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Exam 3 Flashcards

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1
Q

Addiction qualifications

A
  1. Loss of control: can’t cut back
  2. Social impairments: compulsion to use despite cost (finances)
  3. Risky use:physical danger
  4. Pharmacological indicators: tolerance and withdrawal
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2
Q

Tolerance

A

Need for increased dose to achieve high or avoid feeling bad

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3
Q

Relapse triggers

A

Emotional: negative emotions(stress)
Environmental: drug paired cues(place)
Exposure: drug itself

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4
Q

Mesolimbic dopamine reward pathway

A

Brains natural reward system that includes prefrontal cortex, nucleus accumbens, ventral tegmental area

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5
Q

Drugs hijack what to make individual seek drug instead

A

Mesolimbic dopamine reward pathway

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6
Q

How does the brain respond when cocaine is take

A

Dopamine increases in the synaptic cleft because cocaine blocks dopamine re-uptake pump

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7
Q

Extinction learning define

A

Removing the pairing of a cue with the reward such that they lose their association

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8
Q

With addiction, even with extinction learning, what can still occur

A

Renewal: relapse when exposed to drug associated environment
Reinstatement: relapse when exposed to drug itself
Spontaneous recovery: relapse by passage of time

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9
Q

reconsolidation

A

Stable memories become susceptible to change every time they’re retrieved, altering the memory

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10
Q

Reconsolidation window

A

10 mins

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11
Q

How did xue reduce heroin cravings in humans

A

Day 1: baseline cue induced heroin craving
Day 2: 5 min retrieval of heroin memories
10min reconsolidation window
60 min extinction training
Cue induced heroin craving

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12
Q

Extinction training steps

A
  1. Pics of heroin use
  2. Videos of heroin use
  3. Handling heroin paraphernalia

But no drug use so it unpairs drug from cues

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13
Q

Prefrontal cortex useless facts

A

Present in mammals

Associated with expansion of cognitive abilities

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14
Q

Prefrontal cortex functions

A

Abstract reasoning, executive function, social behavior, personality

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15
Q

Core deficits with PFC lesions

A

Motor planning, gaze, speech
Loss of complex thinking
Impaired response inhibition
Increased impulsivity, inspired social behavior, personality change

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16
Q

Matrix reasoning test: what it tests and effected by lesion where

A

Logic and abstraction, sensitive to front lobe damage

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17
Q

Wisconsin cars sorting test: tests?

A

Ability to adapt to rules of experimenter

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18
Q

Stroop task tests and affected by lesions where

A

Ability to juggle saying color not word, sensitive to frontal and anterior cingulate deficits

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19
Q

Anterior cingulate

A

Connects limbic system and pfc

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20
Q

Iowa gambling task: tests and affected by lesion where

A

Impulsivity, Pfc

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21
Q

Tower construction tasks tests

A

Planning

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22
Q

Verbal fluency: letter fluency

A

Being able to name a bunch of words that start with letter x

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23
Q

Category fluency

A

Being able to name animals

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24
Q

Trail making test part B: protocol and what it tests

A

Sequence numbers and layers by connecting dots

Sensitive to task switching deficits, needs intact working memory, reaction time is key measure, and measures executive function

