Final Exam Flashcards

Lectures 9+

1
Q

Define ADHD.

A

Persistent pattern of inattention and/or hyperactivity-impulsivity.

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2
Q

What is hyperactivity as a symptom of ADHD?

A

Excessive motor activity at inappropriate times

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3
Q

What is impulsivity as a symptom of ADHD?

A

Sudden actions that occur without forethought

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4
Q

ADHD begins in _____, DSM5 requires symptoms present before age ______

A

childhood, 12

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5
Q

Name 4 key features of ADHD

A
  1. Must be present in multiple settings (school, home, work)
  2. Context matters (signs of disorder may be absent under close supervision)
  3. Issues affect social life (academic performance, social rejection)
  4. Not considered an intellectual disorder (language, motor, social development delays still occur)
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6
Q

ADHD is ______ in first-degree biological relatives of individuals with ADHD

A

elevated

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7
Q

The cause of ADHD is __% genetic

A

80%

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8
Q

Does food coloring/sugar elevate symptoms of ADHD?

A

No

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9
Q

Is there evidence for gene-environment interactions with ADHD?

A

Yes

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10
Q

What is the most common treatment for ADHD?

A

Psychostimulants

  • Adderall, Ritalin, Dexedrine
  • Non drug treatments don’t seem to be effective
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11
Q

How do psychostimulants treat ADHD?

A
  • Through boosting dopamine and norepinephrine signaling

- ADHD patients have decreased PFC activity, increasing DA/NE increases attention

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12
Q

Post-DSMV, does asperberger’s exist on the autism spectrum?

A

yes, by numerical grade of impairment

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13
Q

Autism prevalence:

1 in ___ births

A

500

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14
Q

Autism Spectrum Disorder prevalence:

1 in ___ births

A

118

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15
Q

3 points for autism’s clinical description?

A
  1. Impaired communication
    - Over literal understanding of language
  2. Impaired social interactions
    - Reading social cues incorrectly
  3. Restricted behavior (interests/activities)
    - Stimming (rocking, yelling, hand flapping)
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16
Q

What is echolalia?

A

Repeating the speech/intonation of others

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17
Q

What is social cognition?

A

How you think about yourself and your social world

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18
Q

What is theory of mind?

A

Ability to attribute mental states to others

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19
Q

What is affective social competence?

A

Ability to send emotional messages to others/read others emotions

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20
Q

ASD is 4 times more common in ___ than ____

A

men, women

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21
Q

Over ____ genes are associated with ASD

A

1000

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22
Q

ASD has an extremely ___ concordance rate (monozygotic twins having same disease)

A

High

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23
Q

Name 4/7 environmental risk factors for ASD. (These must combine with each other)

A
  1. Maternal diet
  2. Maternal smoking
  3. Air pollutant exposure
  4. Poor socioeconomic status
  5. Low maternal education level
  6. Advanced maternal/paternal age
  7. Folic acid status
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24
Q

In terms of neurobiology, ASD is now viewed as an ____ _____ _____?

A

Overall brain reorganization

  • Accelerated brain development early on
  • Morphological abnormalities at microstructural level
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25
Q

How are the immune systems and GI tracts affected by ASD?

A

Heightened immune system, more GI discomfort

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26
Q

What are three theories of ASD?

A
  1. Extreme Male Brain Theory
    - The male brain’s development may be more at risk (due to size, connections, etc)
  2. Prenatal Testosterone
    - Correlated with psychological traits
  3. Mirror Neuron System
    - Many deficits in autism are precisely the skills controlled by motor neurons
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27
Q

What is person first language?

A

Language that acknowledges someone as a person before their personal attributes
- NO ONE IS AN ADDICT

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28
Q

What is reward and who discovered the human system of it?

A

Reward –> Stimuli that is desirable

- Discovered by olds and Milner through intracranial self-stimulation

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29
Q

What circuit is responsible for reward?

