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PHAR 301 > Anti-Anxiety Drugs > Flashcards

Anti-Anxiety Drugs Flashcards

1
Q

what are the 3 types of anxiety disorder?

A
  1. GAD
  2. Panic disorder
  3. Phobias
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2
Q

what are 3 symptoms of GAD?

A
  1. muscle tension
  2. autonomic arousal
  3. vigilance
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3
Q

what is GAD?

A

constant worry for >6 months

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4
Q

what happens if you stop treatment for GAD?

A

relapse

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5
Q

what are 4 characteristics of panic disorder?

A
  1. episodic
  2. recurrent
  3. brief
  4. extreme fear + stress symptoms
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6
Q

what are 2 types of phobias?

A
  1. social –> ex. speaking in public
  2. specific –> ex. snakes, exams
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7
Q

are drugs a cure for anxiety?

A

no

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8
Q

what are the 4 types of possible drug treatments for GAD?

A
  1. antidepressants (SSRIs, SNRIs)
  2. benzodiazepines
  3. B blockers (if somatic)
  4. Busiprone
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9
Q

what are the 2 types of possible drug treatments for panic disorder?

A
  1. benzodiazepines
  2. antidepressants
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10
Q

what type of drug is used for social phobia?

A

B blockers

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11
Q

what type of drug is used for specific phobias?

A

no drugs

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12
Q

what are 4 risk factors for GAD?

A
  1. women >men
  2. civilian trauma
  3. low socioeconomic status
  4. middle-aged
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13
Q

how did they determine that diazepam binds GABAA receptors?

A

radiolabelled diazepam and added it to rat brain
- diazepam was found in the same locations as the GABAA receptor

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14
Q

does diazepam compete with GABA for GABAA receptors?

A

no –> diazepam binding increases in presence of GABA

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15
Q

what were 3 possibilities for why diazepam binding increases in presence of GABA?

A
  1. GABA could be increasing the number of available receptors
  2. GABA could be increasing the affinity of diazepam
  3. both
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16
Q

what are the axes of a scatchard plot?

A

X = amount of diazepam bound
Y = bound/free receptors

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17
Q

what happens if a scatchard plot shows a change in slope?

A

there is a change in affinity for a receptor

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18
Q

what happens if a scatchard plot shows a change in x-intercept?

A

there is a change in number of receptors

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19
Q

how are the scatchard plots with and without GABA different? and what does this mean?

A

with GABA has steeper line –> GABA increased diazepam’s binding affinity

with GABA doesn’t have different x-intercept –> GABA does not affect the number of receptors

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20
Q

how many subunits are in GABAA?

A

5

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21
Q

how many GABA are required to bind GABAA receptor to open it?

A

2 GABA

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22
Q

what is the relationship btwn GABA and diazepam and their affinities for GABAA receptor? how?

A

GABA and diazepam increase each other’s affinity for the receptor

via conformational changes that promote the binding of the other ligand

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23
Q

what site does diazepam bind?

A

allosteric site

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24
Q

what site does GABA bind?

A

orthosteric site

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25
Q

how do benzodiazepines affect GABA-induced hyperpolarization?

A

benzodiazepines INCREASE GABA’s ability for hyperpolarization due to increased affinity

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26
Q

what occurs during GABA hyperpolarization?

A
  1. GABA binds and opens GABAA
  2. Cl- enters cell based on electrochemical gradient
  3. cell becomes hyperpolarized
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27
Q

do GABAA channels open spontaneously?

A

usually no

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28
Q

describe the opening and closing of channels caused by GABA alone

A

channel opens and closes randomly

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29
Q

describe the opening and closing of channels caused by BZ alone

A

channel does not open at all

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30
Q

describe the opening and closing of channels caused by GABA and BZ

A

channel opens with increased frequency (BZ requires GABA to work)

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31
Q

describe the opening and closing of channels caused by GABA and barbiturates

A

channel opens for longer time (but barbiturates does not require GABA to work)

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32
Q

do benzodiazepines and barbiturates bind at the same site on GABAA?

A

no

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33
Q

when is IV diazepam used?

A

for epilepsy

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34
Q

describe the entry of BZ at the brain and periphery when injected thru IV

A

BZ rapidly enters the brain, then slowly redistributes to the periphery

it is fat-soluble so it quickly enters fatty brain/spinal cord with high blood supply
then reaches fat in periphery with lower blood supply

takes longer to equilibrate btwn brain and fat

fast onset and loss of effect

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35
Q

what is the problem with BZ metabolites?

A

they are active and have long half lifes

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36
Q

what is the main active BZ metabolites? what is its half life?

A

NORDIAZEPAM
T1/2 = 30-200H

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37
Q

Which 3 drugs are used for short term procedures? why?

