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Pharmacology > Anxiolytics&Sedative > Flashcards

Anxiolytics&Sedative Flashcards

1
Q

Benzodiazepines can be used for

A
  • generalized anxiety disorders
  • panic disorders
  • social anxiety disorders
  • performance anxiety
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2
Q

Buspirone can be used for

A
  • generalized anxiety disorders

- social anxiety disorders

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3
Q

Tricyclic can be used for

A

panic disorders

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4
Q

SNRIs can be used for

A
  • generalized anxiety disorders

- social anxiety disorders

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5
Q

selective 5-HT uptake inhibitors can be used for

A
  • generalized anxiety disorders
  • panic disorder
  • OCD
  • social anxiety disorders
  • performance anxiety
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6
Q

what can MAO inhibitors be used for

A

-performance anxiety

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7
Q

Gabapentin pregabalin can be used for

A

-social anxiety disorders

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8
Q

what is the main drug used for the short-term treatment of generalized anxiety disorder and sleep disorders

A

benzodiazepines

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9
Q

what is the MOA of benzodiazepines

A
  • release of GABA in GABA containing neurons
  • release of GABA opens Cl- channels on the postsynaptic site
  • Cl hyperpolarizes cell, making it more difficult to depolarize, therefore reducing neuronal excitability
  • binding of GABA is enhanced by benzodiazepine resulting in greater chloride entry
  • benzodiazepines facilitate GABA-ergic neurotransmission and potentiate postsynaptic inhibition by binding to sites on the receptor complex and allosterically increasing the affinity of GABA receptors for GABA and increasing the amount of chloride current generated by GABA receptor activation
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10
Q

what drugs affect GABA/BZD receptors

A
  • BZD receptor agonist (Zolpidem)
  • Omega site (Zaleplon)
  • Zolpiclone (GABA/BZD site)
  • BZD antagoinst (Flumazenil)
  • inverse agonist (experimental)
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11
Q

pharmacological action of Benzodiazepines

A
  • sedation/sleep induction
  • anti-anxiety
  • skeletal muscle relaxation
  • anticonvulsant
  • anterograde amnesia
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12
Q

how do Benzodiazepines induce sedation/sleep induction

A
  • low doses decrease activity and reduce conscious excitability; larger dose promote sleep
  • excessive doses cause stupor/light coma w/o respiratory failure
  • rapid tolerance develops to sedation
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13
Q

how do Benzodiazepines induce anti-anxiety

A
  • reduce the negative effects of punishment and produce disinhibition
  • tolerance does not develop readily to these actions
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14
Q

how do Benzodiazepines produce skeletal muscle relaxation

A

-exert depressive effects on multi synaptic pathway used in flex reflexes; they also decrease spasticity

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15
Q

how do Benzodiazepines produce anticonvulsant effects

A
  • effective, rapid acting anticonvulsants

- tolerance may develop quickly

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16
Q

what effects do Benzodiazepines have on respiration

A
  • sedative hypnotic doses of BZDs do not exert significant effects on respiration in normal subjects
  • may worsen sleep apnea
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17
Q

what effects do Benzodiazepines have on the CV sytem

A
  • CV effects are minor

- some coronary vasodilation may occur after i.v. admin

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18
Q

what effects do large IV doses of BZDs for preanesthetic medication have

A

depress alveolar ventilation and BP

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19
Q

pharmacokinetics of BZDs

A
  • single doses [absorption; lipid solubility (Kp)]

- chronic doses (active metabolites)

20
Q

metabolism of BZDs

A

-some converted to an active metabolite

21
Q

metabolism of Oxasepam and Lorazepam

A

no active metabolites

22
Q

Metabolism of Alprazolam

A

short-lived active metabolite

23
Q

AE of BZDs

A
  • varying degree of CNS impairment
  • dose-related dizziness, lightheadedness, motor dysfunction
  • anterograde amnesia/memory impairment
24
Q

tolerance of BZDs

A

-develop to the sedative and ataxic effects of the benzodiazepines w/ continued administration of the same dosage

25
Q

tolerance of the anti anxiety effect of BZDs

A

-tolerance develops slowly and has relatively minor consequences

26
Q

tolerance to the hypnotic effect of BZDs

A
  • rapidly develop (tachphylaxis)

- respiratory and CV depressant effects w/ overdosage

27
Q

depending on the dose and pd of use, discontinuation of BZDs may result in the appearance of symptoms that can be classified as

A

rebound
recurrence
withdrawal

28
Q

drug interactions w/ BZDs

A

CNS depression

hepatic metabolism

29
Q

what are other uses of BZDs

A

alcohol withdrawal
seizure disorders
spasticity
localized skeletal muscle spasm
preanesthetic medication
induction of sedation or amnesia prior to certain procedures
reduction of periodic movements in sleep

30
Q

use of Buspirone

A

antianxiety

31
Q

MOA of Buspirone

A

partial agonist at 5-HT 1A receptors; also has moderate to weak affinity for DA2, 5-HT2, and alpha2 adrenoceptors

32
Q

how does Buspirone different from BZDs

A
  • lacks sedative-hypnotic, anticonvulsant, or muscle relaxant properties
  • does not cause memory impairment or psychomotor deficits
  • dependence liability appears to be negligible
  • one to 2 weeks are required for onset of anti anxiety effects
  • has also been used in treatment of depression or to augment the actions of actions of antidepressants in depression, OCD, and smoking cessation
33
Q

MOA of barbiturates

A
  • reversibly depress activity of excitable tissues; CNS most sensitive
  • potentiation of GABA at lower doses
  • decrease in Ca currents and glutamate depolarization
  • direct impairment of Na+ and K+ channels at higher [ ]
34
Q

name a long acting barbiturate

A

phenobarbital

35
Q

medium-short acting barbiturates are

A

secobarbital, pentobarbital, amobarbital

36
Q

short acting barbiturates are

A

thiopental; thioamyl; methohexital

37
Q

MOA of low dose barbiturates

A

potentiate GABA action

38
Q

MOA of large dose barbiturates

A
  • directly impair Na+ and K+ channel operation

- direct depression of neuronal activity

39
Q

pharmacodynamics of barbiturates

A
  • depression of the CNS sedation –> [paradoxical agitation] –> hypnosis –> anesthesia –> coma –> death
  • respiratory depression
  • CYP enzyme induction
40
Q

pharmacokinetics of barbiturates

A
  • weak acids that are well absorbed orally

- distribution, in turn is related to lipid solubility and plasma and protein binding

41
Q

how are barbiturates metabolized

A
  • redistribution from brain to less well vascularized tissues
  • hepatic metabolism
  • alkaline urine enhances excretion, particularly of phenobarbital
42
Q

AE of barbiturates

A

-CNS related; drug hanover; rarely, connective tissue disorders

43
Q

precaution of barbiturates

A
  • acute intermittent porphyria
  • addiction
  • drug interactions
  • P450 enzyme induction
  • additive effects w/ other CNS depressants
44
Q

therapeutic uses of barbiturates

A

Epilepsy (phenobarbital; primidone)
Intravenous anesthesia
Kernicterus of the newborn(historical)
Sleep induction; daytime sedative or “anxiolytic” (replaced by BZDs)

45
Q

Miscellaneous agents

A 
Paraldehyde
Chloral  hydrate
Meprobamate
Trazodone
OTC sleep aids (antihistamines)

Pharmacology (23 decks)

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