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
How are the immune systems and GI tracts affected by ASD?
Heightened immune system, more GI discomfort
26
What are three theories of ASD?
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
27
What is person first language?
Language that acknowledges someone as a person before their personal attributes - NO ONE IS AN ADDICT
28
What is reward and who discovered the human system of it?
Reward --> Stimuli that is desirable | - Discovered by olds and Milner through intracranial self-stimulation
29
What circuit is responsible for reward?
Mesocorticolimbic dopamine circuit - Begins in midbrain in Ventral tegmental area - Axons project to limbic and cortex
30
The VTA produces __ (1) when rewarding stimuli is present and projects to _____ (3)
(1) Dopamine (3) Hippocampus, nucleus accumbens, prefrontal cortex - Every addictive drug activates this circuit
31
Addictive drugs lead to ________ dopamine
Supraphysiological
32
Unexpected rewards lead to ____ dopamine release
Larger
33
What is addiction?
State of uncontrolled drug use that persists in spite of negative consequences of taking that drug (Develops over multiple exposures)
34
Name 3 of the 8 diagnostic criteria for addiction.
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
35
What is drug tolerance?
Needing an increased quantity to feel the effect
36
What is drug withdrawal?
When behavioral/physiological symptoms occur upon cessation
37
Define Addiction.
A syndrome at the centre of which is loss of control over a reward-seeking behaviour
38
What are Cannabis' two main cannabinoids?
1. Delta-9-Tetrahydrocannabinol - Main psychoactive ingredient 2. Cannabidiol - Also psychoactive
39
Loss of ability to retain and coordinate information is?
Temporal disintegration
40
What are the two main cannabinoid receptors?
1. CB1 - Forebrain 2. CB2 - Immune system/brain stem
41
What are the two endogenous ligands of the eCB system?
1. Anandamide (AEA) 2. 2-Arachidonoylglyverol (2-AG) - Both are retrograde messengers (carry opposite direction in synapse)
42
How does THC work in the brain?
- 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
43
What are 3 harms of chronic cannabis use?
1. Possibility of epigenetic psychosis 2. Cancers from carcinogens 3. Increasing baseline anxiety/depression
44
What is psychosis?
The loss of contact with reality
45
What are 3 myths about schizophrenia?
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
46
What are the three groups of schizophrenia symptoms?
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
47
What is affective flattening?
A negative symptom of schizophrenia characterized by the absence of visible emotions and facial expressions
48
What age is schizophrenia usually diagnosed?
Late adolescence/early adulthood
49
True or False: | There is a clear genetic, prenatal, and stress link to contributing to schizophrenia
True
50
Degree of ____ degradation in Schizophrenia brains is correlated with illness severity.
Hippocampus
51
Anatomical studies of schizophrenic brains show enlarged ______ ______, and a degraded _____.
Lateral ventricles, hippocampus
52
PET scans of schizophrenia brains show dopamine surplus in striatum (part of basal ganglia), this suggests ____ is due to too much dopamine activity.
Psychosis
53
Blocking __ receptors relieves positive symptoms of schizophrenia
D2
54
The ideal drug to treat schizophrenia would block __ and activate __ (dopamine receptors)
- Block D2 | - Activate D1
55
What is a PET scan
Positive Emission Tomography | - Detects changes in blood flow through radioactive molecules injected in blood stream
56
Females have ___ the rate of depression than males
twice
57
True or False: | Major Depressive Disorder is the most commonly diagnosed mood disorder
True
58
Is environment or genetic a larger factor in depression?
Environment
59
What is the monoamine hypothesis of depression?
- 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
Name three pieces of evidence against the monoamine hypothesis of depression
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
What is the glucocorticoid hypothesis of depression
- Stressful live events impact etiology of depression | - Dysfunctional regulation in HPA axis contributes to this etiology
62
What is hypercortisolemia?
Elevated levels of cortisol is found in the blood at all times of depressed patients
63
How is the HPA Axis related to depression?
- 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
How do SSRI's work?
