Chapter 16: Schizophrenia, Affective Disorders, Anxiety Disorders, And OCD Flashcards

1
Q

Schizophrenia

A

Serious mental disorder characterized by disordered thoughts, delusions, hallucinations, and bizarre behaviors

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2
Q

Schizophrenia: Positive Symptoms

A

Presence of unusual behaviors, in excess of typical functioning

- Thought disorders
- Delusions
- Hallucinations
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3
Q

Thought Disorders

A

Disorganized, irrational thinking

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4
Q

Delusions

A

Believe that is clearly contradiction to reality (persecution, grandeur, and control)

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5
Q

Hallucinations

A

Perception of nonexistent object or events

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6
Q

Schizophrenia: Negative Symptoms

A

Absence or decrease in some typical behaviors

- Social withdrawal, lack of affect, anhedonia, and reduced motivation

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7
Q

Schizophrenia: Cognitive Symptoms

A

Cognitive deficits
- Difficulty sustaining attention, low psychomotor speed, deficits in learning and memory, poor abstract thinking, poor problem solving

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8
Q

Genetic Factors of Schizophrenia

A
  • Heritability plays a role, but no “schizophrenia gene”
  • Evidence of susceptibility to develop schizophrenia, but triggered by other factors
  • Higher rate in monochorionic monozygotic twins
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9
Q

Schizophrenia Mutations

A

Mutations of DISC1 gene increases likelihood of schizophrenia and other mental disorders

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10
Q

Schizophrenia Paternal Age

A

Children of older fathers are more likely to develop schizophrenia
- Increased likelihood of mutations in chromosome of cells that produce sperms (mutations in spermatocyte)

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11
Q

Schizophrenia Epigenetic

A
  • Rare mutations of epigenetic factors may predispose people to schizophrenia
  • Methylation leads to suppression of gene
    • DNA is wound more tightly
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12
Q

Epidemiology

A

Study of distribution and causes of diseases in populations

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13
Q

Environmental Factors of Schizophrenia

A
  • Season of birth
  • Viral epidemics
  • Vitamin D deficiency
  • Population density
  • Prenatal stress
  • Substance abuse
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14
Q

Seasonality Effect

A

Increased incident of schizophrenia in people born during late winter and early spring

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15
Q

Dopamine hypothesis

A

Positive symptoms of schizophrenia are caused by hyperactivity of dopaminergic synapses in the mesolimbic pathway

- Drugs acting as agonists produce and reinforce positive symptoms
- brain may contain more dopamine receptors
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16
Q

D2 receptors and Schizophrenia

A

Increased in people with schizophrenia, but not main reason for schizophrenia

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17
Q

Chlorpromazine

A

DA-R blocker antipsychotic drug

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18
Q

Mesolimbic Dopamine Pathway and Schizophrenia

A
  • Drugs acting as agonists produce and reinforce positive symptoms
  • Some studies show those diagnosed with schizophrenia release excessive dopamine; brains may contain more dopamine receptors
  • Certain thoughts are hijacking the mesolimbic system
    • More DA
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19
Q

Consequences of Long-Term Drug Treatment of Schizophrenia

A
  • Early drugs used for treatment had side effects
    • Parkinson’s-like symptoms
    • Tardive dyskinesia
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20
Q

Tardive Dyskinesia

A

Opposite of Parkinson’s

- involuntary movements of face and neck
- Supersensitivity of D2 receptors in caudate nucleus
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21
Q

Supersensitivity

A

Caused by damage to afferent axons or long-term blockage of NT release

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22
Q

Hypofrontality

A

Decreased activity of PFC (especially DLPFC)

- believed to be responsible for negative symptoms
- may also be responsible for hyperactivity in the mesolimbic pathways related to positive symptoms
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23
Q

Atypical Antipsychotics

A

Unlike original antipsychotics, they increase DAergic activity in PFC and reduce it in mesolimbic system
- Aripiprazole

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24
Q

Clozapine

A

Blocks D4-R in NAc

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25
Q

Aripiprazole

A

Acts as a partial agonist at DA-R

- Increase DA activity in PFC (low DA)
- Decrease DA activity in mesolimbic system (high DA)
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26
Q