A

Mesocorticolimbic dopamine circuit

  • Begins in midbrain in Ventral tegmental area
  • Axons project to limbic and cortex
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30
Q

The VTA produces __ (1) when rewarding stimuli is present and projects to _____ (3)

A

(1) Dopamine
(3) Hippocampus, nucleus accumbens, prefrontal cortex
- Every addictive drug activates this circuit

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31
Q

Addictive drugs lead to ________ dopamine

A

Supraphysiological

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32
Q

Unexpected rewards lead to ____ dopamine release

A

Larger

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33
Q

What is addiction?

A

State of uncontrolled drug use that persists in spite of negative consequences of taking that drug
(Develops over multiple exposures)

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34
Q

Name 3 of the 8 diagnostic criteria for addiction.

A
  1. Using in spite of consequences
  2. Preoccupation with obtaining the drug
  3. Lots of time spent trying to obtain drug
  4. Cravings
  5. Failing to fulfill major role obligations
  6. Tolerance
  7. Withdrawal
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35
Q

What is drug tolerance?

A

Needing an increased quantity to feel the effect

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36
Q

What is drug withdrawal?

A

When behavioral/physiological symptoms occur upon cessation

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37
Q

Define Addiction.

A

A syndrome at the centre of which is loss of control over a reward-seeking behaviour

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38
Q

What are Cannabis’ two main cannabinoids?

A
  1. Delta-9-Tetrahydrocannabinol
    - Main psychoactive ingredient
  2. Cannabidiol
    - Also psychoactive
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39
Q

Loss of ability to retain and coordinate information is?

A

Temporal disintegration

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40
Q

What are the two main cannabinoid receptors?

A
  1. CB1
    - Forebrain
  2. CB2
    - Immune system/brain stem
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41
Q

What are the two endogenous ligands of the eCB system?

A
  1. Anandamide (AEA)
  2. 2-Arachidonoylglyverol (2-AG)
    - Both are retrograde messengers (carry opposite direction in synapse)
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42
Q

How does THC work in the brain?

A
  • Anandamide (AEA) usually binds to presynaptic CB1, inhibiting the release of inhibitory NT’s into synapse
  • THC mimics AEA’s shape, blocking inhibitory NT release, allowing dopamine into synapse
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43
Q

What are 3 harms of chronic cannabis use?

A
  1. Possibility of epigenetic psychosis
  2. Cancers from carcinogens
  3. Increasing baseline anxiety/depression
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44
Q

What is psychosis?

A

The loss of contact with reality

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45
Q

What are 3 myths about schizophrenia?

A
  1. People who have schizophrenia are violent and dangerous
  2. People who have schizophrenia have multiple personalities
  3. People who have schizophrenia see things that aren’t there
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46
Q

What are the three groups of schizophrenia symptoms?

A
  1. Positive symptoms –> Extreme’s of normal experiences
    - Delusions, paranoia, hallucinations (auditory most common)
  2. Negative symptoms –> Deficit or absence of normal behavior
    - Apathy (can’t perform day-to-day), social withdrawal, anhedonia (no pleasure)
  3. Cognitive symptoms –> Erratic speech, motor behavior, and emotion changes
    - Disorganized speech, inappropriate emotions, , disorganized behavior
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47
Q

What is affective flattening?

A

A negative symptom of schizophrenia characterized by the absence of visible emotions and facial expressions

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48
Q

What age is schizophrenia usually diagnosed?

A

Late adolescence/early adulthood

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49
Q

True or False:

There is a clear genetic, prenatal, and stress link to contributing to schizophrenia

A

True

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50
Q

Degree of ____ degradation in Schizophrenia brains is correlated with illness severity.

A

Hippocampus

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51
Q

Anatomical studies of schizophrenic brains show enlarged ______ ______, and a degraded _____.

A

Lateral ventricles, hippocampus

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52
Q

PET scans of schizophrenia brains show dopamine surplus in striatum (part of basal ganglia), this suggests ____ is due to too much dopamine activity.