Selective serotonin response inhibitors block serotonin reuptake, leaving serotonin in the synapse
65
What is the link between estrogen's protection of depression?
- Negative feedback is more effective in presence of estrogen - SSRI's work better when combined with estrogen
66
What are ketamine's low/high dose effects
Low --> Detachment from body, sensation of floating, dreamlike High Doses --> Lose all mental contact with environment
67
Ketamine is an ______ at NMDA receptor
Antagonist, blocks NMDA receptor, reducing AP chance for memory formation
68
All bipolar disorders involve:
manic or hypomanic (half mania) plus depressive episodes
69
What defines BP1 disorder?
- Distinct manic episode lasting a week or more - Three or more BP symptoms - Major depressive episode
70
What defines BP2 disorder?
- Distinct hypomanic episode lasting 4 days - Three or more BP symptoms - Doesn't impair social functioning - Major depressive episode
71
Name 3/7 Bipolar symptoms of mania
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
Rapid cycling of moods consists of ___ or more cycle in one year
four
73
Define lability
Rapid shifts in mood
74
What is Nesperin-1?
A protein involved in scaffolding for holding nucleotide complex in place with cell membrane
75
Any theory for bipolar neurological origin must explain it's ____ nature
cyclical
76
What is the dopamine theory for BD
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
What is the brain-derived neurotrophic factor theory? (BDNF)
BDNF is decreased in BD patients during manic and depressive episodes
78
What is the mitochondrial theory of BP?
- Mitochondria issues cause oxidative stress and cell death | - Defective mitochondrial are present in BP patients
79
What is seasonal affective disorder (SAD)?
A major depressive disorder with seasonal pattern
80
What are two points to the latitude hypothesis of SAD?
1. Similarity between SAD symptoms and energy-conserving strategies implemented in northern latitudes 2. SAD prevalence roughly increases with latitude
81
Anxiety vs Fear
Anxiety --> Anticipation of fearful event | Fear --> Imminent alarm reaction to present danger
82
Panic disorder is characterized by:
recurrent sudden and debilitating panic attacks | can have specific triggers
83
Panic attacks resemble ____ without provocation
The normal fear response (SNS)
84
Is the amygdala hyper or hypo sensitive in people with panic disorder?
Hyper sensitive
85
What does the COMT gene code for?
Catechol-O-methyltransferase | - Enzyme that degrades catecholamine NT's
86
Panic attacks are linked to what gene?
COMT
87
Panic disorder vs General Anxiety Disorder
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
True or False: | GAD is associated with the sympathetic nervous system
False | - It relates to autonomic restrictors
89
Benzodiazepines act as ____ at GABA receptors
Agonists
90
Name 3 pharmacological treatments of GAD/panic disorders
1. CBT - Challenges distorted cognitions 2. Panic disorder exposure 3. Eye movement desensitization and reprocessing (EMDR)
91
What are the diagnostic features of PTSD?
- An experience of trauma leading to: - Intense prolonged psychological distress - And persistent avoidance of that trauma
92
What are the three steps to the fear circuit
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
What is a structural finding of PTSD patients hippocampi?
Not able to use contextual cues in environment to signal safety
94
True or False: | Having a reduced lobe volume puts you at risk for PTSD
True
95
PTSD patients have an ____ amygdala activation in response to trauma-stimuli
exaggerated
96
What is the biomarker of PTSD?
Dysregulated signalling of noradrenaline
97
What is the durable memory theory of PTSD?
Excessive adrenergic response to traumatic event may mediate formation of durable traumatic memories
98
What is propranolol?
- Beta receptor antagonist (stops binding of noradrenaline) | - Can reduce likelihood of PTSD if administered immediately post-trauma
99
PTSD have ___ numbers of cannabinoid receptors and ____ numbers of endocannabinoids
higher, lower
100
What 5 things does the DSMV include under OCD?
1. OCD 2. Body dysmorphia 3. Hoarding 4. Trichotillomania (hair pulling) 5. Excoriation (skin picking)
101
What is the diagnostic criteria for OCD?
