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Brain and Behavior > Lecture 51: Sedatives, Hypnotics, Anxiolytics, and Alcohol > Flashcards

Lecture 51: Sedatives, Hypnotics, Anxiolytics, and Alcohol Flashcards

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1
Q

Anxiolytic

A

Reduce anxiety, cause calm

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2
Q

Sedative

A

Induce sedation by reducing irritability/excitement; calming

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3
Q

Hypnotic

A

Induce sleep or unconsciousness

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4
Q

Benzodiazepines are considered safe why?

A

Flatter dose-response curve (less likely to cause fatal overdose)

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5
Q

Why are barbituates dangerous?

A

Dose as low as 10x hypnotic dose may be fatal if not discovered in time due to resp/cardio depression

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6
Q

All sedative hypnotics interact with what receptor? What does this receptor do?

A

GABAa; chloride ion channel

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7
Q

Sedative-hypnotic withdrawal includes…

A

Arousal/excitability: anxiety, agitation, tachycardia, seizure

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8
Q

Barbituates we need to know (3) and their length of action

A

Phenobarbital** (long acting), secobarbital* and butalbital (intermediate acting)

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9
Q

Barbituates are now primarily prescribed for what? Which drug in particular?

A

Epilepsy (phenobarbital)

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10
Q

What can butalbital be used for?

A

Combination headaches

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11
Q

What are the mild adverse effects of barbituates? How about the severe ones?

A

Mild sedation, dizziness, impaired coordination –> coma, hypotension, cardio/respiratory failure

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12
Q

Absolute barbituate contraindication

A

Porphyria (barbituates induce ALA synthase in heme pathway)

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13
Q

This short-acting barbituate (name) is no longer used in the US. What was it used for? What odd use does it have in the US today?

A

Thiopental; preanesthetic sedative; part of the capital punishment cocktail

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14
Q

Important point about barbituate metabolism

A

CYP450 inducer (many drug interactions)

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15
Q

Short-acting (

A

Midazolam* (Versed)

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16
Q

Medium-acting (8-16 hours) benzo we need to know (2)

A

Alprazolam* (Xanax), lorazepam*

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17
Q

Long-acting (>16 hour) benzo we need to know (3)

A

Clonazepam* (Klonopin), Diazepam** (Valium), Chlordiazepoxide*

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18
Q

Describe the mechanism of benzos

A

Binds directly to GABAa receptor and increase potency of endogenous GABA signaling by increasing frequency of Cl- channel openings

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19
Q

Describe the method of action for barbituates

A

Binds directly to GABAa receptor and increase potency of endogenous GABA signaling by increasing duration of Cl- channel openings

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20
Q

Benzos are prescribed for…(5)

A

Anxiety, epilepsy, alcohol withdrawal, muscle relaxant, anesthesia induction

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21
Q

Benzo consideration for older patients? Why is this important?

A

Hepatic metabolism slows with age; greater risk for dangerous SEs (cardio/resp depression)

22
Q

What “key drug” benzo should be prescribed for patients with liver disease and why?

A

Lorazepam; no Phase I metabolism so half lives are not increased in patients with hepatic disease.

23
Q

Where are benzos better than barbituates? (5)

A
  1. Rapid onset; 2. Higher therapeutic index; 3. Flumazenil* for overdose; 4. Lower risk of drug interaction; 5. Minimal effects on cardio/ANS functions
24
Q

SEs of benzos and a notable psych risk

A

Drowsiness, impaired judgment, decreased motor skills; dependence

25
Q

Benzo toxicity…(5)

A

Ataxia, slurred speech, somnolence, diplopia, hallucinations, coma

26
Q

What is the one non-benzo (new) hypnotic we need to know? Two other drugs in this category?

