Week 10 - Chapter 34 Sedative-Hypnotic Drugs

Question 1

Anterograde Amnesia

Answer 1

impaired recall of events that take place after dosing/injury

Question 2

Drug-Dependency Insomnia

Answer 2

particular problem with older hypnotics (eg, barbiturates), and develops as follows:
1. Insomnia motivates treatment with hypnotics.
2. With continuous drug use, low-level physical dependence develops.
3. Upon cessation of treatment, a mild withdrawal syndrome occurs and disrupts sleep.
4. Failing to recognize that the inability to sleep is a manifestation of drug withdrawal, the patient becomes convinced that insomnia has returned and resumes drug use.
5. Continued drug use leads to heightened physical dependence, making it even more difficult to withdraw medi­cation without producing another episode of drug-dependency insomnia.
To minimize drug-dependency insomnia, hypnotics should be employed judiciously. That is, they should be used in the lowest effective dosage for the shortest time required.

Question 3

Hypnotics

Answer 3

drugs that depress central nervous system (CNS) function.

Question 4

Melatonin Agonist

Answer 4

analogies of melatonin that bind to and activate melatonin receptors

Question 5

Non-Rapid-Eye-Movement Sleep

Answer 5

NREM sleep is further divided into four stages, labeled I, II, III, and IV. Sleep is relatively light in stages I and II, and deep in stages III and IV.

Question 6

REM Sleep

Answer 6

REM sleep is the phase when most recallable dreams occur

Question 7

Triazolam - use

Answer 7

used to promote sleep

Question 8

Triazolam - category

Answer 8

benzodiazepines

Question 9

Triazolam - mechanism of action

Answer 9

potentiate the actions of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter found throughout the CNS. These drugs enhance the actions of GABA by binding to specific receptors in a supramolecular structure known as the GABA receptor–chloride channel complex

Question 10

Triazolam - adverse effects

Answer 10

Category X. Common retro-grade amnesia. tolerance to hypnotic effects can develop quickly—in 11 to 18 days, which is much faster than with other benzodiazepines; and (2) triazolam causes more rebound insomnia than other benzodiazepines.

Question 11

Zolpidem - use

Answer 11

short-term management of insomnia

Question 12

Zolpidem - category

Answer 12

benzodiazepine-like drug

Question 13

Zolpidem - adverse effects

Answer 13

Short-term treatment is not associated with significant tolerance or physical dependence. Withdrawal symptoms are minimal or absent. Similarly, the abuse liability of zolpidem is low. Accordingly, the drug is classified under Schedule IV of the Controlled Substances Act.
Like other sedative-hypnotics, zolpidem can intensify the effects of other CNS depressants. Accordingly, patients should be warned against combining zolpidem with alcohol and all other drugs that depress CNS function.

Question 14

Zolpidem - mechanism of action

Answer 14

binds to the benzodiazepine receptor site on the GABA receptor–chloride channel complex and shares some properties of the benzodiazepines. Like the benzodiazepines, zolpidem can reduce sleep latency and awakenings and can prolong sleep duration. The drug does not significantly reduce time in rapid-eye-movement (REM) sleep and causes little or no rebound insomnia when therapy is discontinued

Question 15

Zaleplon - use

Answer 15

short-term management of insomnia, but prolonged use does not appear to cause tolerance

Question 16

Zaleplon - category

Answer 16

pyrazolopyrimidines

Question 17

Zaleplon - adverse effects

Answer 17

well tolerated. The most common side effects are headache, nausea, drowsiness, dizziness, myalgia, and abdominal pain.

Question 18

Zaleplon - mechanism of action

Answer 18

binds to the benzodiazepine1 receptor site on the GABA receptor–chloride channel complex, enhancing the depressant actions of endogenous GABA. In contrast to zolpidem, zaleplon has a very rapid onset and short duration of action, and hence is good for helping patients fall asleep, but not for maintaining sleep.

Question 19

Secobarbital - use

Answer 19

daytime sedation, induction of sleep, suppression of seizures, and general anesthesia

Question 20

Secobarbital - category

Answer 20

Barbiturates

Question 21

Secobarbital - mechanism of action

Answer 21

nonselective depression of CNS function and are the prototypes of the general CNS depressants. Because they depress multiple aspects of CNS function

Question 22

Secobarbital - adverse effects

Answer 22

high abuse potential, and are subject to multiple drug interactions.

Question 23

Ramelteon - use

Answer 23

treating chronic insomnia 379characterized by difficulty with sleep onset, but not with sleep maintenance.

Question 24

Ramelteon - adverse effects

Answer 24

None. Ramelteon does not bind with the GABA receptor–chloride channel complex, or with receptors for neuropeptides, benzodiazepines, dopamine, serotonin, norepinephrine, acetylcholine, or opioids.

Question 25

Ramelteon - mechanism of action

Answer 25

activates receptors for melatonin—specifically the MT1 and MT2 subtypes, which are key mediators of the normal sleep-wakefulness cycle. Sleep promotion derives primarily from activating MT1 receptors. (Under physiologic conditions, activation of MT1 receptors by endogenous melatonin induces sleepiness.) Ramelteon does not activate MT3 receptors, which help regulate numerous systems unrelated to sleep. Selectivity for MT1 and MT2 receptors explains why ramelteon is superior to melatonin itself for treating insomnia

Question 26

Ramelteon - category

Answer 26

Melatonin Agonist