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Psychopharm Exam 2 > Sedative Hypnotics > Flashcards

Sedative Hypnotics Flashcards

1
Q

What are the sedative hypnotics?

A

alcohols, barbiturates and benzodiazepines

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2
Q

functions of sedative hypnotics

A

-disinhibition of behavior
-sedation
anticonvulsant
-anesthesia
-respiratory & cardiac depression

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3
Q

common alcohols

A
  • isopropyl alcohol
  • methanol
  • ethanol
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4
Q

isopropyl alcohol

A

rubbing alcohol

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5
Q

methanol

A

-methyl alcohol (wood alcohol)
-antifreeze
toxic to the optic nerve due to the accumulation of formic acid

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6
Q

ethanol

A

ethyl alcohol

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7
Q

denatured alcohol

A

acetone/methanol added to ethanol to render it undrinkable

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8
Q

proof

A
  • a measure of alcohol concentration

- twice the percentage of the alcohol content

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9
Q

story behind proof

A

British soldiers poured liquor on gunpowder and lit it, if the power popped in despite it being wet, it was proof that the liquor was 50% alcohol or better (ie 100 proof)

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10
Q

fermentation

A

sugar + water + air is invaded by yeast which consume sugar, ethanol & CO2 are produced

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11
Q

distillation

A

the process of concentrating ethanol after fermentation (remove water)

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12
Q

oral administration

A
  • readily crosses membranes

- 20% alcohol absorbed in stomach, 80% in liver

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13
Q

absorption of alcohol is altered by:

A
  • stomach contents

- carbonation

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14
Q

effects of stomach contents on absorption

A
  • empty stomach: blood levels from 1 drink peak in 20-30min

- carbonation: speeds gastric emptying & absorption

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15
Q

distribution

A

evenly distributes throughout the water of the body

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16
Q

What is the basis for the breathalyzer test?

A
  • levels of alcohol in blood reflect levels in brain

- ethanol in blood is carried to lungs and vaporized

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17
Q

result of women tending to have higher proportion of body fat to body water

A

higher blood ethanol concentrations

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18
Q

alcohol metabolism

A

liver metabolizes 90-95% of the alcohol

  • antabuse blocks the metabolism of alcohol
  • 50% of Asians lack one of the enzymes to metabolize ethanol
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19
Q

alcohol metabolism pathway

A
  • alcohol broken down into acetaldehyde by alcohol dehydrogenase
  • acetaldehyde dehydrogenase breaks acetaldehyde into acetic acid
  • acetic acid broken down into carbon dioxide by an oxidation reaction
20
Q

effects of high acetaldehyde levels

A

flushing, nausea, headache and increased heart rate

21
Q

phenotype associated with homozygosity for active form of acetaldehyde dehydrogenase

A

mild or no flushing

22
Q

phenotype associated with heterozygosity for acetaldehyde dehydrogenase

A

flushing

23
Q

phenotype associated with homozygosity for inactive form of acetaldehyde dehydrogenase

A

severe flushing

24
Q

alcohol metabolism in 150lb male

A
  • metabolizes 10g alcohol/hour, or one 12oz beer or 1.25oz whiskey/hour
  • consumption over this level results in intoxication
25
Q

men have more _____ in stomach lining, results of this?

A

alchohol dehydrogenase; may contribute to lower blood ethanol levels in men than women

26
Q

enzyme activity ____ with increased exposure, contributing to ____ and _____

A

increases; tolerance; cross-tolerance

27
Q

metabolic tolerance

A

pharmoacokinetic tolerance; rate of elimination

28
Q

functional tolerance

A

pharmacodynamic tolerance; can develop tolerance to sedative effects, but not all the effects

29
Q

high doses of ethanol

A

increases membrane fluidity:

  • disrupts lipid matrix of membranes
  • non-specific disruption in neuronal function
  • failures in axonal conduction and transmitter release
  • relevant to blackouts and anesthetic properties
30
Q

lower doses

A

indirect GABA receptor agonist, potentiates the effects of GABA

31
Q

GABA

A

most common inhibitory neurotransmitter

32
Q

GABA receptor recognition sites

A

alcohol recognition site, benzodiazepine and barbiturate recognition sites

33
Q

Are GABA receptors metabotropic or ionotropic?

A

ionotropic

34
Q

Will ethanol have an effect in the absence of GABA?

A

no

35
Q

GABA receptor info:

A
  • forms a chloride channel

- most often contains: 2 alpha subunits, 2 beta subunits and 1 gamma subunit

36
Q

Why is GABA inhibitory?

A

the docking of GABA at GABA receptor opens chloride channel, when Cl- flows into cell, it hyperpolarizes the cell making it less likely to fire

37
Q

non-specific actions of GABA

A
  • interacts with polar heads of phospholipids
  • alters lipid composition
  • disturbs the relationship of protein in membrane
38
Q

specific actions of GABA

A
  • acts as a neurotransmtter binding site
  • modifies gating mechanism inside channel
  • direct interaction with channel protein
  • stimlates Gs which is linked to adenylyl cyclase
39
Q

withdrawal after acute intake

A
  • headache, upset stomach, depression, anxiety, thirst
  • severity related to amount consumed and type of beverage
  • partly due to dehydration and alterations in blood sugar levels
40
Q

ethanol withdrawal after chronic intake

A
  • life-threatening
  • tremors, hallucinations, seizures
  • lasts several weeks
  • due to massive rebound excitation in nervous system
41
Q

Why is ethanol withdrawal after chronic intake life threatening?

A

the nervous system increases excitation in response to GABA potentiation, thus when there is no longer increased inhibition one gets way to much excitation

42
Q

Alcohol withdrawal, dopamine and nucleus accumbens

A

since alcohol increases dopamine release, withdrawal decreases dopamine release, linked to rigidity, vocalizations, tremors and depression

43
Q

Wernicke-Korsakoff’s Syndrome

A
  • confusion and memory loss
  • due to deficits in vitamin B1 (thiamine) intake
  • loss of cells in dorsomedial thalamus (not diagnostic criteria, found in other illnesses)
44
Q

cells of dorsomedial thalamus

A
  • lost in Wernicke-Korsakoff’s syndrome and schizophrenia

- these cells form a wall to lateral ventricles, thus in these illnesses the ventricles are widened

45
Q

Symptoms of fetal alcohol syndrome

A
  • slowed pre- and post-natal growth
  • abnormal facial features (small head, flattened nose, thin upper lip, indistinct philtrum)
  • CNS dysfunction
46
Q

CNS dysfunction in fetal alcohol syndrome

A
  • abnormal behavior, mental retardation
  • small brain size
  • under-developed brain
47
Q

Incidence of fetal alcohol syndrome

A

0.05 - 0.3% in general population

Psychopharm Exam 2 (5 decks)

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