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Drugs and Behavior > Exam 4: Anxiety Pharmacokinetics > Flashcards

Exam 4: Anxiety Pharmacokinetics Flashcards

1
Q

drugs that relieve anxiety are

A

anxiolytic

  • relieve tension, worry, stress
  • produce calm relaxed state, without drowsiness!!, mental clouding, and incoordination
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2
Q

sedative-hypnotic drugs

A

CNS depressants
barbiturates, benzodiazepines, alcohol
-sleep aides/sedation - calms people down
-at high doses - CNS depressants induce coma and deah, respiratory depression

make people very tired!!!

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3
Q

benzodiazepines are used for what anxiety disorders

A

GAD, panic disorder, OCD, social phobia, alcohol withdrawal, acute situational anxiety

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4
Q

benzodiazepine trade name

A

valium, xanax

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5
Q

SSRIs are used for

A

social phobia, OCD, panic disorder, PTSD

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6
Q

what schedule drug are barbiturates

A

schedule II: pentobarbital -anesthesia
schedule III: butobarbital
schedule IV: luminal -anti-anxiety, sleep inducing aspects

high abuse and addiction liability dependent on lipid solubility

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7
Q

uses for barbiturates (4)

A
  • surgical anesthesia
  • sleep aid
  • anti-anxiety
  • anticonvulsant - used for seizures
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8
Q

barbiturate ROA

A

IV most common, also oral
short term: IV - surgical anesthesia
long-term: oral - anticonvulsant or antianxiety

intranasal common route for barbiturate abuse!

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9
Q

what is absorption of barbiturates dependent on

A

lipid solubility!
ultrashort acting have highest lipid solubility - get to brain fastest onset 10s-20min
long acting have lowest lipid solubility onset an hour to 12 hrs (ex: phenobarbital)

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10
Q

distribution of barbiturates

A

readily pass thorugh BBB and placental barriers, detectable in milk of nursing mothers

accumulation in skeletal muscle and adipose tissue (depot binding)

  • these drugs do not work well in those obese bc there is lots of depot binding
  • depot binding can be problem: at high levels when some gets stuck over time it leaks out into bloodstream
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11
Q

metabolism and excretion of barbiturates

A

-broken down in liver

INACTIVE metabolites excreted in urine

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12
Q

after chronic use what types of tolerance do you see

A

metabolic tolerance: cyp450 enzyme induction associated with inc drug metabolism, lower blood concentration of drug, and reduced drug effectiveness

cross tolerance: makes other drugs not work as well

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13
Q

pharmacodynamics of barbiturates (2)- what neurotransmitter involved

A

enhance GABA actions in CNS
-positive allosteric modulator: inc affinity of GABA A receptor for GABA, makes it more sensitive

they directly open Cl- ion channels in GABA A receptor without GABA present
- extreme sedation possible bc it acts as a false agonist for GABA

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14
Q

at higher doses what do barbiturates act as - pharmacodynamics

A

antagonists for AMPA and Kainate glutamate receptors
-for seizure disorders - it shuts down hyperexcitability

sedation is good in moderation- remember too high can cause respiratory depression

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15
Q

dangers of barbiturates: tolerance

A

-behavioral tolerance to some sleep-producing and anti-seizure effects of barbiturates

-respiratory depression does NOT show tolerance - reduced margin of safety due to rightward shift on curve
it does not effect the brainstem sedation - short window btw it being fun and causing respiratory depression

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16
Q

dangers of barbiturates - withdrawal and addiction

A
  • they produce significant physical dependence and have high potential for abuse
  • can’t quit cold turkey after chronic use, need to gradually come off to avoid rebound hyperexcitability and seizures like alcohol withdrawal
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17
Q

dangers in high doses of barbiturates

A
  • poor coordination, slurred speech, life-threatening respiratory depression
  • at its height of use, more than 15000 deaths/year in US were from barbiturate overdose
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18
Q

mild/moderate doses of barbiturates causes

A 
nausea/vomiting/diarrhea
drowsiness
impaired cognition/attention/judgement
slurred speech
emotional dysregulation
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19
Q

serious doses of barbiturates effects

A

shock
coma
death
birth defects (prenatal exposure - crossing placental barrier)

