Anxiety Disorders Notes PDF

WEEK 5: ANXIETY DISORDERS Describe the characteristics of anxiety (lecture, tutorial, ch. 5) 4 types of symptoms of anxiety, 3 components of emotion physiological/somatic symptoms ◦ autonomic bodily responses, changes in ANS ◦ e.g., heart rate, shaking, GI, muscle tension, pupil dilat...

WEEK 5: ANXIETY DISORDERS Describe the characteristics of anxiety (lecture, tutorial, ch. 5) 4 types of symptoms of anxiety, 3 components of emotion physiological/somatic symptoms ◦ autonomic bodily responses, changes in ANS ◦ e.g., heart rate, shaking, GI, muscle tension, pupil dilation, breathing ◦ physiological response is fear/stress response to perceived threat (though absent) cognitive symptoms ◦ alterations in specific thoughts while experiencing emotions ◦ e.g., worries, sense of loss of control behavioural symptoms ◦ consequences of certain emotions/thoughts ◦ e.g., avoidance behaviours, behavioural coping mechanisms (substance use) Describe the differences between adaptive fear and maladaptive anxiety (lecture) anxiety: affective state, individual feels threatened by the potential occurrence of a future event ◦ future oriented ◦ panic: an extreme fear response in the absence of a threat (false alarm) fear: primitive emotion, in response to an imminent threat ◦ present oriented ◦ fear response to an identifiable, objective, current threat ◦ fear response elicits behavioural fight/flight response ‣ reaction of ANS, prepares body for danger, physiological arousal symptoms ‣ evolutionary purpose behind why we get anxious - fear is an evolved response and is necessary for survival to a deemed threat (anxiety experiences this in absence of a threat) fear is adaptive anxiety is maladaptive differentiating between adaptive and maladaptive fear/anxiety ◦ are concerns realistic given circumstances ‣ e.g., being scared of seeing a tiger; but unrealistic fear seeing a tiger on campus (given the circumstances, unrealistic to be scared of seeing a tiger on campus) ◦ is the amount of fear proportionate to the threat ‣ e.g., scared of clowns, sitting in back row of circus is proportionate response to threat, but fully avoiding circus isn't ◦ does the concern persist in absence of the threat maladaptive anxiety causes distress and impairment ◦ lowers quality of life, chronic, frequent, distress, suffering, multiple domains of functiooning are impaired Know the key features and criteria for DSM-5 anxiety disorders (lecture, tutorial, ch. 5) Panic Disorder - PD panic attacks: discrete period of intense fear that develops suddenly and peaks (heightened severity) within minutes ◦ may be associated with other anxiety disorders, but in that case are cued by specific situations/ feared objects; PD the attacks are unexpected panic attack DSM-5 symptoms: 4/13 are required ◦ 10 physiological: ‣ disturbances in heart rate ‣ chest pain/discomfort ‣ trembling/shaking  ‣ paresthesias (numbness/tingling) ‣ sweating ‣ sensations of shortness of breath/smothering ‣ dizziness, unsteadiness, lightheadedness, faintness ‣ nausea ‣ chills/hot flashes ‣ feelings of choking ◦ 3 psychological: ‣ derealization or depersonalization ‣ feeling of losing control or going crazy ‣ fear of dying PD DSM-5 diagnostic criteria ◦ 1. recurrent unexpected panic attacks (4/13 symptoms of panic attacks) ◦ 2. a significant change in behaviour (as a result, ie avoidance) ‣ initially experience the unexpected panic attacks, and have marked apprehension and worry over the possibility of having additional attacks prevalence/course: ◦ panic attacks: 28% ◦ panic disorder: 1.5-3% ◦ attacks are more common higher prevalence ◦ onset late adolescence/adulthood treatment: CBT best, benzos and antidepressants for short term, interceptive exposure (component of CBT) is important Agoraphobia agoraphobia: anxiety about being in places where escape is difficult or panic like symptoms in a place where help is not readily available highly comorbid with PD, differential diagnosis is tricky; panic attack occurrence often instigates agoraphobia diagnosis is made when avoidance is persistent and pervasive ◦ feared situations are actively avoided, endured with extreme anxiety, or require presence of companion agoraphobia DSM-5 diagnostic criteria ◦ 1. marked fear about 2 or more (heightened anxiety) ‣ public transportation ‣ open spaces (e.g., parking lot) ‣ enclosed spaces (e.g., mall) ‣ standing in line/being in a crowd ‣ being outside of home alone ◦ 2. fear of not being able to escape ◦ 3. situations almost always provoke fear ◦ 4. situations are avoided ◦ 5. fear is out of proportion ◦ 6. persistent >6 months treatment: exposure therapy, CBT Generalized Anxiety Disorder - GAD GAD DSM-5 diagnostic criteria ◦ 1. pathological anxiety and worry excessive, for more days than not for at least 6 months about number of events or activities ◦ 2. worry is difficult to control  ◦ 3. symptoms 3+/6 present more days than not past 6 months ‣ restlessness or easily keyed up/on edge ‣ easily fatigued ‣ difficulty concentrating or mind going blank ‣ irritability ‣ muscle tension ‣ sleep disturbance ◦ 4. the focus of the anxiety and worry is not confined to features of an axis I disorder ‣ ie the anxiety isn't about having a panic attack PD or contamination OCD or public SAD; but beyond that worry about everything several things at once multiple domains ◦ 5. cause significant impairment and/or distress in important areas of functioning ◦ 6. differential: not due to substance use, GMC, does not occur only during mood, psychotic, or pervasive developmental disorders prevalence and course: ◦ 9% of population Canada ◦ highly comorbidity with other anxiety disorders ◦ chronic but fluctuates - worsened during times of stress ◦ women at greater risk ◦ most worry about: family, money, work, illness compared to normal worry ◦ people with GAD spend significantly more time worrying (350 minutes GAD person vs 60 minutes normal person) ◦ anxiety experienced is in-proportionate and excessive given set of life stressor compared to what would naturally be elicited in normal person ◦ pathological worry is chronic, excessive, uncontrollable and takes joy out of life treatment: CBT best, improve IU (intolerance of uncertainty) - alleviate anxiety by reducing worry ◦ benzos common for short term but bad for longterm, increase symptoms and relapse develop tolerance and dependence Specific phobias specific phobias DSM-5 diagnostic criteria ◦ 1. marked fear about a specific object/situation ◦ 2. phobic object almost always provokes fear ‣ whenever encountering object, excessive anxiety reaction is produced ◦ 3. situation is always avoided or endured with extreme anxiety ◦ 4. fear is out of proportion (excessive, unreasonable) ◦ 5. impairment/distress interfering with everyday function ◦ 6. persistent >6 months normal fear v phobias: ◦ fear is an adaptive reaction to threats in the environment ‣ natural in childhood and tends to decrease with age ‣ predisposed biological preparedness to certain stimuli that are inherently more threatening ◦ phobias are excessive and unreasonable fear reactions; may be adaptive fears to a perceived threat expressed in a maladaptive way 5 categories of specific phobias ◦ animal ◦ natural environment (ocean, natural disasters, heights) ◦ situational (specific situations, bridges, buses, etc) ◦ blood injection injury ◦ other (illness, choking, vomiting, clowns etc)  