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PSYC 2011.11 Day 9 Notes - 10/15/15

by: Oona Intemann

PSYC 2011.11 Day 9 Notes - 10/15/15 PSYC 2011

Marketplace > George Washington University > Psychlogy > PSYC 2011 > PSYC 2011 11 Day 9 Notes 10 15 15
Oona Intemann
Abnormal Psychology
Woodruff, P

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Abnormal Psychology
Woodruff, P
Class Notes
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This 8 page Class Notes was uploaded by Oona Intemann on Friday October 30, 2015. The Class Notes belongs to PSYC 2011 at George Washington University taught by Woodruff, P in Fall 2015. Since its upload, it has received 83 views. For similar materials see Abnormal Psychology in Psychlogy at George Washington University.


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Date Created: 10/30/15
NOTES THURSDAY 101515 Reading for this week Chapter 8 9 Mood Disorders and Treatment Note on page 17 of the study guide dissociative amnesia episodic not semantic role of self hypnosis put instead under multiple personality disorder a little down the page Mood disorders many different disorders the word affect can be used to describe people who have affected disorders Depression takes many forms The DSM recognizes different categories Maj or depression and dysthymic disorder 0 O O Maj or depression can also be called unipolar depression or clinical depression but they all mean the same thing The person can experience a depressed mood or loss of interest plus at least four other symptoms The individual must experience the symptoms for at least two weeks but usually much longer Has to be severe enough to interfere with one s life Dysthymic disorder less severe but more chronic A person much be experiencing a depressed mood two other symptoms for at least two years The person must never have been without the symptoms for more than a two month period You would use comorbidity with depression if it s paired with something Dysthymic despondency in Greek DSM also describes depression as it could be single episode or recurrent This means there s been at least one previous episode perhaps more There are various forms that depression can take and there are subtypes O O 0 Depression with melancholic features I Inability to experience pleasure anhedonia another Greek word with this the depression is much worse in the morning then eases through the day I They wake up before the want to early morning awakening I Excessive and inappropriate guilt I Signi cant weight los sometimes to the point of anorexia I Slow movement psychomotor retardation Depression with psychotic features I Person has delusions and hallucinations I A person can have a delusion that he or she killed or hurt someone I A hallucination can involve any of the five senses Depression with catatonic features I Catatonic a disorder or movement I Could have excited agitation I Often accompanied by speech disturbances I Person remains in exactly one place often where they have been put for very long periods of time I It s impossible to move them or get them to shift their arms or legs I Signi cant weight gain hypersomnia feeling that your legs and arms are very heavy I Sensitivity to being rejected 0 Depression of postpartum onset I Those symptoms will leave after a few weeks I When it s severe you have the difficulty of the woman not bonding well with the child I There are women who have killed their kids Up until age 15 boys and girls have depression at the same rate After that it s more lopsided The adult ratio might not be accurate because men are much less likely to know that they have it etc they talk less about their feelings or turn to alcohol Set of symptoms Emotion symptoms 0 Sadness Dejection Loss of gratification anhedonia Also three a s anger anxiety agitation Crying spells weeping o Losing feelings of love and affection Motivational symptoms 0 Passivity Having no drive Forcing yourself to go to class work The Noonday Demon memoir about depression Sleep disturbances not sleeping enough etc 0000 0000 Misdiagnosis Endogenous internal factors and exogenous external factors depression DSM doesn t make this decision 0 Endogenous brain cells neurotransmitters hormone levels or genetics 0 Exogenous refers to stressful environmental situations 0 Could be a combination of the two hard to differentiate Theories about the causes of depression ls depression a single disorder Some thing no If you look at the biological evidence regarding the heritability of it is not very strong so it s not genetic But what does seem to be inherited is the predisposition to developing it There are been a lot of studies but many have been small examples 0 Concordance rate of monozygotic and dizygotic differs so that we see something genetic is probably going on Biological depression sometimes results come from a lack of certain neurotransmitters of the brain The neurotransmitters of certain interest have a very speci c amino acid group They re referred to as monoamines o The most important monoamines are a group called catecholamine I They re norepinephrine and dopamine o The other group is called classical tryptamines I They re serotonin and acetylcholine Have different distributions and