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20
Q

what type of drug accounts for 2/3 of all medical prescriptions for psychoactive drugs

A

benzodiazepines

  • 30% all anxiety disorders diagnoses treted with benzos
  • over 40% of panic disorder pts prescribed benzos
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21
Q

what schedule drug are benzodiazepines

A

schedule 4 drugs

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22
Q

use patterns of benzodiazepines

A

women twice as likely to use than men
45% use or less than 30 days - short term going on aplane
80% of use is for less than 4 months
15% use is greater than 12 months

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23
Q

suffix of benzodiazepines

A

azolam or azepam

24
Q

suffix for barbiturates

A

atol

25
Q

benzodiazepine ROA

A

oral - most common; xanax
IV, IM (more common) injections (Ativan)
intranasal-common during abuse

26
Q

absorption and distribution of benzodiazepines

A

BDZs have common molecular structure
onset of action determined by lipid solubility (shorter acting have higher lipid solubilities) ex: 90% xanax absorbed from GI tract

high blood albumin protein binding (depot binding!!)
-also from fat and muscle - can extend time drug can be detected in one’s system

27
Q

metabolism and excretion of benzodiazepines

A

short acting: metabolize in one step into inactive metabolites
ex: temazepam (restoril) or lorazepam (ativan)

long acting: metabolized in many steps in liver - ACTIVE metabolites produced
ex: diazepam or flurazepam

DO NOT induce CYP450 liver enzymes
-so less risk for metabolic tolerance, still get behavioral tolerance

28
Q

pharmacodynamics of benzodiazepines (what neurotransmitter)

A

positive allosteric modulator of GABA A receptor

  • enhance GABA A activity by up to 700%
  • inc sensitivity of GABA receptor to GABA, but does not open pore to Cl-

also inc actions of adenosine in the brain

  • blocks adenosine reuptake
  • adenosine accumulates in system for longer - opposite of caffeine
29
Q

benzodiazepines on glutamate neurons

A

decrease glutamate release

anticonvulsant effect

30
Q

benzodiazepines on NE neurons

A

dec NE release
improves concentration and focus
sedative effect

31
Q

benzodiazepines on serotonin neurons

A

dec 5-HT release

antianxiety effect

32
Q

therapeutic uses of benzodiazepines

A

anxiety - short term relief of severe anxiety
anticonvulsant
sleep (reduces insomnia)
muscle relaxant
presurgical anesthesia - patient conscious but less aware - wisdom teeth

33
Q

adverse effects pf benzodiazepines - after chronic use

A

in older people with slower drug metabolism: confusion and reduced cognitive function resemble dementia

  • sleep disturbances in REM
  • dec sex drive/performance
  • tolerance (44% long term users), usually behavioral tolerance, occurs as early as 1-2wks - not for anti-nxiety
  • fetal BNZ syndrome (birth defects, dependence, floppy infant syndrome)
  • amnesia/reduced learning ability!!! - in moment you focus but nothing sticks
  • severe CNS and resp depression if combined with alcohol, narcotics, barbiturates
34
Q

mesolimbic dopamine changes-BDZ

A
  • dependence and reinforcing aspects of BDZ and barbiturates due to inc mesolimbic DA release
  • BDZ binds to GABA A receptor turning GABA off, disinhibiting so DA turned on and VTA releases DA to NaCC
35
Q

Rohypnol

A

BDZ

  • “roofies”
  • 10x potency of valium (diazepam)
  • effective dose = 2mg
  • ground up and dissolved in liquids (clear, odorless)
  • onset of effects 30 min and lasts for hours
36
Q

effects of rohypnol when taken with alcohol

A 
severe blackouts
sedation
loss of muscle control
confusion
complete memory loss
death
37
Q

acute tolerance to BDZ

A

single drug administration
-limited to behavioral tolerance
-motor impairment, perceptual impairment
when blood concentration inc you have more impairments they dec as blood concentration dec