A
  1. Alprazolam
  2. Oxazepam
  3. Lorazepam

they have shorter half lives

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38
Q

what are 2 additional factors that prolong the action of BZs?

A
  1. diazepam is 99% bound to plasma proteins
  2. enterohepatic recycling
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39
Q

how do plasma proteins prolong the action of diazepam?

A

99% is bound to plasma proteins –> acts as a reservoir to delay clearance

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40
Q

what can cause diazepam to be displaced from plasma protein?

A

if you take a drug that binds to the same plasma protein

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41
Q

what is enterohepatic recycling? and how does this prolong the action of BZs?

A

BZs go from GIT to liver, but enterohepatic circulation takes it and brings it back to GIT

the drug can also be glucuronidated in the liver then converted back in GIT

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42
Q

does diazepam cause more sedation or muscle relaxing effects?

A

causes more muscle relaxing effects than sedation (but sedation still present)

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43
Q

is it ideal for BZs to cause sedation?

A

no

44
Q

what does alpha1 subunit cause?

A

sedation

45
Q

what does alpha2 subunit cause?

A

anxiolytic effect

46
Q

what does the sensitivity of GABAA receptor to BZs depend on?

A

depends on alpha and gamma subunits

47
Q

describe the use of frog oocytes to see the effects of each GABAA subunit

A

A. inject cDNA into frog oocytes to produce specific GABAA subunits
B. can pick the subunits you want it to express/not express
C. test diff drugs and see which receptors they interact with

48
Q

how many alpha subunits are there?

A

6

49
Q

describe the distribution of different alpha subunits in the brain

A

each distributed differently but with some overlap

50
Q

Which 2 alpha subunits do not bind BZs?

A

alpha4 and alpha6

51
Q

what amino acid do alpha subunits that bind BZs have?

A

alpha subunits that bind BZs have HISTIDINE in its binding pocket

52
Q

what amino acid do alpha subunits that do not bind BZs have?

A

alpha subunits that do not bind BZs have ARGININE in its binding pocket

53
Q

what happens if you turn the histidine in an alpha subunit to arginine?

A

alpha subunit will no longer be able to bind BZs

54
Q

what happens if there is a point mutation in GABAA receptors with alpha2

A

cannot bind BZs

55
Q

describe the dark and light experiment with mice and mutated alpha2 GABAA receptor. what does this experiment signify?

A
  • normal mice will hide in the dark
  • mice w normal BZ will go into the light (reduced anxiety)
  • mice w mutated BZ will hide in the dark (has anxiety)

therefore, alpha2 subunit is necessary for anxiolytic effect

56
Q

how many BZs are in use?

A

20

57
Q

what is the half life of midazolam?

A

2h

58
Q

what is the half life of diazepam?

A

> 24h

59
Q

should BZs be used short term or longer term?

A

short term

60
Q

why should BZs not be used long-term? (2)

A
  • can lead to dependence
  • can lead to withdrawal –> rebound anxiety, rebound seizures
61
Q

what are 2 unwanted effects of BZs?

A
  1. sedation
  2. overdose (esp w alcohol)
62
Q

what is flumazenil?

A

competitive antagonist for BZ binding site to reverse an overdose

63
Q

what is busiprone?

A

5HT1A PARTIAL AGONIST

64
Q

why may buspirone be better to use than BZs?

A

has none of the side effects of BZs

65
Q

which of the 3 types of anxieties does buspirone work against?

A
  • GAD
  • somatic activity (a bit)
66
Q

how long does buspirone take to work?

A

1-3 weeks

67
Q

what is the main disadvantage of buspirone?

A

takes 1-3 weeks to take effect, whereas BZs take 15 min-2h to work

68
Q

what are the 2 reasons that the buspirone effect is impossible to predict?

A
  1. 5HT1A receptors can inhibit cell firing and release of 5HT but also mimics postsynaptic action of 5HT
  2. partial agonists act as agonist or antagonist depending on 5HT tone
69
Q

how does 5HT1A receptors inhibit cell firing and release?

A

5HT1A acts as an autoreceptor

70
Q

what is the effect of buspirone if there is lots of 5HT?

A

buspirone will get in the way and act as an antagonist

71
Q

what is the effect of buspirone if there is less 5HT?

A

buspirone will act as an agonist

72
Q

what are the 2 endogenous agonists for beta adrenergic receptors?

A
  1. NA
  2. adrenaline
73
Q

what is the target of beta blockers

A

beta adrenergic receptors

74
Q

what are 4 locations of beta adrenergic receptors?

A
  1. heart
  2. blood vessels in muscle
  3. bronchi
  4. brain
75
Q

what is the most common type of beta blocker?

