PSYC 2300 Week 7 Notes
PSYC 2300 Week 7 Notes PSYC 2300
Popular in Abnormal Psychology
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This 13 page Class Notes was uploaded by Liana Sandell on Thursday October 13, 2016. The Class Notes belongs to PSYC 2300 at University of Connecticut taught by Dr. Inge-Marie Eigsti in Fall 2016. Since its upload, it has received 25 views. For similar materials see Abnormal Psychology in Psychology (PSYC) at University of Connecticut.
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Date Created: 10/13/16
Class Notes October 11, 2016 Suicide and MDD (major depressive disorder) 1. people with mood disorders are 20 times more likely to commit suicide than the general population 2. bipolar disorder: 15X Persistent depressive disorder 1. unremitting and unrelenting low mood (graph) 2. depressed mood most days, for at least two years 3. while depressed, presence of 2 or more symptoms: 1. change in appetite 2. sleep change 3. fatigue, lack of energy 4. poor concentration, indecision 5. low self esteem 6. hopelessness Types of PDD (persistent depressive disorder) 1. mild depressive symptoms without any major depressive episodes (with pure dysthymic syndrome) 2. mild depressive symptoms with additional major depressive episodes occurring intermittently (previously called double depression) 3. major depressive episodes lasting 2 or more years (with persistent major depressive episode) Bipolar disorder 1. bipolar disorder I and II (manic depressive disorder 2. alternating episodes of mania and depression 3. “if i see the light at the end of the tunnel, its the light of the oncoming train” (Robert Lowell) Bipolar mood disorders 1. Orange line: depicts typical variability of mood 2. Bipolar I (previously called manic depressive): very high highs and very low low’s 1. most severe form of depression 2. break dancer example in class Manic episode 1. abnormally and persistently elevated or irritable mood, lasting at least a week 2. during this period at least 3 of them: 1. inﬂated self esteem (grandiosity) 2. decreased need for sleep 3. more talkative 4. ﬂight ideas (racing thoughts) 5. distractibility 6. increased goal-directed activity, energy 7. high-risk activity 3. marked by impairment in functioning, risk of self-harm Hypomanic episode 1. less severe version of manic episode: lasting 4 or more days (manic: 1 week), does not impair functioning (manic: does impair functioning) Bipolar I 1. both manic and major depressive episodes 2. one-year prevalence: 0.7% 3. equal gener ratio 4. typical onset: late adolescence or early adulthood 1. but also diagnosed in children— different presentation 5. if untreated, episodes occur Bipolar II (look at graph) 1. at least one amor depressive and one hypomanic episode but no manic episodes 2. one year prevalence: 0.5% 3. equal gener ratio 4. typical onset: late adolescence, early adulthood 1. in children too 5. if untreated episode reoccur DSM-5 Bipolar Disorders (FILL IN) 1. bipolar I 2. bipolar II 1. all between major depressive 3. cyclothymic disorder 1. alternations between less severe depressive and hypomanic periods Cyclothymic disorder 1. chronic version of bipolar disorder 2. alternating between periods of mild depressive symptoms and mild hypomanic symptoms 1. episodes do not met criteria for full major depressive episode, full hypomanic episode or full manic episode) 3. hypomanic or depressive mood states may persist for long periods of time (ex. weeks at a time) 4. must last for at least two years (one year or children and adolescents) Other depressive disorders 1. premenstrual dysphoric disorder 1. signiﬁcant depressive symptoms occurring prior to menses during the majority of cycle, leading to distress or impairment 2. controversial diagnosis 1. advantage: legitimizes the difﬁculties some women face when symptoms are very severe 2. disadvantage: pathologizes an experience may considered to be normal 3. symptoms (above “typical’ level) of: mood swings, irritability, depressed mood, or tension as well as struggles with all of the following activities 1. decreased interest in normal activities, concentration, lethargy, sleep change, appetite change, loss of sense of control, sense of lethargy or fatigue, and discomfort 4. distress Disruptive mood dysregulation disorder 1. severe temper outbursts occurring frequently, against a backdrop of angry or irritable mood 2. diagnosed only in children 6-18 3. criteria for manic/hypomanic episode are not met 4. intended to combat over diagnosis of bipolar disorder in youth 5. symptoms: 1. sever temper outbursts 3X a week for at least a year 2. generally angry or irritable mood Biological correlates of unipolar depression 1. neurotransmitter abnormalities, especially monoamine system concentration in synaptic cleft: 1. differences in concentration in seratonin (5HT) 2. norepinephrine(NE) - catecholamine hypothesis (depletion associated with stress), 3. dopamine (DA) 2. endoctrine dysfunction 1. abnormalities in HPA axis, excess cortisol levels 3. genetic inﬂuence in depression: weak (unipolar) 4. Familial risk of bipolar 1. in contrast there is a strong genetic component of bipolar disease: adoption, family and twin studies links to the 5-HTT gene (“mood gene”) 2. Alfred Lord Tennyson family pedigree studies (he was a poet and this history was found in his poems and writing) 1. 