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25
Frontal temporal dementia symptoms
Poor judgement, apathy, and compulsive overeasting, overall impulsivity, no clear life goals
26
People with FTD will do well with what but badly on what
Well with visiospatial and language functions, bad with tasks of generation and executive function
27
Emotion definition
Feeling that differs from a persons normal affective state(baseline); a biological function of the NS
28
3 central attributes of emotions
Change in physiological arousal Affective(feeling) response, which may be pleasant or unpleasant Capacity to motivate a specific behavioral response
29
James Lange Theory
View that physiological changes occur in response to an event. Emotion is the interpretation of the physiological response.
30
Cannon Bard theory
View that an event activates the thalamus, which stimulates the cerebral cortex to produce the feeling component(the experience) of the emotion and at the same time stimulates the rest of the body to produce expression of the emotion
31
Schachters cognitive model
View that the emotional rxn is caused by attribution of environmental conditions to the physiological arousal experienced
32
Papez Circuit
Emotional expression and experience are mediated by a system of interconnected forebrain structures: Cingulate gyrus, hippo, entorhinal cortex, mammillary body, anterior thalamic nucleus, hypothalamus, septal nucleus, fornix
33
Primary emotions
Innate, built in, hardwired emotions; processed by limbic systems; amygdala
34
Secondary emotions
Experience of an emotion, the feeling of it, and learning is involved; processes not only by limbic sys but also the prefrontal areas and somatosensory cortices ex:guilt
35
Fear
Construct used to describe seemingly regular relationship of particular sensory inputs and particular motor output Used to recognize both innate danger signals and learned ones
36
The neural system for fear
Sensory info comes into the thalamus A subcortical pathway takes unprocessed info directly to the amygdala A cortical pathway brings this info to the neocortex and hippo, where more detailed representations of experience are constructed. Projections from these regions converge on amygdala
37
Kluver Bucy syndrome
Monkeys w/bilateral temporal lobe desertions showed hyperorality, hypersexuality, visual agnosia, loss of fear
38
Case of SM
Woman with rock for amygdala, has no fear but can experience panic
39
Mood disorders
Major Depression: type of depressive disorder characterized by a depressed mood for more than 2 weeks Dysthymia: chronic low level depression Bipolar disorders: affective disorder characterized by episodes of mania and depression Cyclothymia: bipolar disorder characterized by less intense episodes of mania and depression Hypomania: milder form of mania
40
Depression diagnosis
Depressed mood or loss of interest in activities for more ham 2 weeks, deviates from persons baseline, impaired function, specific symptoms like anhedonia and fatigue
41
Depression associated with
Increased levels of cortisol and glucocorticoids in brain which reduce dendritic spines necessary for structural plasticity
42
Depression associated with reduced dendritic spines in
Hippo
43
Depression causes reduced volume in which brain regions
Hippo, amygdala, entorhinal cortex, basal ganglia, and thalamic nuclei and reduced gray mass in orbitofrontal cortex
44
What doe PET scans show about brain activity with depression
Lower than normal activity during depresssive episodes, reduction especially apparent in left frontal cortex, decreased blood flow and metabolism in cingulate gyrus and basal ganglia as well
45
ECT treatment disadvantage
Disadvantage: high relapse, memory deficits
46
What would work as well as a bilateral application of ECT but with fewer side effects
Right unilateral ECT
47
RTMS alternative to
ECT for depression treatment
48
Alzheimer’s disease
Irreversible and progressive neurodegenerative disorder characterized by gradual loss of memory and other cognitive functions, deficits in activities of daily life, behavior, judgment, personality
49
Pathological hallmarks of Alzheimer’s
Amyloid plaques(protein aggregates) and neurofibrillary tangles( Intracell p tau protein)
50
Symptoms of Alzheimer’s
Gradual memory loss, decline in ability to perform routine tasks, disorientation, impaired judgment, difficulty in learning
51
Genesis implicated in Alzheimer’s
APP, PS1 and 2 and ApoE4
52
ApoE4
Only clearly and reliably identified risk factor for AD but it’s only a risk factor doesn’t mean you’ll get it
53
AD progression symptoms mild thru severe
Mild: loss of recent memory Moderate: delusions, aggression Severe: loss of all reasoning, communication disability
