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Psych > Drugs of abuse sedative hypnotics alcohol Lecture > Flashcards

Drugs of abuse sedative hypnotics alcohol Lecture Flashcards

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1
Q

Benzodiazepines

A
  • alprazolam
  • chlordiazepoxide
  • clonazepam
  • clorazepate
  • diazepam
  • flurazepam
  • lorazepam
  • midazolam
  • oxazepam
  • triazolam
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2
Q

Benzodiazepine antagonist

A

-Flumazenil

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3
Q

Barbiturates

A
  • Amobarbital
  • butabarbital
  • pentobarbital
  • phenobarbital
  • secobarbital
  • thiopental
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4
Q

Misc/Newer sedative-hypnotic drugs

A

-Buspirone
-eszopiclone
-meprobamate
-ramelteon
-zaleplon
-zolpidem
(BEMRZZ)

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5
Q

Drugs for tx of acute alcohol withdrawal syndrome

A
  • diazepam, lorazepam, oxazepam

- thiamine (Vit B1)

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6
Q

drugs for prevention of alcohol abuse

A
  • acamprosate
  • disulfiram
  • naltrexone
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7
Q

drugs for tx of methanol/ethylene glycol poisoning

A
  • ethanol

- fomepizole

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8
Q

drugs used to tx dependence and addiction

A
  • opioid R antagonist- naloxone, naltrexone
  • synthetic opioid- methadone
  • partial u-opioid R agonist- buprenorphine
  • nicotinic R partial agonist- varenicline
  • benzodiazepines
  • NMDA R antagonist- acamprosate
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9
Q

Sedative

A
  • dec CNS activity, moderates excitement, and calms recipient
  • fast acting compared to SSRIs
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10
Q

hypnotic

A
  • produces drowsiness and facilitates the onset and maintenance of sleep
  • recipient can be aroused easily
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11
Q

Benzodiazepines and barbiturates- CNS effects

A
  • barbiturates- no plateau

- benzodiazepines- less dangerous- effects plateau!!

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12
Q

Benzodiazepines and barbiturates- moa

A
  • benzodiazepines- GABAa Rs

- barbiturates- GABAa Rs

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13
Q

Benzodiazepines- moa

A
  • hepatic metabolism (CYP3A4), excretion via kidney
  • elimination half-lives vary- cumulative toxicity
  • binds to GABAa R- enhances GABA’s effects (shifts dose response curve to left)- inc chloride influx- inc hyperpolarization- dec number of APs (CNS depression)
  • diazepam, alprazolam, lorazepam
  • risk of dependence, tolerance
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14
Q

Benzodiazepines- cumulative toxicity

A

-drugs w long half-lives are more likely to cause cumulative effects w mult doses!!

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15
Q

Barbiturates- moa

A
  • hepatic metabolism and excretion via kidney
  • binds to GABAa R and inc duration of GABA-gated channel openings- inc chloride influx- inc hyperpolarization- dec number of APs (CNS depression)
  • phenobarbital, amobarbital, secobarbital
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16
Q

Newer hypnotics (sleep aids)- moa

A
  • hepatic metabolism (CYP3A4) and excretion via kidney
  • binds to GABAa Rs that contain the alpha1-subunit- inc chloride influx- inc hyperpolarization- dec number of APs (CNS depression)
  • tx sleep disorders!!!
  • eszopiclone, zolpidem, zaleplon
17
Q

Tx of anxiety states

A

Benzodiazepines

  • advantages- high therapeutic index, antagonist available: flumazenil, low risk of drug-drug interactions, minimal effect on CV or autonomic fxn
  • disadvantages- risk of dependence, depression of CNS fxn, amnestic effects, CNS depression when combined w other drugs
  • Newer antidepressants are sometimes preferred (SSRIs)
18
Q

