Test 3 - sedative-hypnotics Flashcards

(39 cards)

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thiopental has largely been replaced by _____.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
Fomepizole does what in regards to alcohol breakdown
it inhibits the alcohol dehydrogenase pathway. will increase
26
Disulfiram does what in regards to alcohol breakdown?
inhibits the aldehyde dehydrogenase. higher levels of acetaldehyde (causes N/V headache)
27
What medication can we give alcoholics to help them stop? what effects will they have?
disulfiram. (antebuse) increase in acetaldehyde causing hangover like symptoms (N/V/HA)
28
What does alcohol do in regards to GABA and NMDA
Enhances the action of GABA at GABAa receptors inhibits the ability of glutamate to open the NMDA channel
29
Tolerance with alcohol
more of the drug is needed to get the same initial effect
30
dependence with alcohol
body reliant on drug
31
addiction to alcohol
behavior - will seek out drug regardless of neg consequences
32
Neurotoxicity from alcohol can lead to what?
wenicke-korsakoff syndrome. -thiamine deficiency
33
management of acute alcohol intoxication
Prevent respiration depression and aspiration of vomit.
34
management of alcohol withdrawal syndrome
severe can last 1-5 days. delirium tremens is extreme. can have ANS instability
35
What is naltrexone used for?
used to treat alcohol dependence.
36
Acamprosate for alcohol
increases the activity of GABA channels to bring it back to a normal level
37
Buspirone is a 5-HT 1A receptor antagonist that does what?
Relieves anxiety without sedation
38
Zolpidem (ambien) and Eszopiclone (lunesta) are used for what? what is an adverse effect?
sleep aid. abuse potential
39
Ambien and lunesta have a black box warning for what?
somnambulism. sleep walking