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Psych 3313 > Anxiety Disorders and Autism Spectrum Disorder > Flashcards

Anxiety Disorders and Autism Spectrum Disorder Flashcards

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1
Q

When is the amygdala most active during presentation of phobias?

A

Before the patient is shown the phobia

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2
Q

Dendritic spine number in ASD patients overtime

A

Rises above normal in childhood and stays that way through adulthood

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3
Q

What can carbon dioxide cause?

A

Panic attacks

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4
Q

How do PTSD patients end up with a smaller hippocampus?

A

They may be born with it and it shrinks more with stressful situations

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5
Q

Have meds to treat core behavior issues been effective in ASD treatment

A

No

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6
Q

When does anxiety become a problem?

A

When it is in control; we cant control it

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7
Q

What happens with the HPA axis in anxiety?

A

The amygdala sends a stronger response (ends up eventually causing more cort)

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8
Q

Hippocampus of PTSD patients

A

Much smaller

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9
Q

How can a panic attack be stopped?

A

Trying to slow things down and regain control

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10
Q

What does research not support in ASD diets?

A

gluten and casein free diets not supported

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11
Q

Development of PTSD pathway

A

Stress sensitivity, over consolidation of fear, generalization of fear cues, impaired extinction of fear memories

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12
Q

What do smaller hippocampi of PTSD patients cause?

A

Impaired negative feedback from hippocampus to HPA axis which leads to excessive cort release

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13
Q

Stress response just from your thoughts

A

Anxiety

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14
Q

How early can ASD be diagnosed? More in boys or girls?

A

As early as 18 months. Boys 4 times more likely

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15
Q

Minicolumn differences in ASD patients

A

Minicolumns are much more dense in ASD patients

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16
Q

Meds approved for self-injurious behavior in ASD

A

Antipsychotics

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17
Q

Sources of genetic mutations in ASD

A

77% unknown
15% Mendelian disorders/mutations
5% rare and de novo mutations
3% chromosome abnormalities

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18
Q

Medications other than GABA-A agonists used to treat anxiety

A

Beta blockers (epinephrine/NE antagonist) and antidepressants (SSRIs)

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19
Q

Sudden onset of very strong intense fear of discomfort, strong sympathetic nervous system arousal, hyperventilation

A

Panic attack

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20
Q

These genes regulate brain development and synaptic changes and are likely related to ASD

A

Candidate genes

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21
Q

4 major specific phobia categories

A

Natural environment, animals, mutilation/medical treatments, situations

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22
Q

Parts of the brain with structural abnormalities in ASD

A

Cerebellum, amygdala, hippocampus

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23
Q

Strong negative emotion and physiological sensations from the anticipation of threat

A

Anxiety disorders

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24
Q

VR exposure therapy, MDMA assisted therapy, psychotherapy

A

PTSD treatments

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25
Q

Does the GABA-A receptor depolarize or hyperpolarize?

A

Hyperpolarize. Allows Cl- in

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26
Q

What do benzodiazepines increase at the GABA-A receptor? IMPORTANT

A

Increase frequency of opening Cl- channel

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27
Q

What could inappropriate levels of GABA inhibition cause?

A

A person to overreact to a perceived threat

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28
Q

Region of amygdala that receives inputs?

A

Lateral nucleus

29
Q

Where are abnormalities seen in anxiety disorders?

A

Pathways connecting brainstem, amygdala, and related subcortical structures and decision making areas of frontal lobes, HPA axis, and NE, 5HT, and GABA NT systems

30
Q

How is ASD treated not with meds?

A

Intensive, early childhood learning experiences provided during most of the childs waking hours

31
Q

There are lower levels of this NT in ASD

A

Oxytocin

32
Q

Could be a risk factor for PTSD, a result, or both

A

Lower gray matter volume

33
Q

Generalization and how its related to PTSD

A

PTSD patients show fear in response to stimuli similar to the one that first caused the PTSD

34
Q

Stimulation of locus coeruleus (NE) causes this

A

Panic attack

35
Q

Abnormal versions of this glial cell are in ASD patients

A

Abnormal microglia

36
Q

This is more active in ASD

A

Default mode network (DMN)

37
Q

Repeated panic attacks followed by at least one month of worrying about another panic attack

A

Panic disorder

38
Q

Uncontrolled chronic worry, catastrophizing, physical symptoms create anxiety spiral

A

Generalized anxiety disorder

39
Q

What happens in generalized anxiety disorder?