functions but they all originate in the central part of our brain They all work in similar ways they re all part of a system There s also the catecholamine theory of mood disorder 0 It suggests that depression is associated with an increase of certain levels in the brain catecholamines esp norepinephrine 0 Theory based on the effect of different drugs on mood 0 Medicine called Reserpine used to treat hypertension high blood pressure but also to treat agitation in patients with mental illness 0 It has caused depression in some case 0 It depletes norepinephrine and dopamine 0 And other families of drugs that are antidepressants I MAO inhibitors monoamine oxidase inhibitors and tricyclics increase the activity of the catecholamine so they help the level of norepinephrine and dopamine to be increased I The MAO inhibitors do this by preventing monoamine oxidase from breaking down norepinephrine in the synapses in that way more of it is available I Monoamine oxidase inhibitor means the meds are inhibiting this substance in the synapse from being broken down I The tricyclics block the reuptake of the amines I That part where the little vesicle at the end of the axon takes up the chemical it has released it keeps it from taking it back up I The person who discovered this was a man named Julius Axelrod who worked as a chemist at the NIH GW alumni Won the Nobel Prize in medicine There s also the biological theory of depression 0 Suggests that a deficiency of serotonin contributes to the behavior symptoms of depression 0 It s thought to be a similar mechanism to what s going on with the norepinephrine o It was a breakthrough in the biological understanding of mood disorders but today they are considered too simplistic 0 Just a small part of the explanation I One of the holes in the theory put a patient on the meds and within 24 hours you can test whether they have had an increase in those neurotransmitters norepinephrine and serotonin I But their mood hasn t changed they re still feeling depressed I It could be three or six weeks before the mood changes I How do you explain this if you have an increase in the neurotransmitters It s thought that the presynaptic neurons the ones that squeeze out the chemical produce less of the neurotransmitter at rst with the medication and then go back to a normal level It s also thought that maybe serotonin is a neuromodulator where its primary function is to increase or decrease the activity of other key neurotransmitters The serotonin acting as a neuromodulator may disrupt other neurotransmitters Another current theory is that depression may not be related to increase or decrease of activity of the neurotransmitters but rather a failure in the regulation of the system 0 O 0 Focus that has taken place in the postsynaptic neuron that s where the dendrites are Maybe the receivers are less responsive and the medication may make the receptors more responsive and correct for the lack of sensitivity but it just doesn t happen right away We know that nerve cells can be damaged by stress In addition to knowing this we also know that it can take only one traumatic event in order for there to be a change in both the dendrites and the axons This is what we call epigenetics studying genes and how they can be turned on and off Other theories have looked towards neuroendocrine abnormalities because there s a relationship between hormonal activity and what goes on in our body 0 We have found that people with depression have abnormal electroencephalograms They have altered distribution of REM sleep it s supposed to be longer but it s shorter Seasons can affect this Cortisol is a big factor in depression bodies use this under stress I When it s released into our bloodstream it affects our mood food intake sleep cycle motor activity I Cortisol level is easy to measure drop of blood swab in the mouth I It may be a much better key to understanding depression than serotonin and norepinephrine You can give a person a drug that suppresses release of cortisol from adrenal gland I But what happens if you give it to a depressed person It doesn t suppress the cortisol Another theory involves melatonin 0 You can take this to help you sleep you should wear a sleep mask or sleep in conditions that are as dark as possible When it comes to treatments the antidepressant meds are the most common biological treatments 0 Our textbook has a chart of tricyclics and their structure 0 One of the earliest brands of meds was Elavil I Supposed to elevate your mood o Terphenyl Aphrodil were others 0 Tricyclics work better with commonsymptom people dif culties in sleep and appetite 0 Drugs alter the balance of the biogenetic amines I They increase their activity cause them to have more excited neurotransmitters in the synapse I Blocks the reuptake of norepinephrine and serotonin back into the presynaptic neuron Monoamine oxidase inhibitors 0 Inhibit monoamine oxidase o In the synapse it stops the norepinephrine meaning then it can t excite the dendrites o On bottles of some medications there is a warning if you combine the two it can cause psychotic behavior It might take up to six weeks before a patient notices change The prescribing doctorpsychiatrist may have to increase or