Sedative-Hypnotics Flashcards
End Test 3
Differentiate between sedation and hypnosis
Sedation: Calming effect
Hypnosis: encourages sleep
Identify the major subgroups of sedative hypnotics, and major drugs in each sedative-hypnotic subgroup, and their receptor target.
Benzodiazepines: diazepams, midazolam lorazepam Top of GABA-R
Barbituates: phenobarbital, thiopental, methohexital Bottom of GABA-R
Sleep aids: Ambien, Lunesta
Anxiolytics: Buspirone
Ethanol: Alcohol
What is the nickname for propofol?
Milk of amnesia
Describe a GABA receptors
Inhibitory neurotransmitter ion channel
Permits conductance of chloride
Hyperpolarizes the cell
This is where sedatives work
What do sedatives decrease?
Sleep onset latency
What happens in the early stages of sleep?
You’re able to reach stage 3/4 of sleep but you cycle back up to REM sleep
What happened to the second half of sleep?
You cycle between awakening, REM sleep, stage 1, and stage 2.
Where most dreams happen
How does alcohol affect your sleep?
You dont get good sleep
You never reach REM sleep in the first half.
You fall asleep fast
What is the reversal agent for benzodiazepines?
flumazenil
List the four phases of sleep and important changes seen when taking sedative-hypnotics.
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.
Describe alcohol abuse vs alcohol dependence
Abuse: drinking despite AE
Dependence: if you stop drinking there will be AE
Where is alcohol metabolized?
90% in liver
What is the legal limit for intoxication?
0.08
How fast does an adult metabolize alcohol?
7-10g (150-220mmol) per hour
About 1 drink per hour
What is the common pathway for alcohol?
- NAD+ cycles Alcohol dehydrogenase and converts Ethanol to Acetaldehyde and turns into NADH
- NAD+ cycles aldehyde dehydrogenase and converts Acetaldehyde to Acetate and turns into NADH
What drug inhibits alcohol dehydrogenase? aldehyde dehydrogenase?
Fomepizole: Increases ETOH levels
Disulfiram: increases acetaldehyde levels -> hangover effect immediately
What is acetaldehyde?
Toxic byproduct
Produces hangover symptoms
What is the chronic alcohol pathway?
- NADPH+O2 cycles Alcohol dehydrogenase and converts Ethanol to Acetaldehyde and turns into NADP+H2O
- NAD+ cycles aldehyde dehydrogenase and converts Acetaldehyde to Acetate and turns into NADH
What are the calories produces from in alcohol?
NADH
Summarize characteristic pharmacodynamic and pharmacokinetic properties of ethanol.
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.
What happens in Chronic alcohol use?
Liver cell death -> fatty liver -> liver fibrosis -> cirrhosis
What is Wernicke-Korsakoff Syndrome?
D/t chronic alcoholism
Lack of vitamin B1 or thiamine
SE: external eye muscle movements, confusion, ataxia
What is the difference in symptoms in acute alcoholism and chronic alcoholism
Acute: body cannot tolerate = respiratory depression, tachyarrhythmias, vomitting, decrease BP
What is the average fatal alcohol blood level?
0.4%
Tx for acute alcohol intoxication
Correct electrolyte imbalances and hypoglycemia
List the molecular targets of ethanol
- GABA-A receptors: Enhances the inhibitory effects of GABA.
- NMDA receptors: Inhibits the excitatory effects of glutamate.
- Dopamine receptors: Increases dopamine release, contributing to its rewarding effects.
- Serotonin receptors: Modulates serotonin levels, affecting mood and behavior.
- Endorphin receptors: Increases endorphin release, contributing to its analgesic effects.
What drug treats alcohol dependence?
- Naltrexone
Cannot be taking an opioid
Will cause acute withdrawal syndrome - Acamprosate - tx desire for alcohol
- Antabuse (Disulfiram)
What are normally required before prescription of sleep aids? Why?
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
What are most OTC sleep aids?
Antihistamines
What causes bizarre dreams with alcohol?
Prolonged REM in second half of sleep