prevalence/course: ◦ fears (adaptive): 50% ◦ phobias (maladaptive): 11% - most prevalent of other disorders ◦ having phobia from one subtype/category increases probability of developing another within that category (ie fear of hurricanes leads to fear of oceans) treatment: exposure therapy (in vivo, imaginal, virtual reality) Social Anxiety Disorder - SAD experience fear/anxiety in social situations that is out of proportion to actual threat posed by these situations ◦ often aware that their fears are excessive/unreasonable, but persists overt and covert avoidance => leads to being lonely and isolated SAD DSM-5 diagnostic criteria ◦ 1. marked and persistent fear about one or more social situations ◦ 2. fears they will act in a way the will be negatively evaluated ◦ 3. situation is always avoided or endured with extreme anxiety ◦ 4. fear is out of proportion (excessive, unreasonable) ◦ 5. impairment/distress interfering with everyday function ◦ 6. persistent >6 months ◦ 7. exposure invariably provokes anxiety, sometimes situationally bound panic attack ◦ 8. differential: not due to substance use or GMC or other disorder ◦ may be performance only - fear is restricted to speaking or performing, giving speeches, eating or writing in public prevalence: one of the most prevalent disorders ◦ highly comorbid with substance use, depression, etc treatment: CBGT - cognitive behavioural group therapy, both cognitive restructuring and exposure Describe biological, cognitive, and behavioural factors play a role in anxiety disorders (lecture, tutorial, ch. 5) (Etiology) Etiology PD and Agoraphobia biological runs in families, relatives with PD 5x more likely to develop somatic response elicits a sense of losing control cognitive model subjective threat -> misinterpretation of bodily symptoms -> intensification of bodily symptoms -> increased anxiety and fear 1. pay close attention to bodily sensations ◦ high interceptive awareness - highly aware of changes in their bodily sensations ie increased heart rate or temperature 2. misinterpret bodily sensations ◦ misinterpreting what these physiological changes mean, as something must be threatening and physiological symptoms as a sign something is wrong ◦ physiological responses are consistent with threat response, but there is no threat. this is the misinterpretation 3. snowballing/catastrophic misinterpretations ◦ reaction causes more worries about additional symptoms and more apprehension ◦ intend to reduce sensations but paradoxically increase because ANS fight/flight response to a deemed perceived threat ◦ snowballs and continues until person feels out of control or experiences another panic attack anxiety sensitivity - psychological variable associated with PD, trait like tendency fear of anxiety related physical sensations - due to belief that these somatic sensations have harmful consequences (somatic, psychological, social) that extend beyond the panic episode itself risk factor for anxiety, predicts future occurrence of anxiety symptoms and panic attacks integrated model - *important figure* combination of genetic/cognitive vulnerability alarm theory of panic real danger (objective threat) = real alarm occurs = activate adaptive physiological response to face the threat or flee (fight/flight) alarm system activate instead by emotional cues rather than real danger; perceived threat rather than objective = false alarm with the same fight/flight response induced in absence of threat => panic attack classical conditioning associates panic attack or situation that triggered it with neutral cues (physiological symptoms) = conditioned to fear internal sensations or external stimuli ◦ also develop (conditioned) apprehension about experiencing further panic attacks and associate weak bodily sensations with a full-blown attack ◦ because of anxiety, focus intensely on bodily sensations and the environmental cues present during attack to prepare for or prevent further attack Etiology GAD biological theories GABA theory: people with GAD deficiency in GABA receptors resulting in excessive firing in limbic - without GABA inhibition = excessive firing and reaction genetic theory: biological vulnerability to GAD is inherited ◦ general trait anxiety may increase risks cognitive theories cognitive avoidance theory: worry as an avoidance strategy to avoid physiological arousal associated with anxiety; avoidance is reinforcing, worrying decreases somatic arousal ◦ greater IU (intolerance for uncertainty) = greater reductions in heart rate variability by doing worrying-inducing task - due to worrying to prevent arousal ◦ worry creates unpleasant experiences (negative emotions) contrast avoidance theory: worry to avoid significant changes in emotional states = through worrying, maintain constant state of negativity = less drastic of a change in emotion when experiencing negative events ◦ they do this because they are more sensitive to emotional information and changes in emotional states = they experience more distress when shifting from pleasant to negative emotional states ‣ constant worry reduces the distress that is caused by the shift; with instead shift from unpleasant to negative emotional states beck: people with GAD think about threat constantly ◦ over-predict the likelihood and cost of aversive outcomes ◦ under-predict the ability to cope with aversive outcomes the function of worry: to avoid future threat; as a way to prepare or prevent bad things from happening ◦ seen as a coping strategy ◦ worry is negatively reinforced - avoid negative affect, worry reduces anxiety (uncertainty), thinks bad thing won't happen cause worrying and prepared for it intolerance of uncertainty IU: discomfort ambiguity/uncertainties => leads to anxiety and distress and worrying; people with GAD have a lower tolerance/threshold for life's uncertainties  ◦ selective bias for uncertainty (what if questions) and pay greater attention to threatening and uncertain info and interpret ambiguous info as more threatening ◦ etiological vulnerability factor for GAD - correlated with pathological worry and anxiety Etiology of Specific Phobias biological/psychological vulnerability + experience => specific phobia behavioural theories - associative classical conditioning: associative model pair neutral stimulus with aversive unconditioned stimulus = conditioned startle response to neutral stimulus ◦ caveat: equipotentiality premise assumes that all neutral stimuli have equal potential for becoming phobias (ie lamp vs snake) - select number of stimuli consistently related to phobias ◦ support: little albert operant conditioning: avoidance => decreased anxiety; avoidance behaviours are negatively reinforced ◦ support: exposure is opposite of avoidance, and is most effective in treating specific phobia biological theories non-associative model: evolution = humans have evolved (now predisposed) fear response to select group of stimuli and no learning/conditioning is necessary for fear development ◦ stimuli too dangerous or lethal to have to learn to fear/avoid ie heights, would have to fall from to learn its scary (conditioning) ◦ most people habituate eventually to feared stimulus over time, people with specific phobia to that stimuli fail to habituate ◦ support: there is a genetic contribution to fears; heritability = 35-51% biological preparedness: people are more likely to fear certain types of stimuli; natural