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Brain and Behavior Exam 3 > Lec 47 Sedative Hypnotics Anxiolytics Alcohol > Flashcards

Lec 47 Sedative Hypnotics Anxiolytics Alcohol Flashcards

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1
Q

What is an anxiolytic?

A

reduces anxiety, causes calm

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2
Q

What is a sedative?

A

induces sedation, has calming effect

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3
Q

What is a hypnotic?

A

induces sleep or unconsciouness

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4
Q

What are general effects of sedative hypnotics?

A
  • anti-anxiety/calming
  • sedation
  • anterograde amnesia
  • sleep
  • anesthesia
  • anticonvulsant
  • muscle relaxation
  • respiratory drive depression
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5
Q

What are possible toxicities of sedative hypnotic?

A
  • frequently overdose
  • dose-related CNS depression
  • ingestion rarely fatal in benzos
  • resp and cardio depression
  • additive effects with other CNS depressants
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6
Q

Are benzos or barbiturates safer?

A

benzos because flatter dose response curve, harder to

  • taking 10x your prescribed barbiturate dose –> can be fatal
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7
Q

What is struct of GABA-A receptors?

A
  • 2 alpha
  • 2 beta
  • 1 gamma
  • many different permutations of GABA-A receptors b/c different forms of each subunit
  • Cl ion gated channel
  • GABA binds between the alpha and Beta subunits
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8
Q

Where do benzos and newer hypnotics bind on GABA-A?

A

bind at site between alpha and gamma

when they are there –> more GABA can bind, more than usual hyperpolarization

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9
Q

Are benzos, barbiturates, newer drugs selective for specific isoforms of GABA-A?

A

benzos and barbs are not

newer isoforms are –> why they may have fewer side effects and harder to overdose

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10
Q

What is role of a1 subunit?

A
  • mediates sedation, amnesia, ataxia
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11
Q

What is role of a2 and a3 subunits?

A
  • muscle relaxing, anxiolytic
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12
Q

What is role of a5 subunit?

A

memory impairment

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13
Q

What are symptoms of sedative-hypnotic withdrawal?

A 
anxiety/agitation
restlessness
insomnia
tremor
CNS excitability
tachycardia, HT

abrupt cessation can be lethal

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14
Q

What are 2 intermediate acting barbiturates?

A

secobarbital, butalbital

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15
Q

What is one long acting barbiturate?

A

phenobarbital

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16
Q

Are barbiturates absorbed quickly or slowly?

A

rapidly absorbed/distrubuted , they are lipophilic

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17
Q

How are barbiturates metabolized/eliminated? half life?

A

metabolized: slowly into alcohols –> over time cause induction cyt p450 enzyme
eliminated: renal

half life = ~4-5 days

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18
Q

What is clinical use of barbiturates?

A
  • epilepys [phenobarb]
  • anesthesia induction
  • physician assisted suicide
  • lethal injection
  • combo headache remedies [butalbital]
  • induction agent for shock therapy for depression
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19
Q

What are adverse effects of barbiturates? severe?

A
  • mild sedation, dizziness, impaired coordination, slurred speech, nystagmus, confusion, ataxia
    severe: coma, HT, hypothermia, resp failure
    exam: small pupils, diminished reflexes
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20
Q

Why aren’t barbiturates used anymore a lot?

A
  • tolerance to hypnotic effects
  • induction of CYP450 = drug interactions
  • low margin of safety
  • addiction
  • no antidote
  • effects on CV/autonomic
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21
Q

What is difference benzos vs barbiturates at GABA-A?

A

benzos –> increased frequency of Cl channel opening

barbs –> increase duration of Cl channel opening, less selective so can also depress glutamate receptor

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22
Q

What is clinical use of benzos?

A
  • panic/anxiety
  • insomnia (short term)
  • epilepsy (acute status epilepticus)
  • alcohol withdrawal
  • muscle relaxation
  • anesthesia
  • acute agitation/psych
  • parasomnias
  • mania, catatonia
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23
Q

What is clinical use of midazolam?