Glutamate hypothesis

A

Decreased Glu activity (resulting in hypofrontality) may contribute to negative and positive symptoms

- Chronic low doses of Glu antagonist drugs produces negative and cognitive symptoms
- PCP and ketamine (indirect NMDA antagonists)
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27
Q

Developmental Changes Theories in Schizophrenia

A
  1. Abnormalities (suppressed DISC1 expression) in pyramidal neurons of the PFC are primary cause of process that leads to schizophrenia
  2. Abnormalities in the striatal DA system are primary causes of process that leads to schizophrenia
    • result of inhibitory GABAergic transmission in DLPFC
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28
Q

Affective Disorders

A
  • Characterized by disorder feelings
  • Two main types
    • Bipolar disorder
    • Major depressive disorder (MDD)
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29
Q

Bipolar Disorder

A

Cyclical periods of mania and depression

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30
Q

Major Depressive Disorder (MDD)

A

Unremitting depression or period of depression that don’t alternate with period of trauma

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31
Q

Genetic factors of Affective disorders

A
  • Heritability suggests genetic anomalies

- RORA, GRM8, and RORB genes all have associations with affective disorders

32
Q

Antidepressants

A
  • MAO inhibitors
  • Tricyclic antidepressants
  • Selective serotonin reuptake inhibitors (SSRIs)
  • Serotonin and norepinephrine reuptake inhibitors (SNRIs)
  • Ketamine
  • Lithium
33
Q

MAO Inhibitors

A

5-HT and catecholamines DA, Epi, and NE

34
Q

Tricyclic Antidepressants

A

Inhibit reuptake of 5-HT and NE

35
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A

Prozac, Celexa, and Paxil

36
Q

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)

A
  • Antagonist action on NAergic transporters

- Milnacipran, duloxetine, and venlafaxine

37
Q

Therapeutic Lag

A

Period of time between beginning antidepressant treatment and experiencing therapeutic effects
- autoreceptor densensitization

38
Q

Ketamine

A

For treatment resistant depression

39
Q

Treatment resistant depression

A

MDD whose symptoms aren’t relieved after trials of different treatment methods

40
Q

Lithium

A
  • For bipolar
  • Taken as LiCO4
  • positive response within 1-2 weeks
  • side effects: hand tremors, weight gain, excessive urine production, and thirst
  • Eliminates mania
  • increased gray matter= neural.glial growth
41
Q

Electroconvulsive Therapy

A

Involves brief electrical shock used to induce a seizure

- used to treat mania and depression
- decreased brain activity and increased seizure threshold
- rapid effects
- risk of cognitive impairment or memory loss
42
Q

Vagus Nerve Stimulation

A
  • Indirect form of brain stimulation, but doesn’t induce seizures
  • Used for treatment-resistant depression
43
Q

Transcranial Magnetic Stimulation

A
  • TMS provides similar benefits to ECT without risk of cognitive impairments or memory loss
  • Used to treat depression
44
Q

Deep Brain Stimulation

A
  • useful for treatment-resistant depression

- implanted electrodes under subgenual anterior cingulate cortex

45
Q

Subgenual ACC

A

Focal point in regulation of mood

46
Q

Depressed patients show hyperactivity of […] along with decreased activity in […]

A

Depressed patients show hyperactivity of subgenual ACC along with decreased activity in DLPFC. VLPFC, VMPFC, and orbitofrontal cortex

47
Q

Monoamine Hypothesis

A

Depression is caused by insufficient activity of monoaminergic neurons
- roles of norepinephrine and 5-HT

48
Q

Tryptophan Depletion Procedure

A

Procedure involved low-Trp diet and Trp-free amino acid “cocktail” that lowers brain Trp and decrease synthesis of 5-HT

- Depletion of Trp in brain causes recurrence of depressive symptoms
- 5-HT plays a role in mood, although exact nature is unknown
49
Q

5-HT transporter and depression

A
  • stressful life events increase probability of depression for those with 1-2 copies of short alleles for 5-HTT promoter
    • less likely to respond to treatment
50
Q