selection/evolution result in => predisposition to fear stimuli (objects/situations) that represent threats to our species ◦ this is just predisposition to fear, normal, everyone has biological preparedness ◦ associative learning classical conditioning necessary for phobia development but to stimuli that represent threats disgust sensitivity: people have individual differences in level of disgust reaction to certain stimuli; higher disgust sensitivity (more sensitive to having disgust reaction) = more sensitive to developing specific phobia Etiology SAD biological genetic factors 40% variance in risk for GAD there is inherited predisposition to develop anxiety about social situations rather than the disorder itself behavioural inhibition an early marker risk for SAD brain structures interactions in areas for fear conditioning (amygdala), arousal and stress (HPA axis), monitor negative affect (anterior cingulate cortex, prefrontal and obitofrontal cortex) neurotransmitter dysregulation during stress response - 5Ht, norepinephrine psychosocial negative peer and family influence = develop lack of confidence and negative self focus that creates and reinforces anxiety in social situations ◦ bullying, 92% of adults with GAD were bullied ◦ greater level of parental criticism, overprotection as a child cognitive theory exaggerated likelihood and cost of negative evaluation make negative beliefs and judgements about self and others, process social information  abnormally, greater concern about making mistakes (in general), more doubtful about accuracy of decisions self-focused attention excessive attention inward on self, high in public self conscious, awarenss of self as an object of attention Etiology for Anxiety Disorders barlow's triple vulnerability etiological model of anxiety generalized biological, non-specific psychological, and specific psychological vulnerabilities interact to increase risk generalized biological: biological predisposition for some traits, ie for being high strung, behaviouraly inhibited, nervous, IU, non-specifc psychological: diminished sense of control, low self esteem (internal, overall) specific psychological: experiencing a real danger, false alarm, or vicarious experience (external, specific thing) biological factors genetics family/twin studies: all disorders moderate level of concordance ◦ heritability 30-50% ◦ non-genetic variation accounted for more by individuals specific environmental factors, rather than shared family factors broader genetic risks for temperamental and/or dispositional traits rather than inheiriting specific types of AD, inherit risk factor traits ◦ ie behavioural inhibition - tendency of children to respond to new situations with heightened arousal) and neuroticism (dispositional tendency to experience negative emotions) ◦ individual differences in these = early risk factor for developing AD< when co-occurring with stressors neuroanatomy/NT neural fear circuit: sensory info registered at thalamus -> amygdala -> hypothalamus -> thru midbrain area preiaquaductal grey -> brain stem spinal cord -> connect to autonomic output components for expression of fear ◦ autonomic physiological components, heart rate, bp, body temp, GI GABA inhibitory and receptors distributed along fear circuit, anxiolytic medication acts on GABA mediated inhibition of fear system psychological factors behavioural factors pavolv, watson - anxiety and fear acquisition thru learning two factor theory: acquisition of fears and maintenance of anxiety ◦ fear development = classical conditioning - perviously neutral stimulus paired with inherently negative stimulus UCS (frightening event) = CS ◦ fear maintenance = operant conditioning - avoidance, negative reinforcement caveat: not all fears develop thru CC ◦ develop by vicarious learning (observing reactions of other people) ◦ can develop fears by hearing fear relevant information ◦ we are biologically prepared to fear certain types of stimuli cognitive factors beck's cognitive model for anxiety: people experience fear because of biased perceptions about the world, future, and themselves ◦ world = dangerous, future = uncertain, themself = unable to cope with life threats ◦ core beliefs that they are helpless and vulnerable; they selectively attend to/recall info consistent with their biased perceptions interpersonal factors  ◦ anxious parents interact with children in ways less warm and positive, more critical and catastrophic, less granting of autonomy ◦ parents can protect against anxiety with challenging parenting behaviour - encourage risk taking, outside comfort zones to foster self-efficacy in dealing with unfamiliar/frightening situations ◦ early attachment relationship contribute to anxiety development - leads to development of general belief systems (internal working models) for how relationships operate in general ‣ anxious-ambivalent attachment (inconsistent emotional parenting) = fear of abandonment = predict anxiety in adulthood Know effective treatments for anxiety disorders (lecture, tutorial, ch. 5) most effective: CBT and exposure therapy pharmacotherapy caveat: teach that symptoms are pathological, can only be controlled with medication benzodiazepines: anxiolytic drugs; bind GABA receptor sites, inhibits activity (like brain systems for generating fear/anxiety) ◦ relieve physiological symptoms, short term rapid relief ◦ many side affects, many negative ones antidepressants: most widely used and effective anxiolytic medication ◦ MAOIs - interfere with monoamine oxidase enzyme ◦ TCAs - block norepinephrine and 5HT reuptake ‣ especially effective for OCD ◦ SSRIs - most well prescribed ◦ SNRIs - 5Ht, dopamine, norepinephrine ◦ anticonvulsant pregabalin for GAD SAD cognitive restructuring CBT based on idea: anxiety disorders due to maladaptive, unhealthy, faulty thinking patterns ◦ thoughts of future-oriented, looming imminent threat ◦ over-estimate probability and severity of threats (risk) and underestimate ability to cope (resources) goal: help patients develop healthier more evidence based thoughts to help adjust the imbalance between perceived risk and resource ◦ and find out what deeper beliefs and schemas are triggering patients automatic thoughts principles: ◦ Identifying automatic thoughts ◦ Recognizing cognitive biases the thought record: to understand important relationship between what they're thinking and how they're feeling ◦ increased anxiety, patients ask "what was i thinking before i started to feel this way" ◦ patients learn to monitor and catch their automatic thoughts and beliefs systematically so they can examine the utility and validity of them ‣ patient examine evidence for or against various beliefs ‣ taught strategies for developing more balanced thinking styles ◦ therapist uses the Socratic approach questions to query and evaluate beliefs and behaviours that contribute to anxiety ◦ therapist engage in collaborative empiricism - as a team conceptualize patients difficulties and modify their beliefs exposure techniques facing anxiety provoking stimuli = fears extinguished, new coping skills developed, significant cognitive change habituation: repeated exposure to feared stimulus results in diminished behavioural response  (anxiety) to that stimulus inhibitory learning: anxiety is reduced through repeated exposure learn that the feared stimulus no longer predicts the feared consequence ◦ old fear