54
AD disrupts 3 essential jobs of neurons :
Communication, metabolism, repair
55
Amyloid plaques
Insoluble extracell deposits which accumulate in the cortex and hippo Composed of AB40 and AB42
56
Neurofibrillary tangles
Bundles of insoluble helical fibers within neurons | Hyperphosphorylated tau proteins that are normally associated with MT
57
How amyloid plaques form
APP protein broken down by B-secretase results in AB fragments=plaques
58
Symptomatic relief of Alzheimer’s through drugs that
Increase amount of Ach in synapses by inhibiting it’s breakdown Or reduce glutamate excitotoxicity
59
How is Down syndrome asssociated w/AD
APP protein coded by gene on chromoseb21, people with a downs got 2 21 chromosomes, increases chance of accumulation of neurotic plaques
60
Schizophrenia
Psychotic disorder involving disturbance of thought, emotion and behavior
61
Characteristics of schizophrenia
Broad impairments, thought disorder, delusions, hallucinations,disorganized speech, inappropriate emotions, catatonia, loss of touch with reality
62
Positive symptoms of schizophrenia
Symptoms that are present, but shouldn’t be ex: hallucinations
63
Negative symptoms
Lack of characteristics that should be present ex: reduced speech, lack of emotion
64
Cognitive deficits
Difficulties w/aspects of cognition can make it hard to live a normal life: memory, attention, planning, decision making
65
Hallucinations
Sensory experiences that happen in absence of environmental stimulation. Hearing voices most common
66
Schizophrenics brain when responding to auditory stimulation during hallucinations
They have a competition between the auditory stimulus and hallucinations so the activity level has a small difference compared to baseline cuz baseline got hallucinations
67
Delusions
Beliefs held w/strong conviction despite evidence to the contrary
68
Delusions of grandeur and persecution
Grandeur: believes they’re special Somehow Persecution: believe they’re being targeted or attacked somehow
69
Thought disorder
Trouble orgnazjnf thoughts and logical connecting them Tangential thoughts Lack of observance for the main subject of discourse
70
Observed psychotic symptoms
Voice speaks ones thoughts out loud Hallucinated voices discussing the person Bodily sensations are imposed by an external force
71
Negative symptom examples
Avolition: lack of energy and inability to persist in routine activities Alogia: reduction in amount or content of speech Anhedonia: inability to experience pleasure Asociality: impairment in forming social relationships
72
Catatonia
Prolonged motor immobility states that alternate with periods of excitability
73
External signs of schizophrenia
``` Train of thought is incomprehensible Incapacity for emotional empathy Delusions Hallucinations Sudden hostility Neglect of everyday obligations ```
74
Cognitive deficits of SZ
``` Verbal fluency Reasoning/problem solving Attention/vigilance Visual and verbal learning/memory Working memory Social learning ```
75
Neural deficits in SZ
Basal ganglia, frontal and occipital lobes, auditory system, hippo , limbic sys
76
Etiology of SZ-causes
Genes but not deterministic genes Early brain damage Stressful episode during adolescence
77
Dendritic spines numbers IN SZ
Low, especially in adulthood
78
SZ treatment stabilizes
Only positive symptoms by stabilizing dopamine based psychotic symptoms
79
NAPLS
Consortium of clinical research programs dedicated to early detection and prevention of psychotic disorders and other forms of serious mental illness
80
Cleckley psychopath
``` Superficial charm Lack of remorse Failure to learn by experience Untruthful Pathologic egocentricity Impaired relationships No life plan ```
81
DSM psycho criteria’s
``` Pervasive pattern of disregard for and violation of the rights of others shown in: Failure to conform to social contracts Deceitful ness Impulsivity Aggressive Consistent irresponsibility Lack of remorse ```
82
Hare psychopathy checklist
Structured interview Collateral info(fam/friends) Assess nature and severity of psychopathy Forensic app
83
HARE psycho criteria
Superficial charm (great stories) Grandiosity(inflated view of self and victim) Deceitful:pathological liar Lack of remorse: no capacity for guilt or concern Lack of empathy: disregard for welfare of others Doesn’t accept responsibility: rationalizes harmful behavior Impulsivity: short attention span Poor behavior control Lacks realist long term goals
84
Brain parts implicated in sz
Orbitofrontal cortex Amygdala Anterior and posterior cingulate, limbic structures

Neuropsych (3 decks)

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