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Neur 101 > Psychopathology > Flashcards

Psychopathology Flashcards

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1
Q

Biopsychosocial Model

A

Brings together biological, psychological and sociocultural factors to understand abnormal (atypical) behavior

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2
Q

What is schizophrenia?

A

It is defined as split mind’
It is common psychosis
negative=> lack of function/ behavior
=> positives mean more behavior
-Broad spectrum of cognitive and emotional dysfunction => makes lost of connection with real world.
- Can disrupt perception, thought, speech, and movement

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3
Q

Downside to SZ

A

Because of its heterogeneity it is not well understood

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4
Q

SZsymptoms (two or more need to diagnose)

A

• delusions
• Hallucination
• Disorganized Speech
• Grossly disorganized or catatonic behavior
• Negative symptoms

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5
Q

Delusions

A

• A system of beliefs that would be seen b most members of society as a misrepresentation of reality
• delusion of grandeur (being famous)
• delusion of persecution ( false powerful enemies)

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6
Q

Hallucinations

A

• The experience of sensory events without any input from the surrounding environment
• Auditory hallucinations are most common

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7
Q

Disorganized speech

A

• word salad & Neologisms
=> making own vocabulary and sentences, incomprehensible
• Jump Topics

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8
Q

Grossly disorganized or catatonic behavior

A

• Erratic motor behavior and emotional reactions
• catatonic => waxy flexible (even can stay in uncomfortable position until someone turn them right)

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9
Q

Negative symptoms

A

• emotional and social withdrawal
• Apathy ( lack of interest)
• poverty of thought or speech

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10
Q

What does the presence of large ventricles indicate?

A

• Atrophy or damage to brain areas bordering ventricles

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11
Q

Specific about structural differences

A

Smaller => hippocampi & Amygdalae
Communication Bridges =>
• Entorhinal cortices
• Parahippocampi
• Cingulate cortex

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12
Q

• Entorhinal cortices
• Parahippocampi
• Cingulate cortex

A

_ communication between cortex and hippo
_ surrounded the hippo
_ error detection and monitoring the reality

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13
Q

Treatment likelihood

A
  • Larger the ventricles=> less the recovery
  • Extend to which neural inputs and outputs are disorganized
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14
Q

Functional differences for SZ

A

Hypofrontality hypothesis
- less metabolic activity in the prefrontal during high cognitive tasks

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15
Q

What causes SZ differences

A

• Genetic and environmental factors
• Likely gene-environment interactions epigenetic effects

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16
Q

What is genetic vulnerability?

A

• Genes are responsible for making some individuals vulnerable to schizophrenia

• In adoption studies, children with biologica parent with schizophrenia more likely to suffer from schizophrenia

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17
Q

Monozygotic disadvantage of SZ

A

• Case of the Genain quadruplets
• Monozygotic
• Time of onset, symptoms and diagnoses, course of disorder, outcomes different

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18
Q

Genome-wide association studies

A

• Ask whether particular genes are associated with particular traits (or disorders)
• Associations between single-nucleotide polymorphisms (SPs) and SZ.

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19
Q

Define SNP

A

It can change the protein/enzyme activity
- by altering the conformation
- inefficient cofactor binding
— lower the enzyme activity

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20
Q

Impacts of SNP

A

• +100 loci containing SPs associated with risk of Sz (+600 genes)
- SP can regulate expression of genes upstream or downstream of loci
- SNP can impact non-protein-coding genes or coding genes

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21
Q

What specific changes these genes bring

A
  • NMDA receptor signaling
  • Immune system
  • Calcium Signaling
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22
Q

How NTs involved in SZ

A

In general: The dopamine system is too active (hyperdopaminergic) in individuals diagnosed with schizophrenia

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23
Q

What is effectiveness of Drugs

A

1970s: Clinical effectiveness of antipsychotic drugs directly related to affinity for DA receptors.

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24
Q

Too much DA signaling is SZ. What is driven by?

A
  • too much DA being made?
  • not enough clearance of DA from synapses
  • too many DA channels
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25
Q

What problem actually cause too much DA activity?
Evidence:

A
  1. The number of DA active transporters (DATs) at the synapse, which are important for clearing excess DA, is not significantly different in Sz patients vs. controls
  2. The amount of tyrosine hydroxylase, an enzyme necessary for DA synthesis, is significantly increased in the substantia nigra in Sz patients, compared to controls
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26
Q

Remain evidence about D2 receptors about SZ

A
  1. Patients that are acutely psychotic (this means they are currently displaying psychotic symptoms) show significantly greater DA release than controls.
  2. In treated patients, there is an increased number of D2 receptors expressed, compared to controls. In untreated patients, there is no difference in D2 receptor number, compared to controls.
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27
Q

What cause the more DA activity

A

• Not an issue with clearance at synapse (evidence from DAT)
• Not an issue of having too many D2 receptors
(but upregulation may be a response to medication)
• More tyrosine hydroxylase - more DA

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28
Q

How do antipsychotics act on SZ?