Neurogenesis and Depression

A
  • Stress and depression are associated with reduced hippocampal neurogenesis (dentate gyrus)
  • Antidepressant treatment increases hippocampal neurogenesis in lab animals
51
Q

Exercise and Neurogenesis

A

Increased blood volume in dentate gyrus leads to neurogenesis

52
Q

Circadian Rhythms and Depression

A
  • Sleep disturbances
  • Sleep deprivation can reduce depression in some people
  • Seasonal affective disorder
53
Q

Seasonal Affective Disorder

A

Mood disorder characterized by depression, lethargy, sleep disturbances, and craving for carbs during winter season when days are short

- can be treated by phototherapy
- genetic basis: allele of gene responsible for production of melanopsin
54
Q

Phototherapy

A

Treatment of SAD by daily exposure to bright light

55
Q

Sleep and Depression

A

Reduced sleep latency, reduced REM latency, lack of slow-wave sleep, and general fragmentation of sleep

56
Q

Anxiety Disorders

A
  • Characterized by unrealistic, unfounded fear and anxiety
    • Most common psychiatric disorder
  • Overactive ANS
    • Panic disorder
    • Generalized anxiety disorder
    • Social anxiety disorder
57
Q

Panic Disorder

A

Episodic attacks of acute anxiety

- Anticipatory Anxiety
- Agoraphobia
58
Q

Anticipatory Anxiety

A

Fear of having panic attack

59
Q

Agoraphobia

A

Fear of being away from home or other protected places

60
Q

Generalized Anxiety Disorder

A

Excessive anxiety and worry serious enough to cause disruption of person’s life

61
Q

Social Anxiety Disorder

A

Excessive fear of being exposed to scrutiny of other people that leads to avoidance of social situations in which person is called on to perform

62
Q

Anxiety and Genetic Factors

A
  • Genes for BDNF protein likely play a role
63
Q

Anxiety Biology

A
  • Increased activation of amygdala

- Decreased of VLPFC

64
Q

BDNF

A

Neuronal survival and differentiation during development and LYP

65
Q

Amygdala and vmPFC: Anxiety

A

Adolescents with generalized anxiety disorder show increased activation amygdala and decreased activation of vmPFC
- vmPFC-role in extinction and inhibition of fear and anxiety

66
Q

Anxiety Pharmacological Treatment

A
  • Benzodiazepines

- SSRIs

67
Q

Benzodiazepines: Anxiety

A
  • Bind to GABAa-R
  • Fast acting; often used for emergency treatment
  • Less appropriate for long-term treatment
68
Q

SSRIs: Anxiety

A
  • Preferred treatment option

- Used in conjunction with cognitive behavior therapy

69
Q

Obsessive-Compulsive Disorder

A
  • Individuals experience unwanted thoughts and uncontrollable behaviors
    • Commonly begin in young adulthood
  • Four categories: counting, checking, cleaning, and avoidance
70
Q

Obsession

A

Unwanted thought or idea with which person is preoccupied

- also seen in schizophrenia

71
Q

Compulsion

A

Feeling that one is obliged to perform a behavior

72
Q

OCD Genetics

A

Heredity plays a role

73
Q

OCD Environment

A
  • Brain damage at birth, encephalitis, and head trauma
  • Group A b-hemolytic infection
    • Autoimmune disorder
74
Q

Brain changes OCD

A
  • Damage to the basal ganglia, cingulate gyrus or PFC
  • There was an increase in size to the basal ganglia for those with b-hemolytic streptococcus
  • Increased activity of frontal lobe and caudate nucleus in those with OCD
75
Q

OCD Drug Therapies

A

Serotonergic agonists such as clomipramine, fluoxetine, and fluvoxamine used for treating OCD

- Clomipramine also used for three other compulsions
- Symptoms relieved by increasing the activity of serotonergic pathways with inhibitory role in behaviors
76
Q

Deep Brain Stimulation: OCD

A

DBS in basal ganglia or subthalamic nucleus

77
Q

Serotonin can be seen in 3 different compulsions

A

Trichotillomania, onychophagia, and actual lick dermatitis