A

Psychosis

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53
Q

Blocking __ receptors relieves positive symptoms of schizophrenia

A

D2

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54
Q

The ideal drug to treat schizophrenia would block __ and activate __ (dopamine receptors)

A
  • Block D2

- Activate D1

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55
Q

What is a PET scan

A

Positive Emission Tomography

- Detects changes in blood flow through radioactive molecules injected in blood stream

56
Q

Females have ___ the rate of depression than males

A

twice

57
Q

True or False:

Major Depressive Disorder is the most commonly diagnosed mood disorder

A

True

58
Q

Is environment or genetic a larger factor in depression?

A

Environment

59
Q

What is the monoamine hypothesis of depression?

A
  • Suggests depression is caused by reduced synaptic activity of norepinephrine and serotonin (two monoamines)
  • This is based on the effectiveness of monoamine inhibitors/SSRI/SDRI in treating depression
60
Q

Name three pieces of evidence against the monoamine hypothesis of depression

A
  1. There is little evidence that low NT levels in brain cause depression
  2. Long lag between antidepressant consumption and results
  3. Not everyone is cured
61
Q

What is the glucocorticoid hypothesis of depression

A
  • Stressful live events impact etiology of depression

- Dysfunctional regulation in HPA axis contributes to this etiology

62
Q

What is hypercortisolemia?

A

Elevated levels of cortisol is found in the blood at all times of depressed patients

63
Q

How is the HPA Axis related to depression?

A
  • Normally cortisol binds to hippocampus to shut down stress response
  • Depressed people cannot shut this down as easily
  • Continuous cortisol exposure further damages hippocampus
64
Q

How do SSRI’s work?

A

Selective serotonin response inhibitors block serotonin reuptake, leaving serotonin in the synapse

65
Q

What is the link between estrogen’s protection of depression?

A
  • Negative feedback is more effective in presence of estrogen
  • SSRI’s work better when combined with estrogen
66
Q

What are ketamine’s low/high dose effects

A

Low –> Detachment from body, sensation of floating, dreamlike
High Doses –> Lose all mental contact with environment

67
Q

Ketamine is an ______ at NMDA receptor

A

Antagonist, blocks NMDA receptor, reducing AP chance for memory formation

68
Q

All bipolar disorders involve:

A

manic or hypomanic (half mania) plus depressive episodes

69
Q

What defines BP1 disorder?

A
  • Distinct manic episode lasting a week or more
  • Three or more BP symptoms
  • Major depressive episode
70
Q

What defines BP2 disorder?

A
  • Distinct hypomanic episode lasting 4 days
  • Three or more BP symptoms
  • Doesn’t impair social functioning
  • Major depressive episode
71
Q

Name 3/7 Bipolar symptoms of mania

A
  1. Inflated self-esteem
  2. Decreased need for sleep
  3. More talkative
  4. Racing thoughts
  5. Distractibility
  6. Psychomotor agitation
  7. Involvement in activities that have high potential for painful consequences
72
Q

Rapid cycling of moods consists of ___ or more cycle in one year

A

four

73
Q

Define lability

A

Rapid shifts in mood

74
Q

What is Nesperin-1?

A

A protein involved in scaffolding for holding nucleotide complex in place with cell membrane

75
Q

Any theory for bipolar neurological origin must explain it’s ____ nature

A

cyclical

76
Q

What is the dopamine theory for BD

A

Failure of dopamine receptor and transporter homeostasis might underlie the pathophysiology of bipolar disorder

Cycle:

  • Elevated dopamine receptor availability
  • Increased dopamine signal
  • Compensation for increase in dopamine transporters
  • Decreased dopamine signal
77
Q

What is the brain-derived neurotrophic factor theory? (BDNF)

A

BDNF is decreased in BD patients during manic and depressive episodes

78
Q

What is the mitochondrial theory of BP?

A
  • Mitochondria issues cause oxidative stress and cell death

- Defective mitochondrial are present in BP patients

79
Q

What is seasonal affective disorder (SAD)?

A

A major depressive disorder with seasonal pattern

80
Q

What are two points to the latitude hypothesis of SAD?

