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PSYC370 Ch 18.pdf

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Department
Psychology
Course
PSYC 370
Professor
Janet L Menard
Semester
Winter

Description
PSYC  370     Chapter  18   Biopsychology  of  psychiatric  disorders     -­‐ Schizophrenia   -­‐ Affective  disorders   -­‐ Anxiety  disorders   -­‐ Tourette’s  syndrome     Psychiatric  disorders:  disorders  of  psychiatric  function  severe  enough  to  require  treatment.     -­‐ Hard  to  diagnose   -­‐ Pathological,  or  at  an  extreme  of  the  normal  range?     Problems  with  diagnosing  from  the  DSM   -­‐ Patients  with  the  same  disorder  often  have  different  symptoms   -­‐ Patients  with  different  disorders  often  have  the  same  symptoms     Schizophrenia     Schizophrenia  –  splitting  of  psychic  functions.  The  original  characteristic  function  was  thought  to   be  lack  of  integration  among  emotion,  thought,  and  action.     Positive  symptoms:  excess  or  distortion  of  normal  function.   -­‐ Delusions   -­‐ Hallucinations   -­‐ Inappropriate  affect   -­‐ Incoherent  speech  or  thought   - Echolalia   -­‐ Odd  behaviour   - Catatonia   - Difficulty  carrying  out  daily  tasks   - Lack  of  hygiene   - Talking  in  rhymes     Negative  symptoms:  reduction  or  loss  of  normal  function.   -­‐ Affective  flattening   -­‐ Alogia   -­‐ Avolition   -­‐ Anhedonia     Alogia:  reduction  or  absence  of  speech.     Avolition:  reduction  or  lack  of  motivation.     Diagnosis:  experiencing  any  two  of  the  above  symptoms  for  at  least  one  month.   18  :  1   PSYC  370     1%  population  incidence   10%  family  incidence   45%  MZ  twins     Current  view  of  the  etiology  is  that  of  a  stress-­‐diathesis  model.       Early  factors  that  increase  risk  of  developing  schizophrenia   -­‐ Birth  complications   -­‐ Early  infections   -­‐ Autoimmune  reactions   -­‐ Toxins   -­‐ Traumatic  injury   -­‐ Stress     Chlorpromazine:  first  discovered  antischizophrenic  drug.   -­‐ Studies  found  that  chlorpromazine  does  not  decrease  extracellular  dopamine  levels,  and   that  it  increases  dopamine  metabolite  levels.  The  conclusion  was  that  chlorpromazine   binds  to  DA  receptors     Reserpine:  drug  isolated  from  the  snakeroot  plant  that  has  been  used  in  treating  schizophrenia.   Works  by  depleting  levels  of  dopamine  in  the  brain.   -­‐ No  longer  used   -­‐ Dangerous  drop  in  blood  pressure     Trends  associated  with  both  drugs   -­‐ Effects  took  2  –  3  weeks     -­‐ Induced  Parkinsonian  symptoms     Recall  that  Parkinsonian  patients  have  depleted  dopamine  in  the  striatum  (caudate  and  putamen).       Dopamine  theory  of  schizophrenia:  posits  that  schizophrenia  is  caused  by  excessive  dopamine   and  that  antischizophrenic  drugs  work  by  decreasing  dopamine  levels.     Receptor  blocker:  mechanism  of  action  of  chlorpromazine;  works  by  binding  to  dopamine   receptors  (so  that  dopamine  molecules  cannot)  without  activating  the  postsynaptic  cell.     With  the  discovery  of  chlorpromazine’s  mechanism  of  action  came  the  amendment  to  the   dopamine  theory:  schizophrenia  is  caused  by  excess  activity  at  the  dopamine  receptors.       Haloperidol:  potent  antischizophrenic  drug  that  has  a  low  affinity  for  dopamine  receptors  (where   most  effective  antischizophrenic  have  a  high  affinity).       Neuroleptics:  antischizophrenic  drugs.           18  :  2   PSYC  370     Phenothizines:  chemical  class  of  drug  that  includes  chlorpromazine.   -­‐ Bind  to  D  1nd  D recepto2      Butyrophenones:  chemical  class  of  drug  that  includes  haloperidol.   -­‐ Bind  to  D  2eceptors  only     The  discovery  that  haloperidol  works  when  it  only  binds  to  D  receptors  lead  to  yet  an2ther   amendment  to  the  dopamine  theory  of  schizophrenia:  schizophrenia  is  caused  by  excessive   activity  at  dopamine  D  receptors. 2    It  is  now  acknowledged  that  the  revised  dopamine  theory  still  does  not  account  for  all  research   findings.     Limitations  of  the  dopamine  theory.     1. Receptors  other  than  D receptors  are  implic2    in  schizophrenia.     -­‐ Glutamate,  GABA,  and  serotonin  have  all  been  implicated     Atypical  neuroleptics:  antischizophrenic  medications  that  do  not  bind  to  D receptors.   2   -­‐ Weight  gain,  diabetes,  fat  dysregulation     -­‐ Consider  the  implications  that  atypical  neuroleptics  can  work  in  treating  schizophrenia     Clozapine:  atypical  neuroleptic  that  has  affinities  for  the  following  receptor  types.     -­‐ D 1   -­‐ D 4   -­‐ Several  serotonin  receptors     Atypical  neuroleptics  do  not  cause  Parkinsonian  side  effects.       2. It  takes  weeks  for  neuroleptics  to  reduce  symptoms.     -­‐ And  yet,  neuroleptics  block  D  receptors  with2n  hours     3. Schizophrenia  is  associated  with  widespread  brain  damage.     -­‐ Reductions  in  gray  and  white  matter   -­‐ Drastic  reductions  in  the  temporal  lobes     -­‐ Patients  present  with  significant  brain   damage   -­‐ Damage  increases  with  time   -­‐ Rates  of  degradation  are  not  constant   across  brain  structures     18  :  3   PSYC  370     4. Neuroleptics  are  only  marginally  effective.     -­‐ Do  not  help  all  patients  (about  1  in  7)   -­‐ Effects  are  small   -­‐ 74%  dropout  rate  (due  to  unpleasant  side  effects)     Affective  disorders:  depression  and  mania     Affective  disorders:  psychiatric  disorders  characterized  by  disturbances  in  emotion  or  mood;   also  called  mood  disorders.     Bipolar  affective  disorder  versus  unipolar  affective  disorder.     Reactive  depression:  triggered  by  an  external  event,  such  as  a  death.     Endogenous  depression:  not  triggered  by  any  apparent  external  cause.     10%  incidence  rate  for  clinical  depression   15%  for  bipolar  disorder   5%  suicide  rate  of  those  experiencing  clinical  depression     -­‐ Women  twice  as  likely  to  have  unipolar  affective  disorder   -­‐ Equal  rates  for  bipolar  affective  disorder     60%  concordance  of  affective  disorders  in  MZ  twins   15%  in  DZ  twins     Stress  has  not  shown  to  be  a  predictor  of  clinical  depression,  despite  the  fact  that  many  people   think  that  they  two  are  related.  Extreme  stress  manifests  as  PTSD.     Seasonal  affective  disorder:  symptoms  of  depression  and  lethargy  that  occur  in  the  winter.   -­‐ Sunlight   -­‐ Can  be  treated  with  light  therapy     Postpartum  depression:  sustained  depression  after  giving  birth.     Antidepressant  drugs.     -­‐ MAO  inhibitors   -­‐ Tricyclic  antidepressants   -­‐ Selective  monoamine  reuptake  inhibitors   -­‐ Mood  stabilizers     Iproniazid:  first  antidepressant  discovered,  beloning  to  the  MAO  inhibitor  family.     18  :  4   PSYC  370     MAO  inhibitors:  increase  levels  of  monoamines  (norepinephrine  and  serotonin)  in  the  brain  by   inhibiting  monoamine  oxidase,  which  normally  breaks  down  the  NTs.       Cheese  effect:  certain  foods  can  have  lethal  side  effects  when  taken  with  MAO  inhibitors.     -­‐ Foods  that  contain  tyramine  (elevates  blood  pressure),  which  is  normally  broken  down  by   monoamine  oxidase     Imipramine:  tricyclic  antidepressant.     -­‐ Block  serotonin  and  norepinephrine  reuptake     SSRIs  are  widely  popular  because  they  have  few  side  effects  and  can  be  used  for  multiple   disorders  (?)     Mood  stabilizers:  treat  depression  without  inducing  mania  (or  vice  versa).     -­‐ Lithium   -­‐ Unknown  mechanism  of  action   -­‐ Treatment  of  epilepsy     ~~     Abnormal  structures  in  patients  with  affective  disorders   -­‐ Amygdala   -­‐ Anterior  cingulate  cortex     No  model  of  the  cause  of  depression  adequately  addresses  its  frequent  co-­‐occurrence  with  mania.     Support  for  a  diathesis-­‐stress  model   -­‐ Depressed  individuals  release  more  stress  hormones     Severe  depression  can  be  treated  with  brain  stimulation  to  the  anterior  cingulate  cortex.                                   18  :  5   PSYC  370     Anxiety  disorders     Anxiety:  chronic  fear  that  persists  in  the  absence  of  any  direct  threat.       Anxiety  disorder:  when  levels/duration  of  anxiety  interrupts  normal  functioning.   -­‐ Anxiety   -­‐ Physiological  stress  reactions   - Tachychardia   - Hypertension   - Nausea     - Breathing  difficulties   - Sleep  disturbances   - High  glucocorticoid  levels     Classes  of  anxiety  disorders   -­‐ Generalized  anxiety  disorders:  stress  responses  and  extreme  anxiety  that  persist  in  the   absence  of  any  threatening  stimulus.     -­‐ Phobic  anxiety  disorders:  stress  responses  and  extreme  anxiety  in  response  to  a   particular  conditioned  stimulus.     -­‐ Panic  disorders:  rapid  onset  attacks  of  extreme  anxiety  and  severe  stress  symptoms.     -­‐ Obsessive-­‐compulsive  disorder:  characterized  by  uncontrollable,  recurring  anxiety-­‐ provoking  thoughts  (obsessions)  and  impulses  (compulsions).     -­‐ Post-­‐traumatic  stress  disorder:  persistent  psychological  distress  following  exposure  to   an  extremely  stressful  event.     30  –  40%  heritability  of  anxiety  disorders     Pharmacological  treatment  of  anxiety  disorders   -­‐ Benzodiazepines     -­‐ Serotonin  agonists   -­‐ Antidepressants     Benzodiazepines:  anxiolytic  drug  that  also  acts  as  a  hypnotic,  anticonvulsant,  and  muscle   relaxant.  Work  on  the  GABA  system.  Should  only  be  used  as  a  short-­‐term  drug.     10%  of  all  Americans  take  benzodiazepines  –  most  prescribed  psychoactive  drug               18  :  6   PSYC  370     Side  effects  of  benzodiazepines   -­‐ Sedation   -­‐ Ataxia  (disruption  of  motor
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