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Brain and Behavior Part 2 > Week 4 Lectures > Flashcards

Week 4 Lectures Flashcards

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1
Q

_____ is based on the premise that emotional disorders involve systematic biases, distortions, and/or deficits in thinking that cause people to have exaggerated maladaptive reactions to manageable situations

A

cognitive model

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2
Q

collaborative empiricism

A

cbt is directive and active, psychoeducational, and collaborative between pt and doctor

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3
Q

T/F CBT involves focus on unconscious vs. conscious thought processes.

A

F –> more conscious

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4
Q

schemas

A

unwritten rules by which individuals live their lives and adapt (e.g. unloveability, abandonment, mistrust, incompetence, dependence, entitlement)

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5
Q

T/F CBT focuses on present and future more than the past

A

T

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6
Q

rational responding

A

automatic thought records and open-ended questioning

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7
Q

basic premise of psychodynamic therapy

A

people act the way they do for a reason, though often are not fully aware of these motivations

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8
Q

assumption in psychodynamic therpay

A

patterns develop because of mind’s desire to replay old pain as an attempt to master it –> repetition compulsion

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9
Q

Unorganized instinctual drives

A

id

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10
Q

contact with reality, perception

A

ego

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11
Q

moral compass, thoughts and feelings vs values and ideals

A

super ego

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12
Q

individual deals with internal conflict by falsely attributing his/her own unacknowledged feelings, impulses, thoughts onto others

A

projection

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13
Q

individual has intolerable feelings of powerfulness, unimportance, etc and compensate by attributing exaggerated positive qualities to others

A

idealization

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14
Q

individual deals with disturbing feeligns by describing a situation with excessive use of abstract generalizations

A

intellectualization

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15
Q

individual has intolerable feelings of powerlessness, etc and compensates by exaggerating negative qualities of others

A

devaluation

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16
Q

individual deals with unwanted instincts, ideas, emotions by being unable to remember them

A

repression

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17
Q

acute paroxysms of anxiety indicate

A

panic anxiety –> panic attacks are unconscious conflicted feelings that break through to the surface

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18
Q

transference

A

replay of feelings, thoughts, perceptions about early relationships with the therapist

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19
Q

T/F some amount of anxiety promotes optimal functioning

A

T

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20
Q

Yerkes-Dodson Law

A

medium level of arousal is best for performance

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21
Q

Which GABA receptor is linked to anxiety?

A

A –> allows CL ions t`o enter cell, leading to ap inhibition

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22
Q

Which NE receptor has been more studied in relationship to anxiety and depression?

A

Alpha 2 –> excessive sympathetic activation may produce dysfunctional arousal

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23
Q

Behavioral inhibition

A

anxiety related: timidity and withdrawal in novel situations, exaggerated autonomic and HPA responses, slow habituation, familial trait, predisposed to panic disorder and social phobia

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24
Q

Neuroticism

A

chronic worry with intermittent periods of dysphoria, moderately heritable

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25
Q

Neuroticism is associated with allelic variations in promoter region of ____

A

serotonin transporter gene

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26
Q

Neuroticism is associated with a smaller _____

A

amygdal and cingulate –> abnormal activity of hippocampal and fronto-limbic circuits

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27
Q

T/F Neuroticism predisposes to generalized anxiety disorder

A

T

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28
Q

Reinforcement

A

increases likelihood of behavior

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29
Q

Punishment

A

decreases likelihood of behavior

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30
Q

Mowrer’s Two factor theory

A

anxiety begins with classical conditioning, maintained through operant conditioning (negative reinforcement)

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31
Q

Fear Extinction

A

learning not to fear or new learning and not forgetting –> present CS without US (unconditioned stimuli)

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32
Q

T/F fear response can occur in contexts different than where extinction occurred

A

T –> renewal

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33
Q

Modern Learning theory

A

exposure treatment: new safety learnign to compete with original fear learning; competition resolved by context (internal and external–> time, drug state, therapist office)

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34
Q

T/F extinction learning is particularly context specific

A

T –> must conduct extinction is multipel contexts

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35
Q

T/F Extinction abolishes CS-US association

A

F –> renewal, spontaneous recovery, reinstatement can all occur

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36
Q

Which brain region? stress response

A

locus coeruleus –> noradrenergic

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37
Q

Which brain region? emotional representations

A

Papez circuit –> thalamus to cortex (stream of thinking) to hypothalamus (stream of feeling) and sensory cortex to cingulate

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38
Q

The ___ is responsible to fear in response to cue.