A
  1. Similarity between SAD symptoms and energy-conserving strategies implemented in northern latitudes
  2. SAD prevalence roughly increases with latitude
81
Q

Anxiety vs Fear

A

Anxiety –> Anticipation of fearful event

Fear –> Imminent alarm reaction to present danger

82
Q

Panic disorder is characterized by:

A

recurrent sudden and debilitating panic attacks

can have specific triggers

83
Q

Panic attacks resemble ____ without provocation

A

The normal fear response (SNS)

84
Q

Is the amygdala hyper or hypo sensitive in people with panic disorder?

A

Hyper sensitive

85
Q

What does the COMT gene code for?

A

Catechol-O-methyltransferase

- Enzyme that degrades catecholamine NT’s

86
Q

Panic attacks are linked to what gene?

A

COMT

87
Q

Panic disorder vs General Anxiety Disorder

A

Panic Disorder

  • Primarily fear based
  • Decreased PFC activity and increased limbic/SNS activity

General Anxiety Disorder

  • Primarily anxiety based
  • Increased PFC activity and decreased SNS activity
88
Q

True or False:

GAD is associated with the sympathetic nervous system

A

False

- It relates to autonomic restrictors

89
Q

Benzodiazepines act as ____ at GABA receptors

A

Agonists

90
Q

Name 3 pharmacological treatments of GAD/panic disorders

A
  1. CBT
    - Challenges distorted cognitions
  2. Panic disorder exposure
  3. Eye movement desensitization and reprocessing (EMDR)
91
Q

What are the diagnostic features of PTSD?

A
  • An experience of trauma leading to:
  • Intense prolonged psychological distress
  • And persistent avoidance of that trauma
92
Q

What are the three steps to the fear circuit

A
  1. The medial prefrontal cortex (mPFC) appraises threat
  2. If present, signals to amygdala/HPA axis
  3. Amygdala signals to hippocampus to learn context and hypothalamus to activate brainstem
93
Q

What is a structural finding of PTSD patients hippocampi?

A

Not able to use contextual cues in environment to signal safety

94
Q

True or False:

Having a reduced lobe volume puts you at risk for PTSD

A

True

95
Q

PTSD patients have an ____ amygdala activation in response to trauma-stimuli

A

exaggerated

96
Q

What is the biomarker of PTSD?

A

Dysregulated signalling of noradrenaline

97
Q

What is the durable memory theory of PTSD?

A

Excessive adrenergic response to traumatic event may mediate formation of durable traumatic memories

98
Q

What is propranolol?

A
  • Beta receptor antagonist (stops binding of noradrenaline)

- Can reduce likelihood of PTSD if administered immediately post-trauma

99
Q

PTSD have ___ numbers of cannabinoid receptors and ____ numbers of endocannabinoids

A

higher, lower

100
Q

What 5 things does the DSMV include under OCD?

A
  1. OCD
  2. Body dysmorphia
  3. Hoarding
  4. Trichotillomania (hair pulling)
  5. Excoriation (skin picking)
101
Q

What is the diagnostic criteria for OCD?

A

Presence of obsessions, compulsions, or both

102
Q

What is the difference between obsessions and compulsions in OCD?

A

Obsessions
- Recurrent unwanted thoughts that can’t be suppressed
Compulsions
- Repetitive behavior that individuals feel driven to follow strictly

103
Q

What are the 4 dimensions to OCD?

A
  1. Symmetry –> People liking order
  2. Taboo Thoughts –> Post-partum etc.
  3. Contamination –> Germs
  4. Hoarding –> Holding onto items for lengthy periods
104
Q

Explain the direct pathway of the cortical striatal thalamic loop

A
  • Cortex excites striatum with glutamate
  • Striatum inhibits GPi with GABA
  • Thalamus is disinhibited, and excites the PFC
105
Q

Explain the indirect pathway of the cortical striatal thalamic loop?

A
  • Cortex excites striatum with glutamate
  • Striatum inhibits the GPe with GABA
  • Subthalamic nucleus is disinhibited, and excites the GPi
  • GPi inhibits Thalamus, not exciting the PFC
106
Q

What are the three principle NT systems implicated in OCD?