A

Zolpidem** (Ambien); Zalepon* and Eszopiclone* (Lunesta)

27
Q

Describe mechanism of non-benzo hypnotics and relationship to produced effects

A

Bind to specific GABAa receptor subtype (w/ alpha 1 subunits) so only produces sedation/anxiolytic effects w/out producing muscle relaxant/anticonvulsant effects

28
Q

What SEs of non-benzo hypnotics led to FDA labeling? (2)

A
  1. Next-morning impairment and 2. Abnormal nocturnal behavior
29
Q

Zolpidem is prescribed for…Why?

A

Short-term treatment of insomnia; 1-2 weeks leads to tolerance to sleep effects

30
Q

How does Zolpidem effect sleep?

A

Decrease latency to sleep, decrease REM but little change on slow-wave sleep

31
Q

How would you treat a benzo overdose?

A

With Flumazenil*!

32
Q

What is the mechanism of Ramelteon* and its clinical use. Advantages?

A

Melatonin receptor agaonist; insomnia; does not effect sleep architecture w/ minimal risk of abuse

33
Q

What is the mechanism of Buspirone** and its clinical use. Significant SE?

A

Partial 5-HT1A agonist; GAD; tachycardia

34
Q

What is the mechanism of dexmedetomidine* and its clinical use. Advantage/disadvantage

A

Presynaptic alpha2 agonist –> downregulation of NE; perioperative sedation, analgesia. Advantage: no respiratory depression; disadvantage: caution in patients with heart dysfunction

35
Q

All sedative-hypnotics cross the what? Discuss the issue.

A

Placental barrier; complicated to use during pregnancy (may cause defects, dependence), must weight risks vs benefits

36
Q

Why do women have a higher peak concentration of ethanol? (2)

A

Lower total body water content and difference in first-pass metabolism

37
Q

How much of ethanol is oxidized by the liver? What is the rate? Where else is it excreted?

A

90%; zero-order kinetics (independent of time/drug concentration); kidneys/lungs

38
Q

Ethanol is oxidized to what by what enzyme? Then to what by what enzyme?

A

Acetaldehyde, alcohol dehydrogenase; acetate, alcohol dehydrogenase (again)

39
Q

Where does disulfiram exert its effect? Causes? What else might cause this reaction in a person?

A

Acetaldehyde –> acetate; flushing, nausea, vomiting, headaches, hypotension; genetic ALDH deficiency

40
Q

How else is alcohol metabolized? What is the relevance of this?

A

CYP2E1/CYP450 enzymes; normally only a small amount but increases with chronic alcohol exposure –> induction of metabolism of other drugs (acetaminophen contraindication)

41
Q

Two main receptor effects of alcohol

A

Enhances GABAa activity and inhibits NMDA activity

42
Q

At what BAC does what possibly black out? BAC of Death?

A

0.15; >0.40

43
Q

Alcohol does what to myocardial contractility? Smooth muscle?

A

Depresses; vasodilator

44
Q

Chronic alcohol increases the risk of death for these reasons (5)

A

Liver disease, cardiovascular disease, cancer, accidents, and suicide

45
Q

Course of alcohol liver damage

A

Fatty liver –> alcoholic hepatitis –> cirrhosis –> liver failure

46
Q

Effects of alcohol on the cardiovascular system (4)

A

Dilated cardiomyopathy, arrhythmias, hypertension, coronary artery disease

47
Q

Four broad categories of chronic alcohol effects on the CNS

A
  1. Tolerance/dependence (receptor changes, DA in NA); 2. Neurotoxicity; 3. Wernicke-Korsakoff (ataxia, opthalmoplegia, confusion –> memory disorder); 4. Eye damage
48
Q

Describe alcohols effects on the blood, endocrine system, immune system, cancer

A

Blood: impairs hematopoiesis; Endocrine: androgen problems; Immune: inhibits in some places (lung) and increases in other (liver); Cancer: upper GI, liver

49
Q

What three drugs are approved for treatment of alcohol dependence?

A

Naltrexone, acomprosate, disulfiram

50
Q

What two other alcohols cause poisoning? Treatment?

A

Ethylene glycol (antifreeze) and methanol; IV ethanol or an ALDH inhibitor to prevent toxic aldehydes

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