4 of 12 had no symptoms 2. 8 had bipolar and manic depressive or recurrent depression 3. George Gordon or Lord Byron 1. if you look at his personal pedigree, you can see that many of his relatives struggled with suicide, grandeur, murder, Robert Schumann: mania and creativity 1. classical composer 2. died because he starved himself to death as an inmate in an insane asylum 3. 1833: severe depression, 1840: hypomanic, 1844: severe depression, 1849: hypomanic, suicide 1854 4. productivity in his art is tied to periods of low moods (producing very little) and periods of hypomania or mania (producing a lot) Cognitive schemes underlying depression 1. hopelessness: desired outcomes will not occur no matter what action is taken 1. learned hopelessness: a sense that it does not matter whether i move i will be shocked either way 2. global, stable, internal attributions: predict a sense of hopelessness Sample attributions 1. non depressive attribution 1. this is out of my control, i may as well relax (external vs, internal) 2. oh well its only one appointment (speciﬁc vs. global) 3. the trafﬁc jam will clear up eventually (unstable vs. stable) 2. depressive attributions 1. this is completely my fault (external vs. internal) 2. my whole day is ruined i am going to fail because i missed this class (speciﬁc vs. global) (far reaching) 3. the trafﬁc will never clear and i will miss class (unstable vs. stable) Aaron Becks Cognitive Triad 1. depressed people tend to have negative thoughts and interpretations of: 1. themsleves 2. the environment 3. the future 2. depressed individuals experience distorted (irrational) interpretations which are especially triggered by upsetting situations Interpersonal model of depression 1. interpersonal relations tend to: 1. elicit rejections from others 2. exhibit fewer/reduced social skills 3. seek reassurance from others, but it does not “stick” 4. limited social support networks 5. challenge is causality 1. are their social skills caused by depression or the outcome of their depression 2. researches are still trying to understand this What do we do about it 1. social skill training: address interpersonal skills 2. cognitive-behavioral approach (ex. beck and cog. triad) to change though patterns and activity levels 1. effective Cognitive Behavioral Therapy (CBT) 1. trying to help people get over irrational and negative thoughts about themselves, the world around them and the future 2. goal is to identify, monitor, challenge and replace irrational thoughts 1. increase activities to elevate mood 2. identify negative thinking and biases 3. monitor negative thoughts 4. challenge these thoughts 5. replace them with more adaptive and positive attitudes Effective: 5-6/10 people have near elimination of symptoms 1. fast (fewer than 20 sessions) 2. cheap (group therapy) Class Notes October 13, 2016 Situation 1. what happened? Emotion collum: what was the emotion you were feeling? 1. understand their emotions 2. rate how strong the emotion was Automatic thoughts 1. what was the belief or thought you had in the moment 2. how did it make you feel Rational response 3. rethink the belief, write down alternatives 4. rate how convinced Outcome 1. how do you feel now do you feel a little less negative about this ﬁnding? Transmission at the synapse 1. axon receives nerve impulse 2. charge causes it to open and release neurons into presynaptic gap 3. release serotonin or norepinephrine 4. post synaptic receives enough neurotransmitters and then if enough ﬁres message 5. reuptake 6. in people with depression, reuptake is too constant and there is not enough neurotransmitters to reach the post synaptic neuron 7. what antidepressants do is block the reuptake sights in the presynaptic neuron, leaving more neurotransmitters for the postsynaptic neuron Biologically oriented interventions 1. catecholamines (epinepherine, norepinephrine, dopamine) 1. decreased norepinephrine associated with stress, mania and depression 2. serotonin 1. presence of serotonin metabolite (precursor) associated with depression severity 3. MAOIs bind to MAO: this prevents MAO from breaking down catecholamines and other monoamines 1. tricyclics and MAO inhibitors: block reuptake of NE and seratonin; increased presence in the synapse Antidepressants: change neurotransmitter levels in the synaptic cleft 1. older medications (from 1950ss) 1. MAO inhibitors (Nardil, Parnate) 2. slows down production of MAO, which breaks norepinephrine 3. MAOIs potentially pose a serious danger 1. blood pressure may rise to a potentially fatal level if one eats food with tyramine (cheese, bananas, wine) while taking MAOIs 4. Newer MAOIs (reversabile and selectedtive) are less dangerous 2. tricyclic antidepressants (amitriptyline, imipramine) 1. effective and show improvement in 60-65% of patients 1. 