A

propranolol

76
Q

what do beta blockers require to have an effect?

A

requires presence of agonist to have an effect –> i.e. acts preferentially when SNS is overactive

77
Q

describe the experiment for stage fright and results of BP and HR and self-evaluation

A

Test 1 and 2: random order of propranolol and placebo
Test 3: beta agonist

HR: placebo has same HR as beta agonist, but higher than propranolol

BP: unchanged across all 3 drugs

self-evaluation –> most thought they played better w B blocker

78
Q

if propranolol lowers HR, how does this affect sympathetic activity?

A

propranolol is decreasing sympathetic activity

79
Q

why did the beta agonist not increase HR compared to placebo?

A

could be because it was the 3rd performance so they felt more comfortable –> poor control

80
Q

what are 5 adverse effects of propranolol?

A
  1. bronchoconstriction
  2. cardiac failure
  3. blocks warning signs of hypoglycemia
  4. physical fatigue
  5. bad dreams
81
Q

describe bronchoconstriction due to propranolol and the cause

A
  • occurs in asthma patients
  • inhalers mimic fight or flight to open the airways which is blocked by propranolol
82
Q

describe cardiac failure due to propranolol

A
  • occurs in ppl with heart disease
  • if SNS is what is allowing heart to function, blocking this = fatal
83
Q

what type of ppl does propranolol block warning signs of hypoglycemia?

A

diabetic patients

84
Q

what are the warning signs of hypoglycemia that are blocked by propranolol? (2)

A
  1. increased pulse rate
  2. increased sympathetic tone
85
Q

why does propranolol cause physical fatigue?

A

blocks oxygen supply to muscle

86
Q

what is pindolol?

A

partial agonist at beta adrenergic receptor

87
Q

what is the role of pindolol? when does it have little effect?

A

blunts EXCESSIVE sympathetic tone

(little effect if low sympathetic tone)

88
Q

what is psychic anxiety?

A

anxiety in brain

89
Q

what is somatic anxiety?

A

anxiety in periphery –> tremors, sweating

90
Q

what is the effect of diazepam on somatic and psychic anxiety?

A

diazepam reduces both types of anxiety

91
Q

what is the effect of propranolol on somatic and psychic anxiety?

A

propranolol only reduces somatic anxiety NOT psychic anxiety

92
Q

why does propranolol have effects only against somatic anxiety?

A

propranolol only blocks peripheral effects of SNS, doesn’t really affect brain

93
Q

how does the efficacy of BZs, buspirone, and SSRIs differ?

A

all are similar

94
Q

what is not known about the efficacy of antidepressants?

A

we don’t know efficacy beyond 12 weeks –> i.e. don’t know efficacy with chronic use

95
Q

what does the choice of drug depend on? (2)

A
  1. adverse effects + risks
  2. if need fast onset
96
Q

which drug is useful for short-term/immediate treatment?

A

diazepam

97
Q

which drug is useful for long-term treatment?

A

use diazepam + SSRIs until SSRI effect kicks in, then wean off diazepam

98
Q

what drug is considered second-line treatment? why

A

beta-blockers

second line bc certain patients and situations where they shouldn’t be used

99
Q

what is the elevated plus maze and what does it show?

A
  • closed sections are dark –> mice like to be here
  • open sections are bright and high up –> mice don’t like to be here

if anxiety drug works, mice will spend more time in the open arms

100
Q

what is optogenic stimulation?

A

modify neurons so they express a light-sensitive gene
then can inhibit/stimulate neurons with light to control neuron activity

101
Q

describe what optogenetic stimulation of the amygdala-hippocampus pathway showed

A

inhibiting pathway –> less anxiety –> more time in open arms

stimulating pathway –> more anxiety –> less time in open arms

therefore, stimulation of the amygdala-hippocampus pathway is responsible for anxiety response

102
Q

describe the 3 stages of the fear-potentiated startle response

A
  1. training –> pair light and shock
    - light comes on before shock
  2. testing –> noise
    - mouse jumps due to loud noise
  3. testing –> pair light and noise
    • mouse jumps MORE bc conditioned to associated light with shock
103
Q

what are 3 advantages of fear-potentiated startle response?

A
  1. detect broad range of anxiolytics
  2. can test old and new drugs
  3. reveals brain mechanisms
104
Q

what system is the amygdala part of?

A

limbic system

105
Q

describe the fear-potentiated startle response in the brain

A

the conditioned visual stimulus and the unconditioned shock stimulus meet at the amygdala

this combined with loud noise sends signal to muscles to jump

106
Q

where is the origin of many symptoms of anxiety that are acted on by propranolol and BZs?

A

amygdala

PHAR 301 (11 decks)

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