A

Amygdala –>Amygdala essential for fear conditioning regardless of type of stimulus

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39
Q

____ responds to fear in response to context

A

hippocampus and amygdala –>Hippocampus essential for contextual fear conditioning but not for cued conditioning
Consistent with role of hippocampus for spatial and contextual processing

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40
Q

Which anxiety disorder? Excessive or unreasonable fear of specific objects/situations with self-recognition of unreasonable fear w/significant distress and interference with functioning

A

specific phobia

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41
Q

T/F specific phobias have a significant genetic factor

A

T

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42
Q

One session treatment

A

for specific phobia; rapid and effective; durable

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43
Q

Which anxiety disorder? fear of being embarrassed or humiliated in social situations

A

social phobia

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44
Q

Tx for social phobia

A

nefasodoen –> increase in insula, middle frontal gyrus, ACC, hippocampus; decrase in dorsolateral and medial PFC and dorsal ACC (cognitive control and self-reference)

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45
Q

Panic vs anxiety

A

panic = intense, physiological fear (peak in 10 minutes) –> immediate

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46
Q

Which anxiety disorder? persistent unexpected panic attacks w/ fear of other attacks and/or concern about implications

A

panic disorder

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47
Q

Which anxiety disorder? fear of places where might have a panic attack

A

agoraphobia

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48
Q

interoceptive fear

A

greater fear of fear

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49
Q

Tx of panic disorders

A

SSRIs, SNRIs, TCAs, benzos w/low starting dose; cbt –> decreased hippocampus, ACC, cerebellu, pons, medial PFC

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50
Q

Which anxiety disorder? excessive and uncontrollable worry >6 months + sleep, muscle, concentration problems

A

GAD

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51
Q

neurobiology of GAD

A

dampened connectivity between amygdala and ACC/insual –> worry to dampen emotional experience + greater connectivity between amygdala and DLPFC

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52
Q

Which disorder? person experienced/witnessed/confronted with event that involved actual or threatened death or serious injury or threat to physical integrity of self or others with response involving intense fear, helplessness, or horror w/ reexperience

A

PTSD (required symptoms > 1 month)

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53
Q

Fear conditioning process

A

CS (e.g. tone) + US (e.g shock ) –> freezing to tone

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54
Q

Traumatic fear conditioning process

A

dark street cs + mugging us= fear of dark streets

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55
Q

T/F PTSD seems to involve impaired fear extinction

A

T

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56
Q

Which fear response return? after passage of time

A

spontaneous recovery

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57
Q

Which fear response return? in specific context

A

contextual renewal

58
Q

Which fear response return? after unpaired US presentation

A

reinstatement

59
Q

Which two memories compete for fear extinction

A

cs + us = fear and cs + no us = no fear –> eg. that was easy in staples vs in dorm room –> context dependence

60
Q

Which part of brain? fear extinction recall

A

vmPFC essential for recalling fear extinction (if no lesion, can recall fear extinction better –> less fear)

61
Q

Hippocampal size in PTSD

A

smaller (fear learning)

62
Q

T/F PTSD tx can restore some morphology of brain

A

T –> increase in hippocampal size

63
Q

Tx of PTSD

A

exposure therapy

64
Q

Prolonged exposure for PTSD

A

analog of fear extinction: imaginal and in vivo exposure + discussion and reflection

65
Q

T/F neuromodulation can be invasive or non-invasive

A

T

66
Q

T/F ECT is more effective than medication for depression

A

T

67
Q

T/F a contraindication for ECT is cognitive impairment

A

T

68
Q

Antidepressant effect of ECT may be mediated by increased ____

A

BDNF

69
Q

T/F hypoxia is an important surgical risk for ECT

A

T –> have to pre-oxygenate

70
Q

Why is anesthetic followed by muscle relaxant in ECT?

