Exam 4 Material Flashcards

1
Q

Fear is divided into ____ fear and ____ fear.

A

innate; learned

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2
Q

What coordinates the global response to a perceived threat?

A

the amygdala

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3
Q

Sensory input to ___ ____ activates numerous effector sites for physiological and behavioral fear response.

A

central nucleus

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4
Q

What are the 8 physical responses of the amygdala?

A

sympathetic activation (tachycardia, bp increase, etc); urination/defecation; increased vigilance/attention; increased startle; hypoalgesia; fear facial expression; corticosteroid release

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5
Q

Can patients with damage to the amygdala still feel fear?

A

yes- inhaling CO2 can produce a fear response

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6
Q

What neurotransmitter plays a critical role in the circuitry mediating anxiety?

A

corticotrophin-releasing factor (CRF)

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7
Q

What two components make up a memory of a fearful situation and what brain area processes those?

A

1- cognitive processed in hippocampus

2- affective processed in teh mygdala

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8
Q

What type of memory component is the precise setting or context in which the danger is experienced?

A

the cognitive

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9
Q

What type of memory is of emotional salience?

A

the affective

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10
Q

In anxiety there is no what?

A

immediately threatening situation

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11
Q

Anxiety is what kind of association with memory?

A

maladaptive

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12
Q

This is characterized by discrete episodes of intense anxiety with somatic symptoms such as tachycardia, tachypnea, and dizziness.

A

Panic disorder

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13
Q

this is an unrealistic excessive worry for more than six months with symptoms such as motor tension, sympathetic hyperactivity, and excessive vigilance.

A

Generalized anxiety disorder

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14
Q

This happens after serious trauma and is associated with cue-eliceted reliving of traumatic experience, increased startle, and nightmares.

A

Post-traumatic stress disorder

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15
Q

This is fear of social situations or interactions.

A

social phobia

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16
Q

How do you treat acute anxiety?

A

benzodiazepines

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17
Q

How do you treat GAD?

A

antidepressants or benzos

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18
Q

How do you treat panic disorder?

A

long term anti-depressants and behavioral therapy

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19
Q

How do you treat OCD?

A

long term anti-depressants and behavioral therapy

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20
Q

How do you treat PTSD?

A

behavioral therapy, cycloserine, ketamine, prazosin, propranolol

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21
Q

How does cycloserine work?

A

it’s an NMDA agonist

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22
Q

How does parzosin work?

A

it’s an alpha1 antagonist

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23
Q

What is a common ending to generic names for benzos?

A

-azepam

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24
Q

What are the five types of anti-anxiety medications?

A
1- benzos
2- barbiturates
3- beta adrenergic receptor antagonists
4- newer such as CRF and neuropeptide antagonists
5- 5HT 1A recepor agonists
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25
Q

Name four examples of benzos?

A

diazepam, chlordiazepoxide, oxazepam, clorazepate, alprazolam, prazepam, halazepam, lorazepam

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26
Q

What receptor do barbiturates work on?

A

GABA-A

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27
Q

What are additional therpeutic uses for benzos beyond anxiety?

A

muscle spasticity seen in MS and cerebral palsy, seizures, and sleep disorders

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28
Q

Which benzo treats anxiety?

A

diazepam

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29
Q

Which benzo treats muscle spasticity?

A

diazepam

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30
Q

What three benzos can treat seizures?

A

clonazepam, diazepam, oxazepam

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31
Q

Which benzos can treat sleep disorders?

A

flurazepam, temazepam, triazolam

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32
Q

What are the drawbacks to using benzos?

A

they can impair intellectual functions, interact with alcohol, and cause withdrawal if stopped suddenly

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33
Q

Which benzos have the longest half life?

A

diazepam, cholrdiazepoxide, prazepam, clorazepate

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34
Q

Which benzos have shortest have life?

A

lorazepam, oxazepam and flurazepam

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35
Q

How do benzos that are agonists at the recptor behave?

A

they reduce anxiety, muscle tension, convulsions, vigilance and memory

36
Q

How do benzos that are inverse agonists at the receptor behave?

A

they induce anxiety and oppose agonists; only used with research and not used in humans

37
Q

How does flumazenil behave at the receptor?

A

it prevents both types of agonists and blocks access to BDZ receptor

38
Q

Name the three subunit-selective drugs at alpha-1 receptors?

A

zolpidem, zaleplon, eszopiclone

39
Q

What function do alpha-1 selective drugs perform?

A

they are typically used as sleep aids

40
Q

Which alpha-1 selective drug has the longest halflife?

A

eszopiclone (aka lunesta)

41
Q

How do barbiturates work on the receptor?

A

they bind to a different allosteric site than benzos on GABA A receptors and directly activate it

42
Q

What are the drawbacks to using barbiturates?

