Sedatives-Hypnotics-Ethanol (Exam IV) Flashcards

1
Q

What anxiolytic is a non-sedative;non-hypnotic?

A

Buspirone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is GABA inhibitory?

A

↑ GABA = ↑ pCl⁻ = more - Vᵣₘ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are sedative-hypnotics primary MOA?
Secondary?

A
  1. ↑ GABA
  2. ↓ Glutamate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is an IPSP (Inhibitory Post-Synaptic Potential) ?

A
  • Where the post-synaptic cell is hyperpolarized to make it much more difficult for an action potential threshold to be met.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of amnesia is elicited by sedatives?

A

Anterograde amnesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What stage of sleep is bypassed through the use of sedative/hypnotics?

A

REM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 5 categories of sedative-hypnotics?

A
  1. Benzodiazepines
  2. Barbiturates
  3. Sleep Aids
  4. Anxiolytics
  5. Ethanol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which GABA channel does GABA bind to to allow Cl⁻ to flow into the neuron?

A

GABAA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the deepest state of sleep?

A

Stage 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When is REM sleep normally encountered?

A

Later in the sleep cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is undesirable in our sleep cycle?

A
  • Decreased REM
  • Decrease Stage 4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does alcohol related sleep compare to healthy sleep?

A
  • ↑ Stage 4 sleep
  • More wakefulness/REM later in sleep cycle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can persistent post-anesthetic respiratory depression from benzodiazepines be reversed?

A

Flumazenil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Is cardio-respiratory dysfunction noted with normal sedative-hypnotic dosing?
When would this no longer be the case?
Toxic doses of sedative-hypnotic would do what the cardiovascular system?

A
  • No
  • Depressed cardiac function in the presence of cardiac disease.
  • ↓ contractility.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How much of the general population has Alcohol-use Disorder?

A

8-10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which of the following is characterized as a physical need for alcohol:
1. Alcohol Abuse
2. Alcohol Dependence.

A
  • Alcohol Dependence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When does alcohol absorption peak?

A

30 min

18
Q

As a percentage, where is alcohol metabolized?

A
  • 90% Liver
  • 10% Lungs & Stomach
19
Q

The average adult metabolizes ________ of alcohol per hour.
This is about the equivalent of what?

A
  • 7-10grams
  • Equivalent to one standard drink
20
Q

What is alcohol metabolized into?
What are the two pathways by which this metabolism takes place?

A

Acetaldehyde.
- Alcohol Dehydrogenase pathway
- Microsomal Ethanol-Oxidizing System (MEOS)

21
Q

When does alcohol impairment occur? (this is also the legal limit)

A

0.08% BAC (blood alcohol concentration)

22
Q

When does fatality occur from alcohol ingestion?

A

~ 0.4% BAC

23
Q

What metabolite is primarily associated with hangover symptomology?

A

Acetaldehyde

24
Q

Describe the Alcohol Dehydrogenase pathway.
What type of reaction is this?

A
  • NAD⁺ → alcohol dehydrogenase → NADH (This converts EtOH into acetaldehyde)
  • Acetaldehyde → aldehyde dehydrogenase → acetate.
  • Oxidation-Reduction Reaction
25
Q

What product of the alcohol dehydrogenase pathway becomes problematic with chronic alcohol use?
What disease process is the end result of this?

A
  • ↑ NADH (NADH blocks metabolism of fatty acids → fatty acids in the liver)
  • Steatohepatitis (Fatty Liver disease)
26
Q

What drug is used to treat emergency ingestion of methanol or ethylene glycol (anti-freeze)?
What occurs with ingestion of these substances? How does this drug prevent this?

A
  • Fomepizole
  • Methanol & Ethylene Glycol are converted into formaldehyde by alcohol dehydrogenase. Fomepizole blocks alcohol dehydrogenase, preventing formaldehyde formation.
27
Q

What drug blocks the metabolism of acetaldehyde? How does this occur?
What is the purpose?

A
  • Disulfiram (Antabuse) blocks aldehyde dehydrogenase from converting acetaldehyde into acetate.
  • This drug was used to make drinkers have worse hangover symptoms and hopefully quit.
28
Q

How does the MEOS (microsomal ethanol-oxidizing system) differ from the alcohol dehydrogenase pathway?

A

MEOS:
- NADPH utilized instead of NAD⁺ (oxidation reaction)
-CYP450’s used
- NADP⁺ produced (no fatty liver from this method)

29
Q

What physiologic mechanism allows chronic drinkers to become “high-functioning” alcoholics?

A
  • GABA-receptor desensitization. (chronically stimulated GABA receptors causes ↓ number of GABA receptors)
30
Q

What is the mechanism of action of ethanol (alcohol) ?

A
  • ↑ GABA
  • ↓ Glutamate
31
Q

What is the most common complication of alcohol abuse? What percentage of EtOH abusers develop this?

A

15-30% of chronic drinkers develop liver disease

32
Q

What is the progression of liver disease?

A

Acoholic fatty liver (Steatosis) → alcoholic hepatitis (Steatohepatitis) → Cirrhosis → Liver Failure.

33
Q

Differentiate tolerance, dependence, & addiction.

A
  1. Tolerance = ↑ EtOH needed to get same effect.
  2. Dependence = Body is reliant on drug
  3. Addiction = Behavioral; will seek out EtOH regardless of consequences.
34
Q

What is Wernicke-Korsakoff Syndrome?
What symptoms would be typical with this syndrome?

A
  • Decreased normal nutrition & utilization of alcohol as nutrition = thiamine deficiency.
  • Eye problems, ataxia, confusion, coma, death.
35
Q

What symptoms might persist in chronic alcohol abuse even when alcohol use has stopped?

A
  • Gait disturbances/ ataxia
  • Optic nerve degeneration
  • Dementia & demyelination diseases
36
Q

What mechanism results in withdrawal seizures?

A
  • EtOH discontinuation = lack of glutamate inhibition that the body is used to → massive ↑ glutamate signaling.
37
Q

What is the drug of choice for drug-induced seizures/withdrawal?

A

Benzodiazepines

38
Q

What is Naltrexone?
What is this drug used for?
What drug class does the patient need to be completely off of prior to using this drug?

A
  • Long-acting opioid antagonist
  • Alcohol dependence (targeting endorphin release of EtOH)
  • Opioids
39
Q

What is the purpose of giving Acamprosate in treatment of EtOH abuse?

A
  • Adjunct to psychotherapy to normalize brain activity by ↑ GABA signalling.
40
Q

Which two drugs are used for treatment of sleep problems and have abuse potential?
How long is the prescription wrote for to hopefully avoid abuse?
What FDA warning exists for these two drugs?

A
  • Zolpidem (Ambien)
  • Eszopiclone (Lunesta)
  • 7-14 days.
  • FDA warning: Somnambulism.