A
  1. Serotonin
  2. Dopamine
  3. Glutamate
107
Q

What is body dysmorphic disorder?

A

Individuals preoccupied with one of more perceived defects or flaws in their physical appearance

108
Q

What are the three common eating disorders?

A
  1. Anorexia Nervosa
  2. Bulimia Nervosa
  3. Binge-Eating Disorder
109
Q

How is the severity of AN classified?

A

BMI

110
Q

How is the severity of BN classified?

A

Binge/purge frequency

111
Q

Circulating ghrelin (hormone involved in hunger) levels are ___ in AN patients, and leptin levels are ____

A

High, low

112
Q

What is binge-eating disorder?

A

Essentially bulimia without the purge

113
Q

What part of the subthalamic nucleus is involved in BED?

A

Zona incerta

- Releases GABA

114
Q

What is optogenetics?

A

Gene’s from algae that respond to light get put into area of interest for studying

115
Q

What are two critical discoveries about sleep?

A
  1. The brain is active during sleep

2. The brain goes through several stages through sleep

116
Q

Define Somniloquy

A

Sleep talking

117
Q

Define somnambulism

A

Sleep walking

118
Q

What is the activation synthesis theory of sleep?

A
  • While sleeping, we don’t receive sensory input
  • Random info produced by sensory regions
  • Dreams result from interpreting this random info
119
Q

What is the evolutionary theory to sleep?

A

Dreams may serve an adaptive evolutionary purpose by acting as training simulators.

120
Q

How does light intensity impact sleep?

A

It has no effect

121
Q

How does wavelength of light viewed before bed impact sleep?

A

Shorter wave lengths disrupt sleep architecture

122
Q

What does the glymphatic system do?

A

Flushes out waste from brain through CSF and blood vessels

123
Q

What is advanced phase circadian rhythm sleep-wake disorder?

A

Night time sleepiness, morning wakefullness

124
Q

What is delayed phase circadian rhythm sleep-wake disorder?

A

Night time wakefulness, morning sleepiness

125
Q

Is it structure or function that illustrates evidence of the brain’s involvement in mental health?

A

Structure

126
Q

Children with ADHD have reduced striatal volume. This might explain?

A

Why they are insensitive to rewards

127
Q

Exposure to prenatal testosterone reduces?

A

Frequency of eye contact

128
Q

GAD is primarily ____ based and patients show ___ PFC activity. Panic disorder is primarily ____ based and patients show ____ PFC activity.

A

Anxiety, increased; fear, decreased

129
Q

JD reports that she has feeling significant psychological distress lately. When sad, she’s coped by eating a lot of food, more than normal, followed by intense workouts at the gym. Her body weight is in the normal range. What do you diagnose her with?

A

Bulimia Nervosa, non-purging type

130
Q

THC exerts its effects in the brain by:

A

Binding to CB1 receptors, located pre-synaptically on axon terminals; this shuts down pre-synaptic release of GABA or glutamate

131
Q

Considering the C-S-T-C circuit, activity of the direct pathway

A

Disinhibits the thalamus, exciting the cortex

132
Q

Social anxiety and alcohol use disorder (AUD) are highly comorbid. This tells us:

A

The brain circuits that are dysregulated in social anxiety probably also underlie alcohol use disorder

133
Q

What might at least partially account for the decreased hippocampal volume observed among untreated, depressed patients?

A

Reduced rates of neurogenesis

134
Q

Evidence presented in class suggests SAD and excessive screen time at night are both associated with:

A

Disruption of the retinohypothalamic tract

135
Q

What area of the brain is the Iowa Gambling Task testing?

A

Pre frontal cortical control

136
Q

What is the dual ADHD theory?

A

Alterations in striatal and pre frontal cortex may be causing ADHD

137
Q

What does the striatum (both parts) do?

A

Ventral striatum –> Reward

Dorsal striatum –> Motor control (nucleus accumbens)