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Sleep Medicine > Neuropharmacology > Flashcards

Neuropharmacology Flashcards

1
Q

Sleep is a dynamic process. What mediates sleep in the brain?

A

Neurotransmitters

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2
Q

What is the effect of inhibitor blockade on the function of a neurotransmitter?

A

It has an agonistic effect because the inhibitors are blocked.

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3
Q

What is the effect of reuptake blockade on neurotransmitter function?

A

It has an agonistic effect because the reuptake is blocked - the neurotransmitter persists.

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4
Q

What is the effect of receptor blockade on neurotransmitter function?

A

It has an antagonistic effect because the neurotransmitter cannot exert its function.

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5
Q

What is the effect of synthesis inhibition on neurotransmitter function?

A

Antagonistic because there is no neurotransmitter being produced.

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6
Q

Where are the neurotransmitter receptors located?

A

In the post-synaptic nerve ending. The drug travels from the axon across the synaptic cleft and then attaches to receptor in the post-synaptic nerve ending. The post-synaptic area then sends the signal through the neuron.

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7
Q

Which neurotransmitters are responsible for wakefulness?

A

Norepinephrine (adrenaline), Dopamine, Acetylcholine, Histamine, Glutamate (most prevalent neurotransmitter for wakefulness in the human brain)
Location of neurotransmitter may determine its effect - for instance, ACTH is a neurotransmitter that is responsible for REM sleep as well. It’s NOT contradictory.

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8
Q

What area of the brain keeps us awake?

A

Reticular formation. Glutamate is produced here.

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9
Q

Which neurotransmitters are responsible for NREM sleep?

A

Serotonin, adenosine, gamma-amino butyric acid (GABA - the most prominent NREM sleep neurotransmitter - it is inhibitory of the reticular formation function to keep us awake).

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10
Q

How does caffeine affect sleep (neurotransmitters)?

A

Caffeine is an adenosine receptor antagonist.

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11
Q

How do levels of adenosine fluctuate throughout a 24-hour period (pattern)?

A

They begin to rise as soon as we awaken. They are correlated with homeostatic drive. As soon as we fall asleep, they begin to decrease.

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12
Q

How do benzodiazepines function (neurotransmitter)?

A

They stimulate the GABA receptors.

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13
Q

Which neurotransmitters are responsible for REM sleep?

A

Acetylcholine and adenosine.

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14
Q

Why are benzodiazepines prescribed more frequently than barbiturates?

A

Because barbiturates have a very small threshold between therapeutic and toxic doses - there is a high overdose liability with barbiturates compared to a low one with benzodiazepines (Barbs have a low therapeutic index).

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15
Q

What amount of sleep latency is considered the definition of insomnia?

A

Thirty minutes.

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16
Q

Why are non-benzodiazepines (e.g. Lunesta, Ambien) so highly favored right now?

A

Because they do not affect (remember that BZDs stimulate the GABA receptors) the GABA receptors. They are safer in terms of withdrawal.

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17
Q

How do barbiturates, BZDs, and non-BZDs affect TST?

A

Barb: Large increase
BZD: Large increase
Non-BZD: moderate increase

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18
Q

How do Barb, BZD, and non-BZD affect sleep latency?

A

They all decrease it significantly.

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19
Q

Why might the reduced sleep latency induced by sleeping pills cause greater health problems in terms of sleep arousal levels?

A

The sleep arousal is a defense of the body to protect against low oxygen in OSA. The person may feel better rested (fewer arousals with choking) but be at greater risk of CV and other problems.

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20
Q

How much time do most non-BZDs add to sleep time?

A

Four hours, which is less than the BZDs and barbs.

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21
Q

What are the effects of barbs, BZD, and non-BZD on N2 sleep?

A

Barbs and BZDs: increased N2 sleep at the expense of N3 sleep (reduced N3 sleep). Patient sleep more but don’t feel rested.
Non-BZD: no change in sleep architecture.

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22
Q

What are the effects of barbs, BZDs, and non-BZDs on REM sleep?

A

Barbs: large decrease in REM sleep.
BZDs: slight decrease in REM sleep.
Non-BZDs: no change in sleep architecture.

23
Q

What are the withdrawal implications with barbs, BZDs, and non-BZDs?

A

Barbs: Severe adverse events. Slow weaning off of the drug is needed.
BZDs: Rebound Insomnia. Weaning is needed - the rebound insomnia is often worse than the original insomnia.
Non-BZDs: Minor.

24
Q

What are the implications of Barbs, BZDs, and non-BZDs on sleep studies?

A

Non-BZD: They can just stop taking the medication for the study w/o adverse effects or inaccurate results.
Barbs & BZD: They cannot just stop or they will have rebound insomnia - no sleep, no study. If on it, many more spindles (Stage N2).

25
Q

In general, is it recommended that patient stop taking sleep medication for a sleep study?

A

No, because you want to simulate in the sleep lab what happens at home.

26
Q

How many half-lives are needed for a medication to clear from the system?

A

4.5 to 5.

27
Q

What is the primary side effect of long-acting BZDs?

A

Daytime sedation (e.g. Valium half-life is 36 hours). Patient can have resolution of OSA and still feel tired if taking one of these.

28
Q

What is the primary side effect of short-acting BZDs (Xanax, Ativan)?