38
Q

chronic tolerance and BNZ

A

could be due to pharmacodynamic tolerance

  • repeated administration dec BDZ efficacy
  • unlear if this is due to reduced ability to modify GABA or changes insensitivity of GABA receptor to GABA
  • anticonvulsant actions slow to develop tolerance !!! - good
39
Q

list some psychological withdrawal symptoms of BDZ

A 
-anxiety 
panic attacks
intrusive thoughts
insomnia 
depression 
phobias
40
Q

list some physical effects of BDZ withdrwal symptoms

A 
agitation
tremor
nausea
palpitations
tingling, numbness

bc disinhibiting sympathetic NS

41
Q

distorted perceptions of BDZ withdrawal symptoms

A

hypersensitivity to sound, light, touch, taste

abnormal body sensation (itching, pain, stiffness)

feeling self or world to be abnormal

42
Q

major incidents of BDZ withdrawal

-whenhigh doses stopped abruptly

A

delirium
hallucinations
psychosis
fits

43
Q

2 forms of abstinence syndrome, less severe than barbiturate withdrawal symptoms

A

sedative-hypnotic withdrawal

low-dose withdrawal

44
Q

sedative-hypnotic withdrawal

A

tremors, cramps, delirium, possible convulsions

seen in ppl who take the drug at high doses for > 1 month
symptoms last ~10 days

45
Q

low-dose withdrawal

A

seen in people taking lowr doses for longer period of time (6 months)

anxiety, terror, panic, irregular heart beat, inc BP, memory impairment, concentration issues, senstive to light, insomnia, AKATHISIA

46
Q

akathisia

A

state of inner restlessness with outer movement that compels one to pace/move for hours on end
-feel like you are going to explode
-cannot sit still
enhanced insula activation! - notice slight changes in body and freak

47
Q

treatment of BDZ withdrawal

A

detox with tapering drug concentration over an 8-12 wk period

flumazenil: BDZ receptor antagonist can be used to treat BDZ overdoses

48
Q

what drug class would you prescribe to a patient with insomnia?

A

benzodiazepine bc it has a not as steep curve which means more wiggle room to adjust dose without worrying about inducing a coma

higher therapeutic inde than barbiturates - less risk for respiratory depression

49
Q

example of a second generation anxiolytic

A

buspirone (BuSpar)

50
Q

Buspirone (BuSpar)

A

-partial agonist for 5-HT1A receptor - raphe mediated to reduce anxiety
does NOT directly act on GABA system, non-sedative
-more effective at reducing cognitive aspects of worry/poor concentration than the physical symptoms of anxiety
-effective for GAD, less effective for OCD

51
Q

Buspirone effects

A

onset is quite long and its effectiveness is much less than BDZs
-less useful for those who take the drig only when needed for situational anxiety

short haf life so dosing must occur twice a day

52
Q

advantages of buspirone (5)

A
  • treats depression that often accompanies anxiety
  • anxiety reduction is not accompanied by sedation, confusion, or mental clouding
  • does not enhance CNS depressant effects of alcohol or other CNS depressants (no respiratory depression)
  • little/no potential for recreational use or dependence
  • no withdrawal syndrome reported
53
Q

SSRIs

A

antidepressants used to treat anxiety
take 4-6 wks to become effective where BDZs act immediately
-early on may worsen anxiety

can relieve both anxiety and depression

reduces OCD symptoms unlike buspirone

54
Q

tricyclic antidepressants

A

combination drugs
block SERT, NET, weakly DAT
monoamine oxidase inhibitors

55
Q

these are the first choice because they have fewer side effects, a higher therapeutic index, and low abuse potential

A

SSRIs

56
Q

anxiolytics and LC

A

BDZ enhance inhibitory function of GABA
reduced LC firing - anxiolytic effects

serotonin reuptake blockade by SSRIs reduces LC firing also

tricyclic antidepressants (desipramine) and MAOIs enhance NE function which inhibits firing of LC neurons by acting on the a2 autoreceptors

Drugs and Behavior (27 decks)

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