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Pharm Fall '24 > Test 3 - sedative-hypnotics > Flashcards

Test 3 - sedative-hypnotics Flashcards

1
Q

Deep sleep is ______

A

Hypnosis.

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2
Q

CNS effects of sedative-hypnotics

A

sedation, hypnosis, anesthesia

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3
Q

What are the classifications for sedative-hypnotics

A
  1. benzo
  2. barbituates
  3. sleep aids
  4. anxiolytics
  5. ethanol
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4
Q

sedative-hypnotics work at what receptor?

A

GABAa receptor

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5
Q

What happens when we take a sedative-hypnotic in terms of receptor and ion movement.

A

GABAa receptor is activated by inhibitory neurotransmitter GABA.

two binding sites, once activated allows Cl in and hyperpolarizes the cell.

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6
Q

Sedative hypnotics potentiate ______ at all levels of CNS

A

inhibition

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7
Q

what is sedation?

A
  1. calming - anxiolytic
  2. decrease psycho-motor function
  3. dose-dependent anterograde amnesia
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8
Q

what is hypnosis?

A

dose dependent.
1. decreased time to fall asleep
2. increased stage 2 NREM sleep
3. decreased REM
4. decreased stage 4 NREM slow-wave sleep

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9
Q

What is a normal sleep pattern?

A

during the first few hours going between stage 4 and REM.

later hours of sleep is between stage 2 and REM

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10
Q

What do we see in alcohol related sleep patterns

A

staying down in stage 3/4 for longer periods of time and not coming up to REM until much later in the night.

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11
Q

Sedative-hypnotics can be useful as an adjunct to ____

A

anesthesia

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12
Q

Thiopental and methohexital are what class of drugs?

A

barbituates.

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13
Q

thiopental has largely been replaced by _____. It has a ______ duration

A

propofol.
rapid.

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14
Q

diazepam, lorazepam and midazolam are what class of drugs

A

benzo

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15
Q

benzodiazepines may contribute to a persistent post anesthetic _______. this is reversed with ____

A

respiratory depression.
flumazenil

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16
Q

additional effects of sedative hypnotics

A
  1. anticonvulsive
  2. muscle relaxation
  3. respiratory and cardiac function
17
Q

Ethanol as a sleep aid

A

not a good sleep aid, it changes our sleep patterns and we end up having less time in REM

18
Q

Chronic alcohol abuse can lead to

A

Progression of liver damage

19
Q

Alcohol dependence

A

can have withdraw symptoms if it is stopped

20
Q

Alcohol metabolism. and zero order kinetics.

A

90% metabolized in liver.

anything over one standard drink per hour cant be metabolized so it we will start to have a higher level.

21
Q

what are the two major pathways of metabolism to acetaldehyde?

A
  1. alcohol dehydrogenase pathway
  2. microsomal ethanol-oxidizing system (MEOS)
22
Q

what is the alcohol dehydrogenase pathway

A

common pathway.

ethanol is broken down using NAD that is converted to NADH.

NADH is used to make ATP.

23
Q

what is the microsomal ethanol-oxidizing system

A

happens with chronic alcohol use. NADPH converted to NADP. they take in less calories so they can actually be thinner

24
Q

If we drink high amounts of alcohol we will have an increase in acetaldehyde, what breaks this down? and what is it converted to?

A

Aldehyde dehydrogenase;
turns into acetate.

25
Q

Fomepizole does what in regards to alcohol breakdown

A

it inhibits the alcohol dehydrogenase pathway. will increase

26
Q

Disulfiram does what in regards to alcohol breakdown?

A

inhibits the aldehyde dehydrogenase.

higher levels of acetaldehyde (causes N/V headache)

27
Q

What medication can we give alcoholics to help them stop? what effects will they have?

A

disulfiram. (antebuse)

increase in acetaldehyde causing hangover like symptoms (N/V/HA)

28
Q

What does alcohol do in regards to GABA and NMDA

A

Enhances the action of GABA at GABAa receptors

inhibits the ability of glutamate to open the NMDA channel

29
Q

Tolerance with alcohol

A

more of the drug is needed to get the same initial effect

30
Q

dependence with alcohol

A

body reliant on drug

31
Q

addiction to alcohol

A

behavior - will seek out drug regardless of neg consequences

32
Q

Neurotoxicity from alcohol can lead to what?

A

wenicke-korsakoff syndrome.
-thiamine deficiency

33
Q

management of acute alcohol intoxication

A

Prevent respiration depression and aspiration of vomit.

34
Q

management of alcohol withdrawal syndrome

A

severe can last 1-5 days.

delirium tremens is extreme. can have ANS instability

35
Q

What is naltrexone used for?

A

used to treat alcohol dependence.

36
Q

Acamprosate for alcohol

A

increases the activity of GABA channels to bring it back to a normal level

37
Q

Buspirone is a 5-HT 1A receptor antagonist that does what?

A

Relieves anxiety without sedation

38
Q

Zolpidem (ambien) and Eszopiclone (lunesta) are used for what? what is an adverse effect?

A

sleep aid.
abuse potential

39
Q

Ambien and lunesta have a black box warning for what?

A

somnambulism. sleep walking

Pharm Fall '24 (7 decks)

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