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Pharm > Sedative-Hypnotics > Flashcards

Sedative-Hypnotics Flashcards

End Test 3

1
Q

Differentiate between sedation and hypnosis

A

Sedation: Calming effect

Hypnosis: encourages sleep

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2
Q

Identify the major subgroups of sedative hypnotics, and major drugs in each sedative-hypnotic subgroup, and their receptor target.

A

Benzodiazepines: diazepams, midazolam lorazepam Top of GABA-R

Barbituates: phenobarbital, thiopental, methohexital Bottom of GABA-R

Sleep aids: Ambien, Lunesta

Anxiolytics: Buspirone

Ethanol: Alcohol

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3
Q

What is the nickname for propofol?

A

Milk of amnesia

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4
Q

Describe a GABA receptors

A

Inhibitory neurotransmitter ion channel
Permits conductance of chloride
Hyperpolarizes the cell

This is where sedatives work

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5
Q

What do sedatives decrease?

A

Sleep onset latency

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6
Q

What happens in the early stages of sleep?

A

You’re able to reach stage 3/4 of sleep but you cycle back up to REM sleep

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7
Q

What happened to the second half of sleep?

A

You cycle between awakening, REM sleep, stage 1, and stage 2.

Where most dreams happen

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8
Q

How does alcohol affect your sleep?

A

You dont get good sleep

You never reach REM sleep in the first half.
You fall asleep fast

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9
Q

What is the reversal agent for benzodiazepines?

A

flumazenil

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10
Q

List the four phases of sleep and important changes seen when taking sedative-hypnotics.

A

NREM Stage 1: Light sleep, where you drift in and out of sleep and can be awakened easily.

NREM Stage 2: Eye movement stops and brain waves become slower with occasional bursts of rapid waves called sleep spindles.

NREM Stage 3/4: Deep sleep, also known as slow-wave sleep, where it is difficult to wake someone up.

REM Sleep: Rapid eye movement sleep, where dreaming occurs, and brain activity is similar to wakefulness.

Sedative-hypnotics increase stage 2 non-REM sleep but decrease REM and stage 3/4 sleep.

-Decrease sleep latency: The time it takes to fall asleep is reduced.
-Increased total sleep time: The overall duration of sleep is increased.
-Altered sleep architecture: There may be changes in the proportion of time spent in different sleep stages, often with a reduction in REM sleep and deep sleep.

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11
Q

Describe alcohol abuse vs alcohol dependence

A

Abuse: drinking despite AE

Dependence: if you stop drinking there will be AE

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12
Q

Where is alcohol metabolized?

A

90% in liver

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13
Q

What is the legal limit for intoxication?

A

0.08

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14
Q

How fast does an adult metabolize alcohol?

A

7-10g (150-220mmol) per hour

About 1 drink per hour

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15
Q

What is the common pathway for alcohol?

A
  1. NAD+ cycles Alcohol dehydrogenase and converts Ethanol to Acetaldehyde and turns into NADH
  2. NAD+ cycles aldehyde dehydrogenase and converts Acetaldehyde to Acetate and turns into NADH
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16
Q

What drug inhibits alcohol dehydrogenase? aldehyde dehydrogenase?

A

Fomepizole: Increases ETOH levels

Disulfiram: increases acetaldehyde levels -> hangover effect immediately

17
Q

What is acetaldehyde?

A

Toxic byproduct

Produces hangover symptoms

18
Q

What is the chronic alcohol pathway?

A
  1. NADPH+O2 cycles Alcohol dehydrogenase and converts Ethanol to Acetaldehyde and turns into NADP+H2O
  2. NAD+ cycles aldehyde dehydrogenase and converts Acetaldehyde to Acetate and turns into NADH
19
Q

What are the calories produces from in alcohol?

A

NADH

20
Q

Summarize characteristic pharmacodynamic and pharmacokinetic properties of ethanol.

A

a. Ethanol is rapidly absorbed, distributes evenly, and exhibits zero-order kinetics at higher doses.
b. Pharmacodynamics:
i. Ethanol acts as a central nervous system depressant.
ii. It enhances the effects of GABA at GABA-A, an inhibitory neurotransmitter, and inhibits the effects of glutamate, an excitatory neurotransmitter.
iii. It affects various neurotransmitter systems, including dopamine, serotonin, and endorphins.
c. Pharmacokinetics:
i. Ethanol is rapidly absorbed from the gastrointestinal tract.
ii. It is distributed throughout the body, including the brain, where it exerts its effects.
iii. It is metabolized primarily in the liver and the rest unchanged in the urine, breath, and sweat.

21
Q

What happens in Chronic alcohol use?

A

Liver cell death -> fatty liver -> liver fibrosis -> cirrhosis

22
Q

What is Wernicke-Korsakoff Syndrome?

A

D/t chronic alcoholism

Lack of vitamin B1 or thiamine

SE: external eye muscle movements, confusion, ataxia

23
Q

What is the difference in symptoms in acute alcoholism and chronic alcoholism

A

Acute: body cannot tolerate = respiratory depression, tachyarrhythmias, vomitting, decrease BP

24
Q

What is the average fatal alcohol blood level?

A

0.4%

25
Q

Tx for acute alcohol intoxication

A

Correct electrolyte imbalances and hypoglycemia

26
Q

List the molecular targets of ethanol

A
  1. GABA-A receptors: Enhances the inhibitory effects of GABA.
  2. NMDA receptors: Inhibits the excitatory effects of glutamate.
  3. Dopamine receptors: Increases dopamine release, contributing to its rewarding effects.
  4. Serotonin receptors: Modulates serotonin levels, affecting mood and behavior.
  5. Endorphin receptors: Increases endorphin release, contributing to its analgesic effects.
27
Q

What drug treats alcohol dependence?

A
  1. Naltrexone
    Cannot be taking an opioid
    Will cause acute withdrawal syndrome
  2. Acamprosate - tx desire for alcohol
  3. Antabuse (Disulfiram)
28
Q

What are normally required before prescription of sleep aids? Why?

A

Sleep aids are a high risk for abuse

MDs will normally use these as last result

Other nonpharmacological methods and a sleep study will normally happen beforehand

Normally only prescribed for short period

29
Q

What are most OTC sleep aids?

A

Antihistamines

30
Q

What causes bizarre dreams with alcohol?

A

Prolonged REM in second half of sleep

31
Q
A

Pharm (30 decks)

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