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Psychopharm > Test 4: Anxiety > Flashcards

Test 4: Anxiety Flashcards

1
Q

What percentage of Americans suffer from anxiety?

A

18

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2
Q

__% of patients with MDD display anxiety disorders

A

58

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3
Q

[fear/anxiety] is a stress response from immediate danger

A

fear

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4
Q

[fear/anxiety] is a stress response from your thoughts

A

anxiety

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5
Q

structure deep within temporal lobes, major component of emotional processing neural circuitry including limbic cortices, hypothalamus, and hippocampus

A

amygdala

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6
Q

anxiety circuitry evaluates stimuli then directs appropriate response via ___

A

amygdala

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7
Q

What is the function of the lateral nucleus in the amygdala?

A

processes information

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8
Q

What is the function of the central nucleus in the amygdala?

A

orchestrating response

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9
Q

__ cells in the dorsal pons contact the limbic system to increase anxiety and panic

A

norepinephrine

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10
Q

[increased/decreased] firing of LC NE neurons in response to anxiety provoking stimuli, electrical stimulation of LC, or application of NE inhibitory autoreceptor antagonist increases fear and panic behavior

A

increased

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11
Q

panic disorder and PTSD patients have [increased/decreased] NE

A

increased

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12
Q

therapeutic agents that reduce anxiety (BDZ, SSRI, TC) [increase/reduce] LC firing and NE function

A

reduce

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13
Q

GABA A receptor is a __ channel and causes __

A

chloride, hyperpolarization

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14
Q

sedatives/hypnotics [enhance/decrease] GABA A function to cause sedation and reduce anxiety

A

enhance

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15
Q

[BDZ/BAR or ETOH/neurosteroids] bind to modulatory sites on receptor (not GABA site)

A

BDZ/BAR

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16
Q

[BDZ/BAR or ETOH/neurosteroids] binds to distinct area of GABA A receptor (not GABA site)

A

ETOH/neurosteroids

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17
Q

BDZ, BAR, ETOH, and neurosteroids are all positive ____ modulators for GABA

A

allosteric

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18
Q

Which GABA modulating drug is the most clinically useful?

A

BDZ

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19
Q

BDZ sites are widely distributed in the brain with a high concentration in __, __, and __

A

amygdala, limbic areas, PFC

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20
Q

BDZ agonists [increase/decrease] Cl- current

A

increase

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21
Q

BDZ agonists [increase/decrease] anxiety, arousal, seizures

A

decrease

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22
Q

BDZ antagonists cause cellular [excitation/inhibition]

A

excitation

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23
Q

BDZ inverse agonists uncouple GABA receptors from __ channels so GABA is less effective in causing entry of __ into cells - increases [excitation/inhibition]

A

Cl-, excitation

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24
Q

GABA or GABA agonist in which brain area reduces anxiety?

A

amygdala

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25
Q

many anxiolytics are CNS depressants of the __ class

A

sedative-hypnotic

26
Q

anxiolytics function to [increase/decrease] neuronal excitations

A

decrease

27
Q

4 side effects of anxiolytics

A

drowsiness/sedation, mental clouding, incoordination, prolonged reaction time

28
Q

GABA A receptors are __ channels

A

Cl-

29
Q

GABA agonists produce __, create [EPSP/IPSP] and [excite/inhibit] cell firing

A

hyperpolarization, IPSP, inhibit

30
Q

BAR [can/cannot] directly open GABA A channels without GABA

A

can

31
Q

Differences in structure complexity of BAR due to ___

A

side chain

32
Q

differences in complexity of BAR responsible for differences in ___

A

lipid solubility

33
Q

differences in BAR lipid solubility determine __ and __ of action

A

onset and duration

34
Q

three classes of BAR

A

ultrashort acting, short/intermediate acting, long acting

35
Q

ultrashort acting BAR is __ lipid soluble

A

highly

36
Q

short/intermediate acting BAR are __ lipid soluble

A

moderately

37
Q

long acting BAR have __ lipid solubility

A

poor

38
Q

4 side effects of BAR

A

non restful sleep, cognitive side effects, physical dependence and abuse, pharmacokinetic increase in liver enzymes

39
Q

first BDZ

A

librium

40
Q

BDZ increases __ of receptor for __

A

affinity, GABA

41
Q

BDZ [can/cannot] directly open GABA A channels without GABA

A

cannot

42
Q

BDZ binding to ___ receptor modulates clinical efficacy of drug

A

GABA A

43
Q

BDZ that require lower doses to displace Diazepam have [higher/lower] clinical efficacy

A

higher

44
Q

differences in BDZ structure responsible for differences in ___

A

lipid solubility

45
Q

differences in BDZ lipid solubility determine __ and __ of action

A

onset and duration

46
Q

two classes of BDZ

A

short acting, long acting

47
Q

Which class of BDZ uses Phase II metabolism in one step to inactive metabolites?

A

short acting

48
Q

Which class of BDZ uses Phase I to active metabolites and Phase II to inactive metabolites?

A

long acting

49
Q

2 BDZ therapeutic effects

A

conscious sedation and anxiety relief

50
Q

T or F: BDZ have higher therapeutic index than BAR

A

true

51
Q

T or F: BDZ produce pharmacokinetic increase in liver enzymes

A

F

52
Q

Best known 2nd generation anxiolytic

A

Buspirone (Buspar)

53
Q

T or F: buspirone enhances GABA function

A

false

54
Q

Buspirone is a partial __ agonist acting in limbic system, amygdala, and PFC, raphe

A

5HT1A

55
Q

Postsynaptic heteroreceptors of 5HT1A are located in __, __, and __

A

limbic system, amygdala, PFC

56
Q

Somatodendritic 5HT1A autoreceptors are located in __

A

raphe

57
Q

Anxiolytic action of buspirone may be due to [up/downregulation] of 5HT1A autoreceptors

A

down

58
Q

buspirone [increases/decreases] 5HT function postsynaptically

A

increases

59
Q

SSRIs relieve anxiety by enhancing 5HT function by blocking 5HT ___ postsynaptically

A

reuptake

60
Q

SERT blockers are [more/less] effective than NERT blockers in reducing anxiety symptoms

A

more

Psychopharm (6 decks)

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