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SBM psychiatry > PHARM - pharmacology of alcohol > Flashcards

PHARM - pharmacology of alcohol Flashcards

1
Q

major alcohol pharmacodynamics

A

DIRECT

  • binds GABA-A receptor - inhibitory (relaxation, motor slowing, decreased coordination)
  • antagonist to glutamate (sedation, impaired memory and cognition)

INDIRECT

  • opioid (indirect stimulation of B endorphins/u-receptors pleasure and reward)
  • dopamine (indirect in VTA, reward/pleasure/goal oriented)
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2
Q

explain the alcohol dehydrogenase pathway

A

in the presence of ADH, NAD+ and ethanol are transformed into NADH and acetaldehyde.

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3
Q

physiological consequences of ADH pathway

A

increased NADH can result in:

  • increased lactic acid production resulting in hyperuricemia and gout
  • increased ketone bodies (ketosis)
  • increased triglycerides (fatty liver)
  • decreased gluconeogenesis (hypoglycemia)
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4
Q

explain the MEO system

A
  • microsomal ethanol oxidizing system
  • increased contribution to ADH system as ethanol concentration gets above 100mg/dl
  • NADPH (cytochrome P450) and O2 convert ethanol to acetaldehyde and products are NADP+ and water
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5
Q

acetaldehyde metabolism

A
  • also NAD+ to NADH
  • aldehyde dehydrogenase (ALDH)
  • ends in acetate
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6
Q

how is acetate metabolized?

A

oxidized by body organs into CO2, H2O, and Acetyl-CoA

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7
Q

disulfiram

A
  • inhibits ALDH
  • accumulation of acetaldehyde, very unpleasant feeling
  • caution with liver disease
  • helpful in couples behavioral counseling
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8
Q

men have lower BACs largely because….

A

men have higher GI ADH and can metabolize early

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9
Q

difference between legal and hospital BAC

A

law uses whole blood volume whereas hospitals use plasma, so hospitals have higher values (divide by 1.16)

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10
Q

why does faster drinking cause exponentially greater deficits?

A

saturation of ADH

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11
Q

deficiency in wernicke-korsakoff

A

thiamine (vitamin B deficiencies)

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12
Q

wernicke’s symptoms

A
  • opthalmoplegia
  • ataxia
  • nystagmus
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13
Q

korsakoff’s symptoms

A
  • apathy
  • anterograde or retrograde amnesia
  • lack of insight
  • confabulation (fabricated or distorted memories)
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14
Q

percent of heavy drinkers with liver disease

A

15-30%

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15
Q

two likely sources of tolerance

A

1) hepatic enzymes increased

2) compensatory neurotransmitter concentrations (decreased GABA, increased glutamate, decreased dopamine)

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16
Q

abrupt alcohol cessation chemistry

A

1) glutamate up and GABA down (seizures, delirium, tremors)

2) DA down (lack of motivation, anhedonia, dysphoria)

17
Q

primary goals in treatment of alcohol withdrawal syndrome

A
  • prevent seizures, delirium, and WK syndrome
18
Q

what’s in a banana bag

A
  • glucose
  • thiamine
  • multivitamins
  • folate
  • potassium
  • electrolytes
19
Q

lorazepam

A
  • allosterically potentiates GABA
  • helps with withdrawal
  • short acting but more frequent doses
  • good for elderly because few metabolites
20
Q

chlordiazepoxide

A
  • original benzo
  • allosterically potentiates GABA
  • effects well known
  • longer half life than lorazepam, especially due to metabolites
  • metabolites make it bad for elderly or those with liver disease
21
Q

gabapentin

A
  • GABA analogue
  • non-addictive
  • less immediate relapse to alcohol
  • good for long withdrawal
  • off-label use, not good for seizures and not reliable for serious inpatients
22
Q

what are the anti-craving medications?

A
  • naltrexone
  • acamprosate
  • topiromate
  • disulfiram
  • gabapentin
23
Q

naltrexone

A
  • opioid antagonist
  • can be toxic in liver disease
  • inhibits effects of opiates
24
Q

acamprosate

A
  • GABA analogue, NMDA antagonist
  • acts on DA, 5-HT, NE
  • bad for depression and renal impairment
  • positive effect questionable
25
Q

topiramate

A
  • anti-epileptic
  • augments GABA, inhibits AMPA
  • can be taken daily, even if still drinking
  • can take up to 8 weeks for full effect

SBM psychiatry (20 decks)

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