6-8 week lag before effects are seen (2 mo) 2. BUT these improvements are short lived: if discontinued when symptoms improve, relapse in a year 1. continuation therapy (continue medication 5 mo after symptoms remit) then there is a decreased risk of relapse 1. maintenance therapy (take medicine for 3 or more years) there is a decrease in relapse 3. side effects: dry mouth, constipation, sedation, weight gain 4. tricyclics mechanism 1. 3 ring molecular structure: “TRI” 2. tricyclics block reuptake and there are increased amount of neurotransmitters in the synapse (looks like image before) 3. selective serotonin reuptake inhibitors (SSRIs) 1. 2nd generation antidepressants: SSRIs, S-norepinephrine-RI’s (SNRI’s) 1. structurally different from MAOIs and tricyclics 2. they are more speciﬁc in that they act on only serotonin or NE 3. ex. ﬂuoxetine (prozac), sertraline (zoloft), paxil, luvox, celexa 4. effectiveness is similar to tricyclics but more popular (newest thing on the scene and more expensive) 5. side effects: less energy, reduced sex drive 4. atypical antidepressants 1. wellbutrin, effexor, serzone, remeron 2. tackle both serotonin and NE systems Treating bipolar disorders 1. mood stabilizing medication 2. most people rely on: 1. lithium 2. depakote, depekene (valproic acid) 1. primarily used for seizure disorders 2. discovered accidentally 3. psychotherapy alone not effective but helpful for: 1. family intervention; medication arrangement; social skills, relationship issues; circadian rhythms or mood cycles (Ellen Frank) 4. long term treatment to reduce relapse rates Lithium therapy 1. discovered as a treatment in 1949 2. seems to be quite effective but ﬁnding correct dose is extremely difﬁcult: 1. no therapeutic effect: <0.5 m Eq/L 2. effective dose: 0.5-0.7m Eq/L 3. mild toxic effect: 1.0m Eq/L 4. poisoning: 2.0m Eq/L 5. (milliequivilents per liter) 3. 60% of manic patients see improvements 4. cycling is less rapid 5. may be a prophylactic (may prevent systems from emerging) 6. most experience fewer new episodes 7. lithium helped a little for symptoms with depressive episodes Suicidality Suicide 1. the intentional ending of one’s own life 1. 11th leading cause of death in the US (2001) 1. twice as many as for AIDS/HIV 2. many are unreported and there is likely a higher rate 2. 3rd leading cause of death for adolescents 3. 4th leading cause of death for 9-12 yo 2. for psychologists, suicide is one of the most serious assessment problems 3. ﬁrearms account for 55% of all suicides Suicide myths 1. people who talk about suicide won’t do it 2. suicidal people act without warning (in reality they usually show signs of pulling away) 3. people who commit suicide are always depressed 4. suicide is a lonely event 5. suicide people clearly want to die 6. thinking about suicide is rare Demographic factors (graphs) 1. Age 1. highest rate: men ages 74 or higher (lack of social support) 2. fastest increase of suicide in teen and young adults (3rd leading cause of death) 2. gender 1. 4:1 (males are more likely to complete suicide) 1. because men are more likely to use ﬁrearms 2. 3:1 (females are more likely to attempt) 3. ethnicity 1. 2:1 (white are more likely than african americans) 1. driver of this difference is social connection 2. extremely high rates of suicide in native americans in the US 1. alcohol rates 80% Red ﬂags for adolescents 1. 9-20% of college students contemplate suicide in a given year 2. indicators 1. fatigue 2. sleep loss, change in sleep patterns 3. decline in school performance 4. writing goodbye letters to friends 5. giving away possessions 6. social withdraw 7. loss of appetite Psychological risk factors 1. loss of interest/ pleasure (anhedonia) 2. hopelessness/helplesness 3. feelings of shame, anger, worthlesness, sadness 4. poor problem solving skills 5. poor self soothing skills (coming up with something that makes you feel better) 6. limited conception of the future 7. impulsivity 8. fantasies of death Biological/genetic risk factors 1. family history of suicide (6X higher to commit) 2. family history of mood disorders 3. personal history of psychological illness 1. higher for those with mood disorder or schizophrenia 4. changes in activity level, sleeping patterns, appetite 5. low serotonin (increased impulsivity) 6. substance abuse/ dependance 1. alcohol in teens Social risk factors 1. previous attempt (39X more likely to complete suicide later on) 1. seems to be that you are training yourself out of that instinctual revoltion 2. lack of social support and social withdrawal 1. seen especially in recent loss of important relationships (highest in those who are recently divorce) 3. acute stressors (loss of job, natural disaster) 4. long term stresses (economic hardship, chronic illness, history of abuse) 5. increase risk taking behaviors (injection of drugs, sexual risky behaviors) 6. suicide contagion: experience of someone committing suicide is covered heavily (modeling) 1. suicide romanticized in media 2. little information about incomplete attempts Protective factors 1. positive life events 2. social support 3. feelings of self efﬁcacy 4. cognitive ﬂexibility and problem solving skills 5. hope 6. strong religious beliefs 7. treatment When someone is suicidal 1. let others know… despite pleas to “keep it a secret” 2. stay in personal contact 3. hospitalization may be necessary Will asking about suicide inspire it?