structures not replaced by new adaptive ones, but continue to compete with new fear structures for activation ◦ goal of exposure therapy not to weaken the original fear associations (like habituation), but learn and strengthen adaptive associations so they overpower the fear associations how exposure works: ◦ Stops the reinforcing effects of avoidance ◦ Allows practice of skills ◦ Provides evidence against irrational/unhelpful thoughts/beliefs systematic desensitization: develops fear hierarchy - list of feared situations/objects in descending order for how much they evoke anxiety ◦ imaginal: imagine feared stimulus combined with relaxation response - work their way up fear hierarchy to increasingly more feared distressing stimuli ◦ rationale: anxiety is learned, conditioned; pairing feared and relaxation = counter- conditioning/ extinction ‣ relaxation incompatible response to anxiety, patient learns to be less anxious in presence of feared object or situation worry imagery exposure: systemic exposure to images of feared stimulus, hold image in mind for 25-30 minute in vivo exposure (real life): more effective than imaginal exposure; inclusion of relaxtion no better response than exposure alone ◦ exposure works optimally when they try to increase its frequency, duration, and intensity ◦ gradual exposure - approaches fear hierarchy from lower level intensity working up over time to face higher-intensity stimuli ◦ flooding/intense exposure - start at very high level of intensity rather than working gradually through hierarchy variants of exposure ◦ social phobia - engage in social interactions ◦ PTSD - write about, describe and recall details of traumatic event (imaginal exposure) to learn the even is a memory rather than an ongoing occurrence ◦ panic disorder - exposed to both external feared situations and internal situations ‣ interoceptive exposure - exposure to internal cues (bodily sensations) e.g. induce physical sensations like dizziness by hyperventilating, spinning in a chair, exercise, etc ◦ OCD - exposure and ritual prevention (response prevention) - promoting abstinence from rituals that, while reducing anxiety in short term, only serve to reinforce the obsession in the long term ◦ agoraphobia - exposure and reduce their subtle avoidance - don't get the full benefit of exposure if they used distraction strategies or engage in other safety behaviours which are covert avoidance strategies that reinforce anxiety in the long run; or engaged in distraction when facing fears problem solving skills ◦ by generating and implementing effective solutions to problems, patients will experience less anxiety ◦ begins with problem-orientation phase; individuals encourages to approach and deal with their problems constructively rather than worry about, avoid, or deny them ‣ teach them that the occurrence of problems is an inevitable part of life rather than sources of threat or harm, and to view anxiety as as signal of a problem that needs to be dealt with rather than as a feeling to get rid of ◦ defining a specific problem, generating a wide range of alternative solutions, deciding on and implementing one or more of the solution-focused strategies, and evaluating the outcome relaxation - directly reduce anxious arousal ◦ mental relaxation, physical relaxation, breathing retaining relaxation Exercises: ◦ can’t be both relaxed and scared at the same time. ◦ Progressive Muscle Relaxation (PMR) we are teaching people to use relaxation techniques like breathing techniques and over time you can train yourself to be less anxiety induced in certain situations. Differentiate the anxiety and related disorders from one another (lecture, ch. 5) Panic Disorder = “fear of fear” Agoraphobia = “fear of places where panic is likely & escape difficult” (being out in public, scared to be out in public and get a panic attack) Generalized Anxiety Disorder = “worry” Social Anxiety Disorder = “fear of social situations” Specific Phobias WEEK 7: OBSESSIVE COMPULSIVE DISORDER AND TRAUMA RELATED DISRODERS Define obsessions and compulsions (lecture, tutorial, ch. 5) obsessions: ◦ 1. recurrent, persistent thoughts, images, impulses experienced as intrusive, uncontrollable, unwanted, and cause anxiety/distress ◦ 2. makes attempts to ignore, suppress, neutralize unwanted obsessions with some other thought or action (neutralizations) through the performance of a compulsion ◦ e.g.: ‣ dirt and contamination ‣ aggressive impulses ‣ sexual thoughts ‣ anti-moral behaviour ‣ doubting/uncertainty ‣ sexuality (homo) ‣ violence compulsions: must serve the purpose of alleviating anxiety ◦ 1. repetitive behaviour or mental acts that they feel compelled/driven to preform ◦ 2. aimed at preventing/reducing distress or preventing some dreaded event or situation ◦ e.g., common compulsions: doubting obsession = checking behaviours ‣ often clear link, sometimes not e.g., fear of ur kid dying if you walk on a crack Describe the diagnostic criteria for OCD (lecture, tutorial, ch. 5) OCD DSM-5 diagnostic criteria 1. presence of either obsessions or compulsions 2. time consuming (>1hr a day) or cause distress 3. not due to substances or medication 4. not better explained by another mental disorder (differential) Understand the biological theories and treatments for OCD (lecture, tutorial, ch. 5) biological theories genetic risk factor heritability 32-40%  fronto-striato-thalamic circuit: excessive activation; structural functional abnormalities ◦ less brain volume in frontal cortex, more brain volume in basal ganglia ◦ orbital frontal cortex, basal ganglia (caudate nucleus), thalamus ‣ basal ganglia control motor behaviours ‣ frontal cortex higher cognitive functioning ◦ obsessions (worries/thoughts) first activated by prefrontal cortex -> message to caudate nucleus -> feedback to thalamus => lead to compulsions (behavioural outcomes) ‣ thalamus hyperactivity and response due to increased signal received from caudate nucleus cingulo-opercular network: hyper activation serotonin hypothesis: abnormalities in 5HT system -> OCD symptoms biological treatments SSRIs for increasing 5HT (supportive of serotonin hypothesis); reduce activity in caudate nuclues and thalamus Understand the Psychological theories and treatments for OCD (lecture, tutorial) cognitive theories comorbid depression/anxiety makes even minor events likely to invoke thoughts (intrusive thoughts) moralistic thinking/ feelings of responsibility and guilt ◦ thought action fusion: equate thoughts and actions- based on 2 irrational thinking beliefs: ‣ 1. having a thought increases probability it will come true ‣ 2. having a thought is the moral equivalent of a particular action behavioural theories compulsions develop through operant conditioning, they are negatively reinforced ◦ using SUDS (subjective units of distress); obsession SUDS rating at 85, decreased to 35 when preforming compulsion ‣ ie compulsion acts to negatively reinforce distress anxiety associated with obsession ◦ prevents proper learning and habitation cognitive behavioural theories problematic, abnormal obsessions are caused by individual's catastrophic misinterpretation of intrusive thoughts - with high levels of personal responsibility, believe that their thoughts can influence the probability that others will be harmed (misinterpret) obsessions persist because of the persons maladaptive attempts to cope with them - ie neutralizations