Tx of insomnia

A
  • sleep aids- zolpidem, zaleplon, eszopiclone (highly effective, rapid onset w minimal hangover effects)
  • Benzodiazepines can be used- but cause daytime sedation
19
Q

Tx of insomnia- Ramelteon- moa

A
  • agonist at MT1 and MT2 melatonin Rs
  • oral bioavailability is < 2% (first-pass metabolism)
  • metabolized by CYP1A2 to active metabolite
  • avoid coadmin w fluvoxamine (SSRI and CYP1A2 inhibitor)
20
Q

Buspirone

A
  • tx generalized anxiety disorder
  • anxiolytic effects may take more than 1 wk to become established
  • does not cause sedation, hypnotic, anticonvulsant, or m relaxant effects
  • metabolism by CYP3A4
21
Q

Alcohol

A
  • first-pass metabolism by gastric and liver ADH (alcohol dehydrogenase)
  • zero-order kinetics (rate of biotransformation is indep of time and conc of ethanol- enzymes are almost immediately saturated)
  • typical 70 kg adult can metabolize 7-10 g of alcohol per hour (1 drink)
22
Q

Ethanol and methanol biotransformation

A

-ethanol, methanol–alcohol dehydrogenase–> acetaldehyde (hangovers)–aldehyde dehydrogenase (inhibited by disulfiram)

23
Q

alcohol- ion channels

A

NMDA R (glutamate- primary EAA of CNS)
-alcohol inhibits the ability of glutamate to open the cation channel of NMDA R- inc depression of CNS
-memory loss- due to inhibition of NMDA R activation
GABA R (GABA- primary inhibitory Nt of CNS)
-alcohol enhances effects of GABA on GABAa R

24
Q

alcohol- clinical pharmacology

A
  • Acute alcohol intoxication

- chronic alcohol abuse: acute withdrawal syndrome vs alcohol dependence

25
Q

Acute alcohol intoxication- tx

A
  • monitor resp depression ad aspiration of vomit
  • glucose- tx hypoglycemia and ketosis
  • thiamine- protect against Wernicke-Korsakoff syndrome
26
Q

Acute withdrawal syndrome- tx

A
  • can be life threatening
  • prevent seizures, delirium, arrhythmias; electrolyte rebalancing; thiamine tx
  • benzodiazepines
27
Q

Alcohol dependence

A

-psychosocial tx- primary tx!

28
Q

Alcohol dependence- tx

A
  • Naltrexone
  • Acamprosate
  • Disulfiram
29
Q

Naltrexone- moa

A
  • tx alcohol and opiate dependence
  • u opioid R antagonist (long-acting)
  • reduces craving for alcohol and rate of relapse to drinking or alcohol dependence for short term (12 wks)
  • must be opioid-free b/f starting tx!!
30
Q

Acamprosate- moa

A
  • weak NMDA-R antagonist and GABAa R agonist

- reduces short-term and long-term relapse rates (> 6 months)

31
Q

Disulfiram- moa

A

-irreversibly inhibits aldehyde dehydrogenase (build up of acetaldehyde- hangovers)- causes extreme discomfort when drink alcohol

32
Q

schedule 1-IV

A
  • I- no medical use, high addiction potential
  • II- medical use, high addiction potential
  • III- medical use, moderate abuse potential
  • IV- medical use, low abuse potential
33
Q

PSP and LSD- long term effects

A
  • PCP- irreversible schizophrenia-like psychosis

- LSD- flashbacks of altered perception yrs after consumption

34
Q

Disinhibition of DA neurons in the VTA- what drugs?

A

Inhibition of GABA inhibitory neurons (causes Dopamine release)

  • Opioids
  • THC, CBD, other cannabinoids
  • GHB
35
Q

drugs that bind transporters of biogenic amines

A

Inc conc of dopamine in synapse

  • Cocaine- inhibits DA reuptake
  • Amphetamine- gets taken up into vesicle so dopamine is not, so gets exported out

Psych (16 decks)

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