Presence of obsessions, compulsions, or both
102
What is the difference between obsessions and compulsions in OCD?
Obsessions - Recurrent unwanted thoughts that can't be suppressed Compulsions - Repetitive behavior that individuals feel driven to follow strictly
103
What are the 4 dimensions to OCD?
1. Symmetry --> People liking order 2. Taboo Thoughts --> Post-partum etc. 3. Contamination --> Germs 4. Hoarding --> Holding onto items for lengthy periods
104
Explain the direct pathway of the cortical striatal thalamic loop
- Cortex excites striatum with glutamate - Striatum inhibits GPi with GABA - Thalamus is disinhibited, and excites the PFC
105
Explain the indirect pathway of the cortical striatal thalamic loop?
- 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
What are the three principle NT systems implicated in OCD?
1. Serotonin 2. Dopamine 3. Glutamate
107
What is body dysmorphic disorder?
Individuals preoccupied with one of more perceived defects or flaws in their physical appearance
108
What are the three common eating disorders?
1. Anorexia Nervosa 2. Bulimia Nervosa 3. Binge-Eating Disorder
109
How is the severity of AN classified?
BMI
110
How is the severity of BN classified?
Binge/purge frequency
111
Circulating ghrelin (hormone involved in hunger) levels are ___ in AN patients, and leptin levels are ____
High, low
112
What is binge-eating disorder?
Essentially bulimia without the purge
113
What part of the subthalamic nucleus is involved in BED?
Zona incerta | - Releases GABA
114
What is optogenetics?
Gene's from algae that respond to light get put into area of interest for studying
115
What are two critical discoveries about sleep?
1. The brain is active during sleep | 2. The brain goes through several stages through sleep
116
Define Somniloquy
Sleep talking
117
Define somnambulism
Sleep walking
118
What is the activation synthesis theory of sleep?
- While sleeping, we don't receive sensory input - Random info produced by sensory regions - Dreams result from interpreting this random info
119
What is the evolutionary theory to sleep?
Dreams may serve an adaptive evolutionary purpose by acting as training simulators.
120
How does light intensity impact sleep?
It has no effect
121
How does wavelength of light viewed before bed impact sleep?
Shorter wave lengths disrupt sleep architecture
122
What does the glymphatic system do?
Flushes out waste from brain through CSF and blood vessels
123
What is advanced phase circadian rhythm sleep-wake disorder?
Night time sleepiness, morning wakefullness
124
What is delayed phase circadian rhythm sleep-wake disorder?
Night time wakefulness, morning sleepiness
125
Is it structure or function that illustrates evidence of the brain's involvement in mental health?
Structure
126
Children with ADHD have reduced striatal volume. This might explain?
Why they are insensitive to rewards
127
Exposure to prenatal testosterone reduces?
Frequency of eye contact
128
GAD is primarily ____ based and patients show ___ PFC activity. Panic disorder is primarily ____ based and patients show ____ PFC activity.
Anxiety, increased; fear, decreased
129
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?
Bulimia Nervosa, non-purging type
130
THC exerts its effects in the brain by:
Binding to CB1 receptors, located pre-synaptically on axon terminals; this shuts down pre-synaptic release of GABA or glutamate
131
Considering the C-S-T-C circuit, activity of the direct pathway
Disinhibits the thalamus, exciting the cortex
132
Social anxiety and alcohol use disorder (AUD) are highly comorbid. This tells us:
The brain circuits that are dysregulated in social anxiety probably also underlie alcohol use disorder
133
What might at least partially account for the decreased hippocampal volume observed among untreated, depressed patients?
Reduced rates of neurogenesis
134
Evidence presented in class suggests SAD and excessive screen time at night are both associated with:
Disruption of the retinohypothalamic tract
135
What area of the brain is the Iowa Gambling Task testing?
Pre frontal cortical control
136
What is the dual ADHD theory?
Alterations in striatal and pre frontal cortex may be causing ADHD
137
What does the striatum (both parts) do?
Ventral striatum --> Reward | Dorsal striatum --> Motor control (nucleus accumbens)