A

induction agent of anesthesia

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24
Q

What is clinical use of clonazepam?

A

parasomnias

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25
Q

How are benzos metabolized/excreted?

A

hepatic metabolism
– usually phase 1 oxidation with CYP3A4 then phase 2 conjugation

renal excretion

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26
Q

3 benzos that do not undergo phase 1 metabolism? importance?

A

lorazema
oxazepam
temazepam

much safer to use with liver disease

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27
Q

How are half lives of benzos changed in older pts? pts with liver disease?

A

longer half life with older pts and with liver disease

28
Q

Do drugs that have phase 1 metabolism have shorter or longer half life?

A

very long half life! > 40 hrs

29
Q

What is the half life of alprazolam?

A

very short!

30
Q

Categorize as short, intermediate, or long: Midazolam, alprazolam, diazepam, lorazepam, clonazepam

A 
diazepam = very long
clonazepam = intermediate-long
lorazepam = intermediate
alprazolam = intermediate
midazolam = short but IV
31
Q

What are adverse effects of benzos?

A
  • drowsiness
  • disinhibition
  • confusion
  • anterograde amnesia
  • impaired motor skils
  • resp/cardio depression
  • dependence/abuse
  • additive CNS depression with other drugs
  • life threatening withdrawal
32
Q

What is difference between benzo and z drugs in binding of GABA-A?

A

Z drugs = more selective, only bind isoforms of GABA-A that contain alpha 1 subunits

33
Q

What are exam findings of barbituate tox [pupils; reflexes]?

A
  • small pupils

- diminished reflexes

34
Q

Which benzos are safe in liver disease?

A
  • the ones that don’t undergo phase 1 metabolism in liver

- oxazepam, lorazepam, temazepam

35
Q

What are advantages of benzos?

A
  • minimal CV and autonomic effects
  • low risk of drug interactions
  • availability flumazenil for treatment overdose
  • high therapeutic index
  • rapid onset
36
Q

How do you treat barb overdose? benzo overdose?

A 
barb = supportive, no antidote
benzo = treat with flumazenil
37
Q

What is mech of action flumazenil?

A

competitive antagonist at GABA benzodiazepine receptor

38
Q

What is effect of benzos and barbs on sleep [on onset, stage 2, REM, stage 4]?

A
  • decreased latency sleep onset
  • increased duration stage 2 sleep
  • decreased duration REM sleep
  • decreased duration stage 4 slow wave sleep
39
Q

What is effect of zolpidem on sleep [on onset, stage 2, REM, stage 4]?

A
  • decreased latency sleep onset
  • decreased duration REM sleep
  • minimal effect stage 4 slow wave sleep
40
Q

Why are newer hypnotics in theory better than benzos/barbs for sleep?

A
  • newer hypnotics do not decrease slow wave sleep which is important
41
Q

What is function of ramalteon?

A

pt having difficulty falling asleep

42
Q

Which are safe in pregnancy: Buspirone, barbs, non-benzo hypnotics, benzos

A 
buspirone = category B
non-benzos = category C = not a lot of data

others are category D = more dangerous

all cross placental barrier
even though benzos = category D/X use in pregnancy b/c untreated anxiety disorder might be more damaging to pregnant woman/fetus

all can cause newborn to be dependent

43
Q

What other types of drugs besides sedative/hypnotics can be used to manage insomnia/anxiety?

A
  • antidepressants
  • antihistamines
  • atypical antipsychotics
  • antiepileptics
44
Q

When is peak BAC after drinking alcohol if fasting?

A

within 30 min

45
Q

How much alcohol can typical adult metabolize per hour?

A

7-10 g = 1 drink

46
Q

What are kinetics of ethanol elimination?

A

zero order kinetics = independent of time and concentration of drug

47
Q

What are two paths of alcohol metabolism to acetaldehyde? final step of metabolism from acetaldehyde?

A
  • via alcohol dehydrogenase = primary path
  • via MEOS [microsomal ethanol-oxidizing system]

from acetaldehyde –> acetate by aldehyde dehydrogenase

48
Q

What is disulfram?