perpetuate the obsessional (problematic, misinterpreted) thinking; and actually increase their frequency (rebound effect) ◦ avoidance + neutralizations = can't learn that the assumptions/beliefs are problematic, and their personal responsibility is incorrect and their misinterpretations; irrational beliefs are instead strengthened by engaging in compulsive behaviours treatment ERP exposure and ritual prevention - form of CBT fort people with OCD; they confront anxiety- provoking stimuli or situations (exposure) while preventing themselves from engaging in avoidance/compulsive behaviours (ritual prevention) ◦ alters the faulty appraisals and beliefs of people with OCD Describe are the diagnostic criteria for PTSD (lecture, tutorial, ch. 5) ptsd consequences occurs after experiencing stressors, a traumatic or stressful life event; and continue to re-experience intrusive, unwanted recollections of the past traumatic event also experience emotional/physiological distress when exposed to internal (bodily) or external cues that remind them in some aspect of the trauma  may experience flashbacks: transient break from reality, may act or feel as if traumatic event is recurring in the present moment, feel like they are reliving the event, intense fear PTSD DSM-5 diagnostic criteria 01 exposure to traumatic event: actual or threatened death, sexual violence; that was experienced with intense fear, helplessness, or horror ◦ directly experiencing trauma ◦ witnessing, in person, an event to others ◦ learning of an event to a close family member ◦ experiencing repeated exposure to aversive details of an event (e.g., first responders collecting human remains) 2. requires presence of 4 symptoms: ◦ a. intrusive symptoms - distressing memories, flashbacks/recalls ◦ b. avoidance - avoiding reminders ot things similar/related to event (cognitive or behavioural) ◦ c. negative alterations in cognition or mood - inability to remember certain aspects of trauma, low/diminished pleasure in activities, black/white thinking of being at fault, exaggerated guilt or self blame, emotional numbing ◦ d. alterations in arousal or reactivity - sleep problems, hypervigiliance (startle response), anger, irritability, outbursts, sleep problems, difficulty concentrating 3. duration >1 month after event 4. impairment and/or distress 5. differential: not due to substance use Know the key difference between PTSD & Acute stress disorder (lecture) acute stress disorder difference: symptoms last between 3 to 30 days post trauma the purpose of this diagnosis rather than PTSD (which requires symptoms for over one month) is to allow people to get help soon after traumatic experience if they are experiencing these symptoms already, rather than waiting for it to develop to PTSD Describe social, psychological, and biological factors contribute to PTSD (lecture, ch. 5) social factors gender differences in prevalence: men greater prevalence of trauma; women more likely probability of PTSD - 2x more likely ◦ possibly due to type of traumatic experience; women more likely sexual assault, child abuse, gender based violence which is 12% of females and 2% of males ◦ women are exposed to more events that are particularly likely (compared to other events) to be associated with PTSD development ◦ women greater susceptibility once exposed to trauma pre-event social risk factors: ◦ sociocultural background, socioeconomic status, education, intelligence ◦ psychiatric history ◦ duration - repeated traumatic experiences = increased risk post-event social risk factors: stronger predictors (crt pre-event factors) ◦ severity, proximity and duration of trauma greatest predictors ◦ severity of trauma - more severe = more likely PTSD ◦ proximity of trauma ‣ if it happened to you = more likely ‣ proximity of perpetrator to you = increased risk ◦ social support - greater social support is protective of PTSD ◦ additional stressors present and experienced after the trauma = more likely ◦ interpersonal trauma (ie related to physical violence or abuse) more likely to develop PTSD  than non-interpersonal trauma (ie car accident, natural disaster) psychological factors personal assumptions - shattered, personal invulnerability ie “Bad things don’t happen to good people” belief pre-existing distress - ie depression, anxiety, increased likelihood of PTSD development coping styles - poor coping styles increase vulnerability biological factors innate alarm system (AIS) - dysfunction brain regions for quick processing and response to threat (amygdala, brainstem, frontotemporal cortex) - PTSD greater activity and connectivity HPA axis for stress response - PTSD decreased cortisol, so less negative feedback of adrenal function, HPA axis more active? amygdala hyperactivity - involved in fear hippocampus shrinkage - volume decrease may be cause or effect of trauma fight/flight response (ANS, HPA axis?) genetics cognitive theories must integrate conflicting previous beliefs (e.g., the world is a safe place, people are good), with the discrepant realities of the trauma they just faced (e.g., rape) ◦ = alter pre-existing beliefs to reflect their traumatic experience (all men are dangerous, the world is bad) and new beliefs can be maladaptive and lead to sense of current and generalized threat = symptoms of chronic arousal, distress, hyper-vigilance PTSD treatments exposure - facing the trauma and discussing it in detail Most evidence for effectiveness Treatment Rationale ◦ Avoidance maintains PTSD symptoms (of memories, emotions, etc) ◦ Confronting fear cues helps process distressing memories, leads to cognitive change, reduces PTSD symptoms Types of Exposure ◦ In-vivo exposure - confronts specific places, people, or situations associated with the trauma ‣ realizes that these are memories rather than ongoing events, make sense of them, and integrate with other aspects of their lives ◦ Imaginal exposure - envisions or describes the trauma ◦ Re-scripting nightmares CPT cognitive processing therapy NET narrative exposure therapy based on CPT - recount traumatic events with goal of contextualizing the cognitions, emotions, and sensory information associated with these events and reducing the distress they cause ◦ creation of an autobiographical life story that reframes their trauma as a chapter of their lives rather than the entire book WEEK 8: MOOD DISORDERS AND SUICIDE Describe the diagnostic criteria for the various mood disorders (lecture, tutorial, ch. 8) MDE: Major Depressive Episode MDE DSM-5 diagnostic criteria (2, with >5/9 symptoms) 1. at least 5/9 symptoms present most of the time for 2 week duration *differenital  ◦ 1. depressed mood or 2. anhedonia - diminished pleasure in normal activities (one or both of these must be present for diagnosis) ◦ 3. appetite or weight changes (change in >5% body weight) ◦ 4. sleep changes (insomnia/hypersomnia) ◦ 5. psychomotor changes (retardation/agitation) ◦ 6. loss of energy ◦ 7. difficulty concentrating ◦ 8. feelings of worthlessness / inappropriate guilt ◦ 9. suicidality 2. symptoms cause distress/impairment in important areas of functioning mood/emotional symptoms: depressed mood, anhedonia physical symptoms: appetite, sleep, psychomotor, loss of energy cognitive symptoms: worthlessness, indecisiveness, concentration, suicidality MDD: Major Depressive Disorder MDD: Diagnostic Criteria (3) 1. presence of a MDE (major depressive episode) 2. distress