A

to reduce physical risks of seizures

71
Q

T/F sine currents are associated with worse outcomes in ECT

A

T –> instead use alternating current

72
Q

T/F narrower time of current application in ECT has better outcomes

A

T

73
Q

3 factors positively correlated with ECT

A

quality of seizure (higher frequency EEG spikes), duration of seizure, degree of postictal suppression

74
Q

T/F ECT has 100% relapse rate if stop treatment

A

T –>effectively 100%

75
Q

Key benefit of TMS

A

can non-invasively target specific locations in brain –> stimulation AND inhibition depending on frequency

76
Q

T/F no cognitive side effects with TMS

A

T

77
Q

Main indication for TMS

A

depression

78
Q

3 factors influencing effectiveness of rTMS

A

duration, intensity, number of pulses

79
Q

Vagal nerve stimulation

A

stimulus applied to left vagus –> initially for epilepsy, now antidepressant

80
Q

DBS

A

electrodes implanted through burr holes and placed using sterotactic neurosurgery –> parkinson’s/essential tremor, epilepsy

81
Q

Which brain area affected by bipolar/unipolar depression?

A

Cg25

82
Q

Which disorder? unwanted thoughts, images, impulses that cause marked anxiety/distress//not simply excessive worries about real-life problems

A

OCD

83
Q

Doubting obsession

A

e.g. i know i left the oven on

84
Q

Compulsions

A

repetitive behaviors or mental acts performed in response to obsessions: neutralizing –> anxious, try to fix it, anxious, try to fix it, cyclical

85
Q

Area of CBT focus for OCD

A

breaking link between obsession (distress) and compulsion (relief) –> break cycle

86
Q

In OCD CBT: prolonged confrontation with anxiety-evoking stimuli

A

Exposure in vivo

87
Q

In OCD CBT: prolonged imaginal confrontation with feared disasters

A

imaginal episode

88
Q

In OCD CBT: blocking of compulsions

A

ritual prevention

89
Q

In OCD CBT: correcting erroneous cognitions

A

cognitive interventions

90
Q

Primary OCD scale

A

Y-BOCS

91
Q

Tx of OCD

A

SSRI

92
Q

T/F combination CBT and medication therapy for OCD provides additional benefits over meds alone

A

T

93
Q

“the guilty act” objective element of a crime

A

actus reas

94
Q

“the guilty mind” subjective element of a crime needed to produce criminal liability

A

mens rea

95
Q

levels of culpability

A

1st degree/purpose, 2nd degree/knowledge, 3rd degree/recklessness, negligence

96
Q

2 ways to negate actus rea

A

argue you have the wrong person or argue did not commit the act

97
Q

2 ways to negate mens rea

A

self defense or insanity

98
Q

3 reasons why the insanity defense is important to the law

A

protects fairness of law, would otherwise be useless as a deterrent, constitution forbids cruel and unusual punishment

99
Q

Legal standards for insanity

A

m’naghten standard, american law inst. model penal code, irresistible impulse test, durham test

100
Q

M’Naghten test

A

every defendant is presumed to be sane unless he is laboring under a defect of reason from a disease of the mind as not to know the nature and quality of the act he was doing or if he did know it that he did not know that what he was doing was wrong

101
Q

Which test? would the defendant commit behavior if a policeman was at his elbow/right there?

A

irresistible impulse–> difficult to evaluate impulses

102
Q

Which test? If the crime would be a product of the disease, then insanity is automatically the charge.

A

Durham Rule

103
Q

Key cases in defining mental illness

A

McDonald vs. US and Washington vs. US

104
Q

Which test? person is not responsible if at time of event lacked substantial capacity to appreciate criminality of conduct or to conform his conduct to the law as a result of mental disease

A

model penal code of american law institute

105
Q

Which act shifted burden of proof of insanity to defendant?