A
  • inhibits aldehyde dehydrogenase [oxidation acetaldehyde to acetate]
  • causes there to be accumulation of acetaldehyde = unpleasant facial flushing, N/V, dizziness, headache
49
Q

At what BAC do you have coma/death? blackout?

A 
blackout = 0.15
death = 0.4
50
Q

What is the most common complication of alcohol abuse?

A
  • liver disease

- –> alcoholic fatty liver = reversible but may progress to alcoholic hepatitis and cirrhosis/liver failure

51
Q

How does chronic alcohol use affect the CV system?

A
  • dilated cardiomopathy = right ventricle really big and doesn’t pump well
  • heart failure
  • arrhythmias
  • HT
  • coronary artery disease
52
Q

How does chronic alcohol use affect CNS?

A
  • upregulation NMDA glut receptors + voltage-sensitive Ca channels –> seizures
  • increases DA release
  • peripheral nerve injury
  • cerebellar tox
  • wernicke-korsakoff syndrome
53
Q

What is wernicke-korsakoff?

A
  • due to alcoholism
  • paralysis external eye muscles, ataxia
  • confused state
  • associated with thiamine deficiency
  • diabling memory disorder
54
Q

What is fetal alcohol system? features?

A
  • ethanol crosses placenta to fetus
  • fetal liver has no alcohol dehydrogenase
  • intrauterine growth retardation, microcephaly, poor coordination
55
Q

What are alcohol-drug interactions?

A

PK: chronic alcohol use –> induction hepatic cyt p450
- get increased risk hepatotoxicity w/ drugs that are metabolized by P450s [ex. acetaminophen]

  • can increase level of tricyclic antidepressants, sedative-hypnotics
  • additive CNS depression when alcohol combined with sedative hypnotics
56
Q

What is goal of acute alcohol intoxication treatment?

A
  • give thiamine to protect wernicke-korsakoff
  • IVF with electrolytes if dehydrated + vomiting
  • correct electrolyte imbalance
  • treat hypoglycemia w/ glucose

prevent resp depression, prevent aspiration of vomit, support CV system

57
Q

How do you manage alcohol withdrawal?

A

want to prevent seizures, delirium, arrhythmias
- substitute long-acting sedative hypnotic for alcohol [usually benzo –> diazepam if good hepatic function; lorazepam if not]

  • taper dose of long acting drug
  • give thiamine
  • restore electrolytes
58
Q

What 3 FDA approved drugs for treatment of alcohol dependence?

A
  • naltrexone
  • acamprosate
  • disulfiram
59
Q

What is mech of naltrexone?

A

long acting opioid antagonist

60
Q

Who should you avoid giving naltrexone to?

A

pts on opioids or disulfiram

pts with liver disease

61
Q

What is mech of acamprosate?

A

weak NMDA-receptor antagonist and GABA-A receptor agonist

62
Q

What are upsides and downsides to acamprosate?

A

upsides: no drug-drug interaction; safer for pt with liver disease
downsides: avoid in renal disease; poor absorption; need to give many pills / day

63
Q

What is mech of methanol?

A
  • found in commercial solvents
  • absorbed through skin, resp, or GI
  • slow ox to toxic metabolites –> 6-30 hrs before toxic
64
Q

What are signs of methanol poisoning?

A
  • look inebriated; visual disturbance; anion gap metabolic acidosis
65
Q

How do you treat methanol poisoning?

A
  • alkalinization [bicarb] to coutneract metabolic acidosis

- give alcohol or fomepizole to compete with methanol

66
Q

What is ethylene glycol? signs of poisoning?

A
  • in antifreeze
  • metabolized to toxic aldehyde
  • get severe anion gap met acidosis; osmolar gap; oxalate crystals in urine; no visual symptoms
67
Q

How do you distinguish methanol vs ethylene glycol poisoning?

A

both = osmolar gap; anion gap metabolic acidosis

methanol = visual symptoms
ethylene glycol = oxalate crystal in urine

Brain and Behavior Exam 3 (32 decks)

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