and/or impairment 3. no history of a manic or hypomanic episode PDD: Persistent Depressive Disorder PDD: Diagnostic Criteria (2, with >2/6 symptoms) 1. depressed mood most of the time for >2 years *differential 2. at least >2/6 symptoms present ◦ 1. appetite problems ◦ 2. sleep problems (insomnia/hypersomnia) ◦ 3. low energy ◦ 4. low self-esteem ◦ 5. poor concentration ◦ 6. feelings of hopelessness Bipolar Disorders (I &II) manic episode: distinct period of abnormally persistently elevated expansive or irritable mood abnormally persistently increased goal-directed activity or energy lasting ≥1 week present most of the day, nearly every day hypomanic episode: distinct period of abnormally persistently elevated expansive or irritable mood abnormally persistently increased goal-directed activity or energy lasting ≥4 consecutive days symptoms: 3 required (BD1 = 1-10; BD2 = 1-7 only) ◦ 1. increased self-esteem/grandiosity ◦ 2. pressured speak/ more talkative ◦ 3. decreased need for sleep ◦ 4. increased goal directed activities ◦ 5. distractibility ◦ 6. flight of ideas ◦ 7. increased high risk activities ◦ 8. marked impairment in functioning (manic only, BD1) ◦ 9. psychotic features (manic only, BD1) ◦ 10. necessary hospitalization (manic only, BD1) Bipolar I (manic-depressive episode) ≥1 lifetime manic episodes  history of MDE not required but often present may also have hypomanic episodes just full manic episode required Bipolar II ≥1 MDE ≥1 hypomanic episodes no history of manic episodes, cannot be present hypomania + depression Cyclothymic Disorder 1. hypomanic episodes + sub-clinical depression symptoms for ≥2 years ◦ but cannot experience MDE or full manic episodes 2. for 2 months, no symptom free period (ie not depressive or hypomanic) 3. clinically significant distress and/or impairment Describe the key differences between major depression, persistent depressive disorder, Bipolar I, Bipolar II, cyclothymia (lecture, ch. 8) MDD vs PDD duration: MDD=2 week; PDD = >2 years ◦ in symptoms for PDD noted as problems rather than changes, cause persistent MDD episodic, PDD chronic - both recurrent episodes compared to MDD; PDD is: ◦ more impairment ◦ younger age of onset ◦ higher rates of comorbidity ◦ stronger family history influence ◦ higher levels of stress ◦ higher levels of dysfunctional personality traits MDD MDE present, impairment/distress, no manic episode MDE >2 week duration compared to grief/loss: ◦ MDD: depressed mood is persistent, decreased ability to feel pleasure (anhedonia), worthlessness/self-loathing, feeling undeserving of life and unable to cope ◦ grief/loss: wave/pangs of grief and depressive thoughts related to loss, positive affect not as changed some moments of pleasure in between, self-esteem generally maintained, thoughts of death or joining the loss prevalence: ◦ sex difference - 10% women, 5% men but 2:1 sex ratio women more likely sex difference ‣ biological factors: genetic predispositions and hormones contributing to sex difference; ‣ social factors: socioeconomic, discrimination, socialization, abuse victimization ◦ indigenous communities more prevalence course: episodic (6-12 months), following a stressor, 5-6 across lifetime; recurrence risk decreases with longer periods of remission associated features: ◦ elevated suicide risk (2-5%) ◦ physical pain ◦ comorbidity: anxiety, substance use disorders, OCD PDD depressed mood most of the time for >2 years duration, with 2 symptoms (appetite, sleep, energy,  concentration, self-esteem, hopelessness problems) prevalence: lifetime, 3% course: onset before 21, chronic, recurrent MDEs Bipolar I vs Bipolar II vs Cyclothymic Disorder differs in presence of episodes BD1: MDE often but not necessary, full manic episode, hypomanic not necessary ◦ just mania required BD2: MDE necessary, full manic episodes cannot be present, hypomanic episodes ◦ depression + hypomania cyclothymia: hypomanic, subclinical depression Manic vs Hypomanic Episode duration: manic episode at least 1 week; hypomanic episode 4 consecutive days ◦ manic episode any duration with hospitalization manic episode if any of the following 3 are present (and is not hypomanic): ◦ marked impairment in functioning ◦ psychotic features ◦ necessary hospitalization hypomanic/manic episodes last between 2 weeks and 4 months; depressive episodes 6-9 months both - suicide rates 10-15% BD1: prevalence: equally common in men and women, lifetime prevalence 0.6% course: age of onset 18 years, recurrent, chronic BD2: prevalence: equally common in men and women, lifetime prevalence 0.3% (less common) course: may be reluctant to take mood stabilizer cause hypomania as enjoyable CD: prevalence: 0.4-1% (greater than BD); equal in men and women, but women seek treatment more often course: chronic but less severe form of BD Understand biological, psychological, and social theories of the etiology of mood disorders (lecture, tutorial, ch. 8) biological theories genetics - mood disorders run in families; heritability: MDD=0.36; BD=0.75 - greater for BD ◦ MDD increase likelihood of developing depression ◦ BD increase likelihood of developing any mood disorder (more general) adoption studies: BD concordance 32% bio parents, 12% adoptive (double) twin studies: ◦ MDD concordance higher in MZ (50%), DZ (25%) (double) ◦ BD concordance higher in MZ (65%), DZ (15) much higher NT - dysfunction in depression 5HT underactivity: MDD less receptors, less binding at synapse, less action, lower transmission ◦ purpose: mood, anxiety, aggression, eating, sleeping, pain, sexual behaviour, memory NE low: severe depression, BD (most depression not low NE) ◦ purpose: arousal, energy, activity, appetite treatment - first antidepressants tricyclics and MAOi increase 5HT and NE DA low: if 5HT low, so is DA, ◦ purpose: reward, mood, attention, activity; low = reduced experience of pleasure (anhedonia)  full mania - low DA triggers hyperactivity/psychosis; abnormal NE trigger euphoria/grandiosity; low 5HT (inhibitory) = activation/disinhibition of behaviours =. wide swings between depression and mania biopsychosocial theory: environmental events can affect biological aspects (gene expression, brain functioning) leading to increased vulnerability e.g., early life stress -> altered gene expression in hippocampus -> greater HPA stress response in adulthood (increased vulnerability for depression) cognitive theories - of depression beck's cognitive model people with depression = more likely to appraise situations negatively (negative appraisals) = more likely to experience negative mood in response to such situations ◦ emotional response to situation determined by matter situation is appraised ◦ situations not inherently negative, but interpreted as such ◦ negative appraisals - applying cognitive distortions to ambiguous situations = negative mood depressive schema is formed; negative cognitive style associated with depression ◦ schema core beliefs about cognitive triad (self, world, future) ◦ negative depressive schema develop early in life from negative experience early in life, then makes negative appraisals due to schema a diathesis stress model: negative depressive schemas inactive vulnerability factors until activated and primed by a stress event that matches the theme of the schema depressive self-schema -> faulty information processing -> self, world, future cognitive biases - maladaptive thoughts depression schemas ◦ all or nothing thinking ◦ over generalization ◦ jumping to conclusions ◦ "should" statements - connection to guilt, anger towards others ◦ emotional reasoning - feel bad therefore everything must be bad, my life must be bad hopelessness model depression results from internal, stable, global view of negative events ◦ e.g., depressed response to negative event: negative events occur (injury) if internal attribution (this is my fault), stable thought (I won't ever be able to change), global (nothing will work out for me) ◦ e.g., non-depressed response to negative event: external (its the other dogs fault), unstable (I won't get hurt next time), global (this is just one injury) non-depressed, self serving bias to positive events are protective ◦ global (i'm the most popular dog in Canada), stable (I'm always fun to play with), internal (its because i have the best personality) interpersonal theories marriage and interpersonal relationships - dissatisfaction = depression social support - lack = depression stress generation hypothesis: individuals with depression are more likely to generate stressful life events in the interpersonal domain (fights, arguments, interpersonal rejection) excessive reassurance seeking: tendency to repeatedly seek assurance about ones worth and lovability from others, regardless of whether such assurances have already been provided ◦ depression prone person may do this after a negative event (ie argument), reassurance may be provided,, but they doubt its sincerity and continues to demand more reassurance ◦ elicits frustration and irritation in others, setting the stage for more interpersonal conflict  (stress generation hypothesis) interpersonal model of depression: people with depression, their interpersonal relationship problems generated by behaviours in their interactions, that cause and maintain depression ◦ a need for interpersonal attachment, support, and acceptance (interpersonal dependency) psychosocial theories of BD stressful life events - may trigger new episode sensitivity to reward - related to DA, reward seeking and needing changes in bodily rhythms/routines - some treatments effective that manage daily routines What are the treatments for mood disorders? (lecture, tutorial, ch. 8) biological treatments depression - antidepressants and shock tricyclics - first antidepressants, block NE reuptake (increase NE) MAOI - inhibit monoamine oxidase SSRIs - block 5HT reuptake ◦ most widely used, less severe side effects ◦ relief after few weeks SSNRIs - block both 5HT and NE reuptake, more stimulant effect than SSRIs ECT (electroconvulsive therapy) - when severe, treatment resistant depression ◦ 6-12 sessions ◦ relieves depression in 50-60% of people but 85% relapse rTMS (repeated transcranial magnetic stimulation) - magnetic fields to alter activity ◦ few side effects, non-invasive, painless bipolar - mood stabilizers lithium - reduce excitatory NT (DA, glutamate); increase inhibitory (GABA); increases proteins to inhibit cell death and increases brain volume in emotional regulation areas anticonvulsants - increase GABA synthesis/release for inhibitory, or decrease glutamate synthesis/release for excitatory atypical antipsychotics - used for schizophrenia, for depressive episodes, controls psychotic symptoms (hallucinations, delusions) or as sedatives (for insomnia, agitation) bipolar is treated as chronic - remain on medication for rest of their life (not MDD), but problem with compliance psychological treatments IPT interpersonal therapy - depression interpersonal + behavioural techniques to help maintain routine targets interpersonal dysfunction 4 areas: ◦ interpersonal disputes - problems in relationships, identify misunderstanding, do problem- solving ◦ role changes - difficulty adapting to a life change, repraise old and new roles, identify problems in adapting, do cognitive restructuring to alter dysfunctional appraisals of new role ◦ grief - listening, work through morning and encourage new relationships ◦ interpersonal deficits - low number of quality relationships, identify personality issues CBT cognitive behavioural therapy - depression address problematic cognitions to reduce vulnerability to depression/mania (beck cognitive model) by teaching them how to be aware of meanings of attributions, and how these contribute to the emotional reactions that follow effectiveness = that of other psychotherapies (IPT) and antidepressants behavioural interventions: behavioural activation, increase number of positive reinforcements,  decrease negative ones ◦ restore and enhance functioning ◦ counteract withdrawal techniques ◦ increase interest/pleasure cognitive interventions: ◦ identify cognitive biases - identify unhelpful/inaccurate thoughts; less automatic and unconscious ◦ monitor negative thoughts - to increase awareness ◦ examine the evidence - actively trying to see how the thought is inaccurate, and how to change it ◦ change core beliefs - change negative self schemas prevention of relapse IPSRT interpersonal and social rhythm therapy - bipolar based on: disruptions in daily routines and interpersonal conflicts cause bipolar episode relapse by teaching them how to regulate routines, cope more effectively with stressful events FFT family-focused therapy - bipolar focus on interpersonal stress within family education for patient and their family members about disorder and effect on patient's functioning, as well as communication and problem-solving training w all members CT cognitive therapy - bipolar taught strategies for bipolar: ◦ 1. how to regularize sleep/daily routines ◦ 2. how to regularly monitor their mood to identify early triggers for manic episode relapse ◦ 3. the importance of medication compliance relative success of medication and CBT with MDD dropout rates: meds> CBT short term effectiveness: meds = CBT long term effectiveness: CBT> meds cost effectiveness: CBT> Define suicide, suicide attempts, and suicidal ideation (lecture & ch. 8) suicidality - any thoughts or behaviours suicidal (attempt, ideation, act) suicide: intentional fatal injury (intent present desire to die, outcome fatal injury death) suicide attempt: intentional non-fatal injury, engages in behaviour with intent to due but doesn't result in death (intent present, outcome non-fatal) suicidal ideation: thoughts of wanting to die, intention but no behaviour no outcome Describe facts about suicide (lecture) worldwide - lots of deaths, more than accidents, war, homicide; one every 40 seconds, 1 million a year canada - 4000 a year, 9th cause of death overall, 2nd in children/young adults; 10 a day suicide deaths: sex difference 4:1 men 4x more likely to die (use means more likely to be successful and result in death) suicide attempts: sex difference 3:1 women 3x more likely to attempt misconceptions proven wrong ◦ peaks around spring, not holidays ◦ most don't leave a note ◦ most are not intoxicated when they die caring letters study - social support, engagement/sense of belongingness is effective Describe the key tenets of the interpersonal theory of suicide (lecture)  suicidal ideation / desire for suicide results from hopelessness to change and 2 beliefs: ◦ thwarted belongingness: disrupted sense of belonging, low social support, proximal risk ‣ e.g., i dont belong anywhere ◦ perceived burdensomeness: feeling like a burden to family/friends, weight on their shoulders causing problems