A

Rebound insomnia is more pronounced with these because they clear out of the system more rapidly.

29
Q

What are the primary therapeutic effects of BZDs?

A

Anxiolytic, sedative, amnestic, anti-convulsive, mild muscle relaxant.

30
Q

What is a negative adverse event of BZDs in OSA patients (related to muscle function)?

A

BZDs are mild muscle relaxants. They reduce tonicity of the upper laryngeal airway muscles, thus potentially worsening OSA.

31
Q

What are the potential adverse events associated with rapid withdrawal from BZDs?

A

Nightmares, arousals, fragmented sleep.

32
Q

What are the effects of Non-D2 neuroleptics (Clozapine, Olanzapine, Resperidone) on sleep?

A

These antipsychotic drugs can increase sedation (daytime sleepiness), decrease N3 sleep, and increase RLS and periodic limb movement disorder (PLMD) (can result in fragmented sleep).

33
Q

Effects of propanolol (beta blocker, BP, CAD, etc.) on sleep?

A

increased nightmares, increased wakefulness

34
Q

What percentage of patients with refractory hypertension have sleep apnea?

A

Refractory is defined as hypertenstion requiring 3 or more medications. 85% have SA.

35
Q

Effects of clonidine (BP med) on sleep?

A

increased sedation/daytime sleepiness

36
Q

Effects of prazosin (BP and prostate) on sleep?

A

Increased REM, fewer nightmares.

37
Q

What are the sleep effects of dopamine and NE affecting stimulants?

A

Increase wakefulness, sleep latency, wakefulness after sleep onset (WASO), REM latency.
Decrease: TST, REM, N3 sleep.

38
Q

What are the most common DA and NE affecting stimulants?

A

Pemoline (Cylert), Mazindol (Sanorex), Seleginine (Eldepry), Amphetamine (Adderall), D-amphetamine (Dexedrine), L-amphetamine, Methamphetamine (Desoxyn), Methylphenidate (Ritalin), Cocaine and Ecstasy (both are DA and NE reuptake inhibitors).

39
Q

What are the drugs that affect serotonin levels in the brain and how do they affect levels?

A

L-tryptophan (precursor), LSD (antagonist), buspirone (antagonist), cyproheptadine (antagonist), SSRI (agonist).

40
Q

What are the effects on sleep of L-tryptophan?

A

It is a serotonin precursor that increases N3, REM density (more rapid movement of eyeballs), and decreased sleep latency.

41
Q

What are the sleep effects of LSD?

A

Serotonin antagonist. Increased REM, eye movement in N3 sleep.

42
Q

What are the sleep effects of buspirone?

A

Serotonin antagonist, antidepressant. No effects on sleep.

43
Q

What are the sleep effects of cyproheptadine?

A

Serotonin antagonist, prescribed to counter OD of SSRIs. Increased N3.

44
Q

What are the sleep effects of SSRIs?

A

Serotonin agonist. Decreased N3/increased N2, decreased REM sleep, increased daytime sedation, weight gain.

45
Q

Which three antihistamines do I need to be most aware of?

A

Diphenhydramine, triprolidine, promethazine, cetrizine, hydroxizine, and brompheniramine. All three are H1 antagonists, therefore they increase sedation (H2 antagonists, such as loratadine and zyrtec) do not as much).

46
Q

Tricyclic antidepressants and sleep?

A

All end in “mine” or “line”. They increase N3 sleep, significantly decrease REM (especially clomipramine), and increase sedation.

47
Q

What is modafinil?

A

Reduces GABA (which is inhibitory of wakefulness) in sleep promoting regions, increases histaminergic activity and inhibits the area of the brain that induces sleep (inhibits antihistamine production). IT INCREASES WAKEFULNESS.

48
Q

What is Rozerem?

A

Synthetic melatonin receptor agonist - induces sleep. Generally a safe drug.

49
Q

Opiates and sleep?

A

Daytime sedation, worsening of OSA, cause central apneas, sudden withdrawal: insomnia/nightmares.

50
Q

Alcohol and sleep?

A

Reduced SL (transient sedation), hyperarousal after sedation (2-3 a.m.), suppression of upper airway muscles (snoring and OSA), GERD, polyuria, many months of poor sleep after abstinence.

51
Q

Nicotine and sleep?

A

Relaxes, but keeps person in Stage 1 and 2 sleep - reduced N3 sleep. May delay sleep onset. Reduces REM and decreases sleep continuity. Withdrawal can induce insomnia.

52
Q

What are the AASM guidelines on caffeine use?

A

Strategic consumption is key, onset of effect is 15-30 minutes, half-life is 3-7 hours, use for temporary relief of sleepiness. Caffeine is relaxing and has analgesic effects and can actually help one to sleep, but: more arousals (wake up at 2 or 3 a.m. and be wide awake), reduced periods of REM sleep, diuretic effects.

53
Q

Decongestants and sleep?

A

Pseudoephedrine decreases sleep continuity and produces insomnia.

54
Q

Herbal medications and sleep?

A

Valerian root, chamomile, rosemary, kava kava, poppy seeds may induce sedation. Valerian inhibits GABA receptors and increases REM and slow-wave sleep.

Sleep Medicine (14 decks)

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