A
  • Antagonists at D2 receptors
  • Lack of effect
  • NT cannot act
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29
Q

How dosage of drugs impact SZ?

A
  • To be effective, drug must bind optimal
    number of D2 receptor sites
  • < 50% - little to no response
  • > 50% - response increases
  • ~75% - risk of extrapyramidal side
    effects increases
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30
Q

How does an issue with DA relate back to
the actual symptoms?

A

Aberrant salience model:
DA plays a role in assigning motivational salience to internal or external stimuli. In this way, DA determines which stimuli grab our
attention and drive behavior

31
Q

explain ASM in SZ

A
  1. Elevation of DA -> release in absence of
    appropriate stimuli
  2. Dysregulated release leads individual to
    attribute salience to irrelevant stimuli
  3. Everyday occurrences are imbued with a
    sense of inexplicable significance
  4. Individual builds delusions based around
    these occurrences
32
Q

What about negative symptoms relate to ASM?

A
  1. DA dysregulation
  2. Increased ‘noise’ in the system, ‘drowning
    out’ DA signals linked to rewards
  3. Reduced motivational drive
  4. Social withdrawal and neglect of interests
33
Q

Problems with the DA Hypothesis
how patient respond to treatment

A
  • 1/3 of patients show little to no response,
    even with high levels of D2 receptor
    occupancy
  • Don’t respond to manipulations that
    deplete presynaptic DA
34
Q

how functionally not enough the DA hypo. on SZ?

A
  • Too much DA in striatum
  • Not enough DA in prefrontal cortex
    – Hypodopaminergic signaling – associated
    with D1 receptor issues
35
Q
  • Glutamate hypothesis!
A
  • Interaction between DA and Glu systems
  • NMDA antagonists can influence DA
    synthesis and firing patterns
36
Q

recent studies on improving treatment

A

SEP-363856 rose to the top of
the heap. This compound didn’t
touch D2 receptors, the
researchers found, but it
activated two other types of
neural receptors—known as
TAAR1 and 5-HT1A—that help
regulate the synthesis and
release of dopamine. The
mechanisms of the drug aren’t
fully clear, but the researchers
suspect they’ve hit on a new
way to tweak dopamine
signaling.”

37
Q

define mood disorder

A

Psychological disorders in which there is a
primary disturbance of mood (prolonged
emotion that colors the individual’s entire
emotional state)

38
Q

be specific about mood disorders

A

Fundamental experiences of depression and
mania contribute, either singly or together to
all mood disorders

39
Q

Most common example of mood disorder

A
  • Most commonly diagnosed depression
  • Most severe depression
  • Leading disability in the US
  • Symptoms must persist for at least 2
    weeks for diagnosis
40
Q

MDD symptoms

A
  1. Depressed mood most of the day
  2. Reduced interest or pleasure in all or most activities (anhedonia)
  3. Significant weight loss or gain/Significant decrease or increase in
    appetite
  4. Trouble sleeping or sleeping too much
  5. Psychological and physical agitation, or in contrast, lethargy
  6. Fatigue or loss of energy
  7. Feeling worthless or guilty in an excessive or inappropriate manner
  8. Problems in thinking, concentrating, or making decisions
  9. Recurrent thoughts of death or suicide
    v No history of manic episodes
41
Q

most important indicator for MDD

A
  • Physical changes
  • Behavioral and emotional shutdown
42
Q
  • Behavioral and emotional shutdown
A

– anhedonia is more indicative than feeling
sadness, distress, or crying
– anhedonia shows that an individual has low
positive affect, not just high negative affect

43
Q

Structural difference for MDD

A

Individuals diagnosed with MDD
show size reductions in regions in
the limbic system and cortical
structures inolved in
emotional regulation and experience

