Week 13: Psychopathology Flashcards

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1
Q

Walter Cannon

A

Fight or flight response is a physiological response to an acute threat (disturbance in homeostasis)

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2
Q

Hans Selye

A

“Stress” is a non-specific physiological response to demand made on the organism

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3
Q

General Adaptation Syndrome

A
  • Alarm
  • Resistance
  • Exhaustion
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4
Q

Bruce McEwen

A

Allostatic Load is the wear and tear of the organism due to repeated allostasis

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5
Q

Allostatic Load Index

A

*Neuroendocrine system (e.g., NE/E, cortisol)
*Cardiovascular system (e.g., blood pressure)
*Metabolic system (e.g., glucose, lipids)
*Immune system (e.g., C-reactive protein (CRP), interlukin-6(IL-6))

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6
Q

Chronic Stress is associated with:

A

*Cardiovascular disease
*Metabolic disorders (e.g.,diabetes)
*Depression
*Anxiety
*Cognitive impairment
*Accelerated biological aging

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7
Q

Schizophrenia

A

*Originally called Dementia Praecox (“premature dementia”
*Schizophrenia(“splitting of mind”), a split between the emotional and intellectual aspects of experience

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8
Q

Schizophrenia Positive symptoms

A

◼Disorganized speech
◼Disorganized behavior
◼Hallucinations
◼Delusions

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9
Q

Schizophrenia Negative symptoms

A

◼Flattened affect and /or anhedonia
◼Speech minimized
◼Lack of motivation
◼Social withdrawal

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10
Q

Schizophrenia Cognitive symptoms

A

◼Poor sustained attention
◼Low psychomotor speed /catatonia
◼Poor learning and memory
◼Poor abstract thinking and problem solving

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11
Q

Schizophrenia symptoms: complex syndrome

A

◼Psychosis
◼Emotional/Affective Symptoms
◼Motivational impairment
◼Cognitive impairment

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12
Q

Schizophrenia: Etiological theories

A
  1. Genetic theories
  2. Neurodevelopment hypotheses
  3. Dopamine-Glutamate hypothesis
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13
Q

Schizophrenia: Genetic Theories

A

◼Twin studies
◼Adoption studies
◼Gene mutation

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14
Q

Schizophrenia: Neurodevelopment hypotheses

A

◼Seasonal effects
◼Neurology of Schizophrenia

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15
Q

Schizophrenic Gene Mutations: DISC1

A

▪Disrupted in Schizophrenia 1 (DISC1)
▪DISC1 protein is important for neurodevelopment
▪Human studies:
▪High prevalence of “broken copy” in large Scottish
family over 5 generations -development of
schizophrenia, bipolar & other mood disorders
▪Meta-analysis confirmed overall association and
found strongest estimate in Chinese population

▪Animal studies:
▪Mutant mice with no DICS1 in brain stem cells show
behaviors that mimic schizophrenia
▪Down regulation of DISC1 in dentate gyrus leads to
schizo-typo behaviors
▪Transgenic mice expressing DISC1 mutation display
enlarged lateral ventricles

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16
Q

Schizophrenic Gene Mutations: NRG1

A

◼Neuregulin 1 (NRG1) protein important for neurodevelopment
◼Association studies:
◼Icelandic population –NRG1risk allele doubles the
risk of schizophrenia
◼Extended to Scottish, Swedish and Chinese
populations
◼NRG1also associated with bipolard disorder and creativity, independent of schizotypal traits

17
Q

Schizophrenic Gene mutations: Recent popular hypothesis

A
  • not just one gene, but new mutations in any one of hundreds of genes

◼Microdeletions and microduplications
◼Found in 15% schizophrenia patients; 20% if onset before 18 years. Compared to 5% in control group.
◼Not random, but selective for genes that are important for production of proteins involved in neurodevelopment and cognitive function.

18
Q

Schizophrenia: Neurodevelopmental Hypothesis

A

suggests abnormalities in the neonatal development of the nervous system leads to mild abnormalities of brain anatomy and major abnormalities in behavior

19
Q

Schizophrenia Risk Factors

A

◼Poor nutrition of the mother during pregnancy
◼Premature birth
◼Low birth weight
◼Complications during delivery
◼Extreme stress of mother during pregnancy
◼Immunological rejection e.g., Rhesus factor(Rh) incompatible
◼Other infections during pregnancy (Toxoplasma gondii)
- Postnatal stressors

20
Q

Schizophrenia Brain abnormalities

A

◼Enlarged lateral ventricle and prominent sulci
◼Decreased tissue cerebral gray matter
◼Smaller cell bodies in PFC and hippocampus
◼Reduced cortical connectivity and activity
◼Glial reductions (glial theory) : oligodendrocytes and myelin integrity (DISC1); altered microglia in temporal and frontal lobes; astrocyte glutamate transporters in PFC
◼Brain “insults” may not be apparent until later

21
Q

Schizophrenia Dopamine Hypothesis

A

◼positive symptoms are caused by over-activity of synapses between DA neurons of the ventral tegmental area (VTA) and nucleus accumbensand amygdala (Mesolimbic)