decrease the dose in other words triturate it to get one that is the most effective Then repeat dosage for next five months Constant maintenance would be needed sometime for rest of life Effects include dry mouth lack of sexual desire interference with shortterm memory 0 Tricyclics have 65 success rate 0 MAO inhibitors have about 50 0 There is a restriction with the MAO inhibitors I Cannot eat food with tyramine in it see previous notes we ve talked about this 1989 capsule Fluoxetine Prozac o The first SSRI o Paxil followed that then Zoloft Luvox I Appear to alter sensitivity of serotonin receptors I Fewer side effects but there is still a lag time between when medicine is taken and when effects are seen I Biochemically you can see this difference in the brain I There are though two things that can happen tremendous weight gain and loss of interest in sex Starting in 2006 we began research on what some call Special K o Ketamine O I First use it was an anesthetic that vets often used with large animals I Sometimes used in humans also has recreational uses I Related to PCP Phencyclidine Angel Dust I Can have hallucinations with this tend to be fairly mild 2006 study began in patients who were nonresponsive to all other treatments for depression I Patients received the ketamine and within hours the depression lifted even for patients who had been depressed for 27 years I Results lasted for about a week I This is a substance that works on the neurotransmitter glutamate I Currently not approved by the FDA for general use with depression still part of clinical trials I Individuals looking to participate in the study must demonstrate that nothing else has worked for them Another category of antidepressants atypical O O O O Albutren is one of them also Assendin Effexor They operate on multitransmitters systems a number of neurotransmitters They can cause seizures in people Might help some people but they can t take them because of the seizures Question that comes up Why does a drug like Prozac also work in treating panic disorder OCD bulimia premenstrual dysphoric disorder 0 If one drug can help with all of these conditions have we really categorized the illnesses correctly Remember anxiety disorders are often comorbid 2005 study hundreds of studies with thousands of adults taking SSRIs individuals were twice as likely to attempt suicide than those taking the placebo I APA continues to say that it is better to have someone on the SSRIs and monitor them closely than to have them not be taking them at all I Particular concern with children and adolescents I Many parents would say they know it s a risk but they d rather not have their children have the depression I In many countries there is not yet approval for a child to take these medications William Potter National Institute of Mental Health 0 Has been studying drugs that might help with depression Peter Kramer psychiatrist o Wrote a book Listening to Prozac 0 Drug can completely change your personality O 0 When he rst had experience with this there were patients who were not depressed but still wanted Prozac to make them more assertive or pleasant in the workplace He said it was unethical but if you can have plastic surgeons who can change how you look physically can you have medication to change your personality Can we have cosmetic personality change through drugs Other observations with depression in sleep 0 Deprive a person with depression of sleep while on an antidepressant and it works more effectively we don t know why Also ECT treatment we ve had it available for about 75 years see notes from previous classes 0 O O O APA continues to feel this should be used in some cases Other medical authorities think it is a form of brutality About 50000 people receive ECT for depression each year more females than males Normally used if an individual has been unresponsive to any medication and especially if they re suicidal Insulin therapy can also cause seizures 0 O O O O 0 Very dangerous Patient is given a relaxant and something to stabilize the heart Given between 65 and 140 volts to the brain for less than a second Electrodes have to be placed in a very specific way if they are all over the scalp it is more effective but the patient is more likely to have memory loss Usual to have 12 treatments three or four days apart Patient wakes up confused and doesn t remember pain or much of anything Used to be used to control people in mental institutions Seasonal Mood Disorders How do you treat these 0 0 More light in rooms environment Wellbutrin is very helpful but it is suggested to begin taking it in September as the day light hours decrease and stay on it through March 2005 that the FDA approved what we call pacemakers for the brain 0 0 000 Used with severe depression Planted on chest under skin but sends constant current to the vegus nerve which goes up to the brain Two very thin wires that feed up to the left vegus nerve send pulses of electricity Releases serotonin and other neurotransmitters in the brain Low voltage Costs about 25000 0 Not all insurance covers it and it is very expensive for something that might not work but people still use it if they can afford it


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