A

insanity defense reform act of 1984

106
Q

Guilty but mentally ill

A

conviction and criminal sentence –> hospitalized and then prison

107
Q

psychoactive ingredient in marijuana

A

THC

108
Q

T/F marijuana use as an adolescent is linked to schizophrenia incidence

A

T

109
Q

marijuana withdrawal syndrome

A

dysphoria, anorexia, irritability, anxiety, nonspecific somatic complaints

110
Q

marijuana urine test effective in what time span

A

8-96 hours

111
Q

cannabinoid receptors in immune cells

A

cb2:: lymphocytes > macrophages > cytokines

112
Q

cannabinoid receptors in organs and fat

A

cb1

113
Q

which receptors do endogenous cannabinoids bind?

A

cb1 > cb2

114
Q

stimulant epidemics driven by low/high perceived risk and decreasing/increasing supply

A

low and increasing

115
Q

Cocaine administration

A

iv/snort of cocaine powder and smoking of crack cocaine (free base)

116
Q

Cocaine mx

A

blocks dopamine transporter and increases amount of dopamine in the synapse (but also really complex with other nt)

117
Q

Acute effects of cocaine

A

euphoria, racing thoughts, increased hr and bp, anorexia, delusions, anxiety

118
Q

Cocaine is metabolized by ____ and it’s main metabolite is

A

plasma esterases and benzylethylene

119
Q

speedball

A

cocaine and heroin–> enhances positive effects of both drugs, reduce some of the down effects of cocaine

120
Q

cocaine and alcohol

A

most common combo –> reduces anxiety, cocaethylene is psychoactive

121
Q

CNS toxicity of cocaine

A

seizures and stroke

122
Q

Cardiac complications of cocaine

A

chest pain, MI, cardiomyopathy, myocarditis

123
Q

Medical problems of cocaine

A

hyperpyrexia, intestinal ischemia, perforated nasal symptom, crack baby

124
Q

T/F cocaine produces long-term sensitization

A

T –> increased AMPA receptor activity in response to cocaine use –> increased desire to use cocaine

125
Q

T/F cocaine affects cortex

A

T –> reduction in gray matter in prefrontal cortex

126
Q

Process of cocaine addiction

A

increased drug salience and reduced impulse control result in addiction

127
Q

Tx of cocaine dependence

A

few withdrawal symptoms (sleepiness, deprx) –> require inpatient care (at least 30 days) –> less than 1/2 clean at 6 months after treatment // topiramate, disulfuram cocaine vax (relapse prevention)

128
Q

Counseling in cocaine dependence

A

individual drug counseling > group > cbt > supportive therapy

129
Q

contingency management

A

chances to win prizes for clean urine tests have proven to be most effective psychosocial approach to cocaine addiction

130
Q

What is best tx for cocaine addiction in long term?

A

CBT

131
Q

Topiramate MOA in cocaine dependence

A

gaba agonist feedback and glutamate antagonist feedback to dopaminergic neurons in VTA –> less dopamine release with cocaine

132
Q

Disulfuram MOA in cocaine dependence

A

dopamine b hydroxylase blocker –> increase dopamine and reduce NE –> reduce cocaine high // reduce plasma esterase

133
Q

Cocaine vax –> TACD

A

attach cocaine to cholera –> make Ab to cocaine

134
Q

Methamphetamine

A

like cocaine but lasts longer

135
Q

HP Benzodiazepines with short half life

A

alprazolam, lorazepam, triazolam –> most abusable b/c of short half life and high potency

136
Q

HP Benzodiazepines with long half life

A

clonazepam

137
Q

LP benzodiazepines with short half life

A

oxazepam, temazepam

138
Q

LP benzodiazepines with long half life

A

diazepam, flurazepam, chlorazepate, chlordiazepoxside –> alcohol withdrawal

139
Q

benzo MOA

A

gaba a binding –> anticonvulsant, anti anxiety –> cross tolerant with alcohol –> withdrawal treatment

140
Q

benzo withdrawal

A

CNS excitation/seizures because brain has adjusted to benzo use

141
Q

Compare a POD user vs. heroin dependent patient

A

younger, briefer addiction, less overall use, less likely to inject, more psychosocially stable

142
Q

pseudo addiction

A

looks like addiction but disappears with adequate meds

Brain and Behavior Part 2 (6 decks)

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