A

Hypoactivity, reduced inhibition of the amygdala which then overexcites the HPA axis and sympathetic nervous system

40
Q

Do ASD brains have more or less lateralization?

A

More (more symmetry)

41
Q

How has autism prevalence risen over the last 40 years and why?

A

It has gone way up due to rise in incidence in general and relaxation of diagnostic criteria

42
Q

Dysfunctions of this can be seen in ASD patients (debated)

A

Dysfunctions in mirror system function (debated)

43
Q

How can postnatal factors influence gut microbiota and thus ASD

A

Child delivery method, feeding method (breast/formula), use of pre/probiotic supplements and/or antibiotics

44
Q

What happens in the body during a panic attack that is counterproductive?

A

The body does things that won’t help you calm down like hyperventilating (trying to breathe more)

45
Q

Normal response to genuine danger

A

Fear

46
Q

Has a high comorbidity with anxiety disorder or other mood disorders

A

Panic disorder

47
Q

Drugs that reduce anxiety

A

Anxiolytics

48
Q

Associated with agoraphobia

A

Panic disorder

49
Q

2 core symptoms of ASD

A

Social communication deficits and repetitive behaviors

50
Q

Childhood brain development in ASD and what does this cause/what causes this?

A

Brain development is abnormally accelerated through early childhood, producing first brain enlargement, followed by a period of deceleration. High neurotrophic levels and excess CSF

51
Q

What do barbiturates increase at the GABA-A receptor? IMPORTANT

A

Increase duration of opening Cl- channel

52
Q

What do relatives of ASD patients show and what does this help show?

A

Elevated levels of autistic traits. ASD is linked to genetics

53
Q

Severe emotional disturbance after experiencing or witnessing severely stressful event

A

PTSD

54
Q

Do patients with ASD show more or less autophagy?

A

Less. They have less pruning and end up with more dendrites

55
Q

Higher levels of this NT are seen in ASD patents and it is due to ___

A

Elevated 5HT levels. Due to impaired 5HT reuptake

56
Q

Concordance rate of ASD

A

76-88%

57
Q

IV administration of sodium lactate (respiratory stimulant) causes what?

A

Panic attacks in individuals prone to them but not controls

58
Q

Region of amygdala that sends outputs?

A

Central nucleus

59
Q

These types of medications are specific to treating anxiety (IMPORTANT)

A

GABA-A agonists (benzodiazepines, barbiturates, alchohol)

60
Q

This area has lower volume in PTSD patients

A

Anterior cingulate cortex

61
Q

Classical conditioning and how it relates to the amygdala and specific phobias?

A

Strong stimulus becomes paired with weak stimulus that causes stronger input to lateral nucleus of amygdala which creates stronger outputs from the central nucleus of the amygdala which creates stronger signals to the periaqueductal gray region of midbrain

62
Q

How do ASD symptoms vary?

A

All ASD patients have different combinations of symptoms (no combination is better or worse)

63
Q

What does risperidone do in ASD?

A

Provides some therapeutic benefit (5HT antagonist)

64
Q

What altered network communications are seen in ASD patients?

A

Signals are sent broken up, like a dashed line, and not outright, like a solid line

65
Q

Marked and persistent fear that is excessive or unreasonable cued by presence or anticipation of specific object or situation

A

Phobia

66
Q

Symptoms include recurring dreams, flashbacks, hyper-arousal and avoidance of stimuli associated with trauma (respond to more cues overtime), and high levels of vigilance and an impairment in daily functioning

A

PTSD

67
Q

Causes can include perinatal complications, inc parental age, exposure to infection and nutritional factors, maternal use of antidepressants, gut microbiota

A

ASD

68
Q

Observed brain differences in ASD patients

A

unusual patterns of activation and weak connections across many areas. Brain development is abnormally accelerated through early childhood, producing first brain enlargement, followed by a period of deceleration

Psych 3313 (24 decks)

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