A

they creat tolerance, physical dependence, liver issues, and can have withdrawal symptoms

43
Q

What are barbiturates typically used for?

A

anasthesia

44
Q

How do SSRIs work?

A

they block 5-ht reuptake transporter

45
Q

How do SNRIs work?

A

they block 5-ht and NE reuptake transporters

46
Q

What are some drawbacks to SNRIs and SSRIs?

A

they can potentially worsen anxiety for a short time, have side effects including: nausea, diarrhea, decreased sex drive,, anorgasmia, and weight gain

47
Q

SSRIs with a ___ half- life are more likely to cause SSRI discontinuation syndrome.

A

short

48
Q

How does buspirone act at the receptor?

A

it is a 5-HT1a receptor agonist

49
Q

Does buspar cause sedation?

A

no

50
Q

How long does it take for buspar to work?

A

at least a week

51
Q

How effective is buspar when compared to benzos or SSRIs?

A

it is not as effective

52
Q

What is vilazodone?

A

it’s a combination of SSRI and buspar

53
Q

How do beta blockers work at the receptor?

A

they are beta adrenergic antagonists

54
Q

What effect do beta blockers have on NTs?

A

they reduce the effects of catecholamines

55
Q

What effect on symptoms do beta blockers have?

A

they reduce anxiety induced heart palpitations, tremor, sweating

56
Q

What types of anxiety is propranolol good to treat?

A

performance anxiety and PTSD

57
Q

Where are D1 receptors found?

A

neostriatum, cerebral cortex, olfactory tubercle and nucleus accumbens

58
Q

Where are D2 receptors found?

A

neostriatum, olfactory tubercle and nucleus accumbens

59
Q

Where are D3 receptors found?

A

nucleus accumbens and islands of calleja

60
Q

Where are D4 receptors found?

A

midbrain and amygdala

61
Q

Where are D5 receptors found?

A

hippocampus and hypothalamus

62
Q

most antipsychotic drugs block ___ receptors wheras apriprazole is a _____ ____.

A

D2, partial agonist

63
Q

What are the reward pathways that are activated?

A

nucleus accumbens and VTA

64
Q

Output neurons from the NAc are…?

A

GABAergic

65
Q

Rewarding inputs _____ the activity of GABAergic NAc neurons.

A

inhibit

66
Q

___ or ____ receptors on NAc neurons are inhibitory.

A

Opioid, DA

67
Q

Opioids ___ NAc neurons directly but also ____ GABAergic VTA interneurons.

A

inhibit x2

68
Q

Nicotine activates _____ and ___ VTA neurons.

A

opioidergic; DA

69
Q

What do cannabinoid do to glutaminergic input into the NAc?

A

they inhibit it

70
Q

What six thing increase dopamine in the NAc?

A
1- heroin and cocaine
2- nicotine
3- alcohol intake
4- THC
5- food
6- caffeine
71
Q

What causes tolerance to dopamine in the NAc?

A

compensatory regulation

72
Q

What five types of tolerance are there?

A
1- PD tolerance
2- PK tolerance
3- behavioral tolerance
4- cross tolerance
5- reverse tolerance
73
Q

What is reverse tolerance also known as?

A

sensitization

74
Q

This is a physiologic tolerance to others of same drug class or similar action.

A

cross tolerance

75
Q

This is adjustment of behavior to compensate for adverse effects.

A

behavioral tolerance

76
Q

This is increased metabolism due to enzyme reduction.

A

pharmacokinetic tolerance (PK tolerance)

77
Q

This is compensatory change of receptor number or sensitivity.

A

pharmcodynamic tolerance (PD tolerance)

78
Q

Acute cocaine increases dopamine binding to what two receptors?

A

D1 and D2

79
Q

What happens to compensate for chronic cocaine use?

A

reduction of Gi and increase of anaylate cyclate (leading to more cAMP and sensitization)

80
Q

Define addiction.

A

habitual dependence on a substance or practice beyond voluntary control

81
Q

What is the impact of chronic drug use?

A

normal reward function is replaced and it leads to craving/loss of control/addiction

82
Q

What is one potential cause of aura in migraine?

A

cortical spreading depression

83
Q

What is cortical spreading depression?

A

waves of electrical excitability followed by depression that moves across the cortex at approximately 3-6 mm/min

84
Q

Meningeal afferents are sensitive to what types of things?

A

chemical (low pH, inflammatory mediators) and mechanosensitivity

85
Q

What explains the throbbing pain?

A

mechanosensitivity

86
Q

What are abortive therapies for migraines?

A

nsaids, ergots, triptans, CGRP antagonists

87
Q

slide 19 migraines

A

start with ergot questions