44
Q

Specific about structural difference on MDD

A
  • Hippocampus
  • Orbitofrontal cortex
  • Sub-Genual Prefrontal Cortex
45
Q

how illness progresses of MDD

A
  • Amygdala size varies
    throughout course of illness
    – Enlarged at onset of illness
    – Reduced as illness progresses
    – Dependent on gender – more
    pronounced reduction in women
46
Q

how severity of symptoms impact

A
  • The more persistent symptoms
    are, the greater the impact on
    brain volume
    – Episodes are longer
    – Multiple episodes
    – Repeated relapses
47
Q

functional difference of MDD

A
  • Hyperactivity of HPA Axis
    (hypothalamic-pituitary-adrenal axis)
    – Feedback loop for
    responding to stress
48
Q

regions involved in the F diff. of MDD

A

Potential role in
volumetric changes in
hippocampus, OFC,
PFC, and amygdala

49
Q

What causes str. & func. Diff. In MDD

A

• Genetic and environmental factors (and their interaction)
• Neurotransmitter Dysregulation

50
Q

Name & Define functional bias of MDD

A

• Mood-congruent emotion processing bias
• Hyperactivation to negative stimuli and hypoactivation to positive stimuli in amygdala

51
Q

What help can given in response to Mood-congruent emotion processing Bias

A

• Lack of ability to regulate negative emotion
• Asked to downregulate negative feelings
- less activation in dorsolateral prefrontal cortex
- Involved in emotion regulation and executive control

52
Q

MDD symptoms related to Mood

A
  1. Depressed mood most of the day
  2. Fatigue or loss of energy
53
Q

Define anhedonia (MDD symptom)

A

Reduced interest or pleasure in all or most of the activities

54
Q

MDD symptoms related to health

A
  1. Significant weight loss or gain
  2. Decrease or increase in appetite
  3. Problems with thinking, concentration or making decisions
  4. Psychological and physical agitation, or in contrast, lethargy
55
Q

MDD symptoms related to feelings

A
  1. Recurrent thoughts of death or suicide
  2. Feeling worthless or guilty in an excessive or inappropriate manner
56
Q

what are the three psychotic drugs?

A

L-Dopa => extracellular concentration of DA increase => Parkinson’s alleviated
Reserpine => Extracellular concentration of DA decrease => no more psychotic symptoms
Amphetamine => Exracellular cenc. of DA increase => Psychotic symptoms.

57
Q

which drugs are bad to take for SZ

A

L-Dopa & Amphetamine

58
Q

define Tardive dyskinesia

A
59
Q

how much genetic factor is involved in the MDD

A

only 2-3% likely that genes would interfere
- MZ vs. Dz chances are 60% vs. 20 %

60
Q

Which of the following is a drug that, used repetitively, produces a psychotic state akin to paranoid schizophrenia?

A

Amphetamine

61
Q

A common movement disorder produced by antipsychotics, called _______, may affect as many as one-third of patients taking those drugs.

A

tardive dyskinesia

62
Q

Which of the following is a positive symptom of schizophrenia?

A

Hallucinations

63
Q

According to the monoamine hypothesis, depression is caused by

A

a decrease in the synaptic activity of connections that use monoamines.

64
Q

The antianxiety effects of benzodiazepines are related to effects on which transmitter?

A

GABA

65
Q

Benzodiazepine drugs have which of the following effects on GABA synapses?

A

Enhancement of GABA-mediated inhibition

66
Q

For monozygotic twins, the concordance rate of schizophrenia is ________, and for dizygotic twins, the concordance rate of schizophrenia is _______.

A

50%; 17%

67
Q

Transgenic mice that express the mutant version of DISC1 that is associated with schizophrenia, are more likely to have _______________.

A

Enlarged ventricles

68
Q

In general, which of the following is FALSE about common treatments for depression?

A

SSRIs are a class of drugs used to encourage reuptake of transmitters at serotonergic synapses.

69
Q

Functional imaging studies indicate that drugs that alleviate symptoms of schizophrenia tend to increase activation of the

A

frontal cortex

70
Q

How much environment effect the genetic factor to happen in case of MDD

A
  • Adoption studies: more likely to
    be depressed if biological parent
    diagnosed with MDD
71
Q

what gene particularly impact MDD according to genomewide association studies

A
  • RRA gene: most strongly
    associated with occurrence of
    MDD
    – Involved in circadian rhythms
72
Q

Environment factors involve in the MDD

A
  • Low SES
  • Minority women
  • Situational factors
    – 62% individuals show signs of depression
    after death of a close family member
73
Q

what kind of environment develop MDD gradually?

A

Expose mouse to aggressive mouse
10 minutes a day for 15 days
Test response to stress and look at
brain – issues reflect changes found
in depressed human patients

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