for them and others would be better off in absence; death worth more than life; possible inaccurate view of how their family/friends perceive them ‣ e.g., others would be better off without me capability for suicide needed to result in lethal or near lethal suicide attempts ◦ high pain tolerance (withstand pain involved in suicide behaviour) + ◦ fearlessness of death (not afraid to die) ◦ factors that are acquired over time, possibly unrelated to suicide itself thwarted belongingness + perceived burdensomeness + capability for suicide = lethal (or near lethal) suicide attempts treatment - centred around these tenants decrease burdensomeness increase belongingness ◦ increase social support, feelings of worthiness, helping people interpersonal coping strategies challenging untrue beliefs activities that foster connectedness (leadership, volunteering) crisis intervention - when high risk suicidal first deescalate then therapy ◦ hospitalization, suicide hotline, medication WEEK 9: EATING DISORDERS Describe the diagnostic criteria for the various eating disorders (lecture & ch. 10) AN: anorexia nervosa: food restriction leading to a significantly low weight (relative to age, sex, height) with a fear of gaining weight AN DSM-5 criteria (3) 1. restriction of intake leading to low body weight ◦ low weight defined with BMI (age, height, weight), or failure to make expected weight gain during a period of growth 2. intense fear of weight gain 3. disturbance in body image ◦ preoccupation in appearance, body weight, size, hypervigilant ◦ often linked with low self-esteem; uses body weight/shape as a primary method of determining self-evaluation and worth subtypes (2) 1. restricting subtype - dieting, restrictive eating 2. binging/purging subtype - binge eating episodes (loss of control or overindulgence) with compensatory behaviour ◦ difference between AN binging/purging subtype and bulimia is the low weight characteristic of AN, not bulimia ◦ compensatory behaviour may be excessive exercise as means of weight loss, or purging (and weight loss due to dehydration) associated features (8) perfectionism always cold or baggy clothes food rituals / strict rules  preoccupation with food fidgety/restlessness social withdrawal irritability comorbidity - high with depression, anxiety from the ancel keys minnesota semi-starvation study - found that many features of AN are actually the effects of starvation/food restriction rather than causes or risk factors ◦ decreases in heart rate, emotional instability, difficulty concentrating, decreased sex drive and lethargy, preoccupation with body image, food, food rituals, binging, etc. BN: bulimia nervosa: binge eating episodes (consume large amounts of food or feel out of control while they eat, followed by food restriction period), and after binging try to compensate by purging BN DSM-5 criteria (5) 1. recurrent episodes of binge eating 2. recurrent episodes of compensatory behaviour ◦ e.g., self-induced vomiting, laxative use, fasting, exercise 3. behaviours occur ≥1x week for 3 months 4. self-evaluation unduly influenced by shape/weight 5. not occurring exclusively during an AN what is a binge? objective binge eating episode: eating an amount of food within 2-hour period that is definitely larger that most people would eat in similar conditions subjective binge eating episode: experience a sense of loss of control over eating during episode associated features self-esteem based on weight and shape, greater compared to other things in life (family, friends) ◦ measured with SAWBS (shape and weight based self-esteem inventory), WISE-Q (weight- influenced self-esteem questionnaire) social isolation, depression hard to detect because behaviours done in private cyclical pattern restriction, binge eating, purging (due to physical discomfort, shame, guilt, anxiety) escape from self awareness problems episodes to escape from high levels of aversive self awareness binge shifts focus away from perceived failures and toward behaviour and positive sensations associated with eating BED: binge eating disorder: recurrent binge eating episodes in absence of inappropriate compensatory behaviour; often overweight BED DSM-5 criteria (4, with ≥3/5 symptoms) 1. recurrent episodes of binge eating 2. at least 3/5 symptoms: ◦ 1. eating until feeling uncomfortably full ◦ 2. eating more rapidly than normal ◦ 3. eating alone because of embarrassment ◦ 4. eating when not feeling hungry ◦ 5. feeling disgusted, depressed, or guilty about overeating 3. episodes must occur on average at least 1x week for 3 months 4. significant distress about binge eating present What are biological consequences of eating disorders (lecture & ch. 10) highest mortality rate of all other psychiatric disorders ◦ common cause of death: natural (circulatory collapse, cachexia, multiple organ failure); and non-natural (suicide, accidents) medical complications associated with AN: ◦ starvation symptoms: lanugo (fur/body hair grows as compensatory protection), constipation, cold intolerance ◦ major organ failures: ‣ cardiovascular complications (bradycardia, arrythmia, heart failure) ‣ kidney and liver damage ◦ osteoporosis and related bone fractures ◦ impaired immune functioning medical complications associated with BN: ◦ electrolyte imbalance ◦ erosion dental enamel ◦ enlarged salivary glands ◦ ruptured esophagus ◦ ruptured stomach ◦ impaired renal function (kidneys) ◦ hypokalemia (low K+) ◦ cardiovascular complications Know the general prevalence of anxiety, mood, eating disorders, and suicide (lectures & textbook) Anxiety Disorders and OCD PTSD PD prevalence/course panic attacks: 28% prevalence panic disorder: 1.5-3% prevalence attacks are more common higher prevalence onset late adolescence/adulthood GAD prevalence/course 9% lifetime prevalence chronic but fluctuates, worsened during times of stress women greater risk Specific phobias prevalence/course 11% lifetime prevalence having phobia from one subtype/category increases probability of developing another within that category (ie fear of hurricanes leads to fear of oceans) SAD prevalence/course one of the most prevalent disorders high comorbidity with substance use, depression, etc PTSD prevalence/course women more likely 12% vs 2% OCD????? Mood Disorders MDD prevalence/course women more likely 10% vs 5% men indigenous people more liekly episodic following stressor  elevated suicide rate 2-5% PDD prevalence/course 3% lifetime prevalence onset before 21 chronic BD1 prevalence/course 0.6% lifetime prevalence no sex difference equally common onsent age 18 recurrent, chronic BD2 prevalence/course 0.3% lifetime prevalence no sex difference equally as common CD prevalence/course 0.4-1% lifetime prevalence no sex difference equally as common chronic, less severe form of BD Suicide prevalence/course 4000 a year, 10 a day, 9th cause of death, second for kids and teens suicide deaths - men more common 4x suicide attempts - women more common 3x Eating Disorders: AN prevalence/course 1-2% lifetime prevalence 90% are women (given formal diagnosis and treatment) onset in adolescence chronic standardized mortality rate: 5.86 - high BN prevalence/course 1-3% lifetime prevalence more common women onset adolescence to 30s BED prevalence/course 2-3.5% lifetime prevalence; more common ED more common women (but less sex difference compared to other ED) chronic if untreated - mean duration ~8 years