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Psych Pharm > Alcohol: use & abuse > Flashcards

Alcohol: use & abuse Flashcards

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1
Q

What can be given for acute methanol or ethylene glycol intox?

A

ethanol and fomepizole

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2
Q

What drugs are given for EtOH dependence?

A

Disulfiram
Naltrexone
Acamprosate

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3
Q

What to give to a pt in EtOH withdrawal?

A

thiamine and BNZs

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4
Q

how is EtOH metabolized?

A
  1. ethanol to acetaldehyde via alcohol dehydrogenase
    * inhibited by fomepizole
  2. Acetaldehyde to Acetate via Aldehyde DH
    * inhibited by disulfiram
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5
Q

why is disulfiram used?

A

to encourage abstinence from alcohol by preventing the metabolism of acetaldehyde – accumulation of this leads to feeling of nausea and flushing rxn

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6
Q

Asian flush why?

A

polymorphisms in aldehyde DH

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7
Q

What is a problem w/ disulfiram in some alcoholics?

A
  • find acetaldehyde pleasure due to VTA which promotes DA relases.
  • acetaldehyde condenses w/ DA to produce salsolinol
  • still unpleasant in periphery
  • Asians w/ polymorphism experience more positive feelings after alcohol. Allele is associated w/ lower prevalence of abuse and alcoholism
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8
Q

What effects does alcohol have on other drugs

A
  • inducer of CYP2E1
  • this increases acetaminophen conversion to highly reactive NAPQI (highly toxic)
  • give N-acetylcysteine to provide fresh conjugate substrate for reactive intermediate to be safely detoxified
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9
Q

What happens w/ the following BAL levels?
0
400

A

< 50 : limited muscular coordination
50-100: pronounced incoordination
100-150: mood and personality changes, intoxication over the legal limit in most states
150-400: N/V, marked ataxis, amnesia, dysarthria
>400: coma, respiratory insufficiency and death

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10
Q

impact of EtOH on key neurochemical systems

A
  1. GABA release, increase receptor density
  2. inhibits NMDA, w/ chronic use up-regulation
  3. increase DA and effects on ventral tegmentum/nucleus accumbens
  4. increase ACTH
  5. release of Beta endorphins, activation of mu receptors
  6. in crease 5HT
    - increased CB1 activity (cannabinoid)
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11
Q

what effects does EtOH have on other systems besides the CNS

A
  • CV depressant
  • relaxes vascular SM: vasodilation, hypothermia, increased gastric bloodflow
  • relaxes uterine SM
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12
Q

factors affecting blood alcohol level

A
  • Vd: more weight = larger Vd = lower BAL
  • BMI: more body fat = smaller Vd = higher BAL
  • Female gender: higher BAL
  • Metabolism: 0 order, 1 drink per hour
  • Adaptation: behavioral and neural adaptation, enzyme induction
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13
Q

Chronic effects of EtOH

A
  1. Liver: decreased gluconeogenesis –> hypoglycemia, fatty liver –> hepatitis, cirrhosis, liver failure
  2. GI: bleeding, scarring –> absorptive and nutritional deficiency
  3. CNS - peripheral neuropathy, Wernicket Korsakoff syndrome (ataxia, confusion, ocular muscle paralysis)
  4. endocrine - gynecomastia, testicular atrophy
  5. CV - HTN, anemia, dilated cardiomyopathy, arrhythmias w/ binge, modest consumption increases HDL and may protect against CHD
  6. Neoplasia- GI cancer
  7. Immune system - pancreatitis, infectious pneumonia
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14
Q

What is thiamine deficiency crucial

A
  • can’t make and replenish critical amino acids and proteins
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15
Q

Fetal alcohol syndrome

A
  • crosses placenta easily and fetal blood reflect maternal levels.
  • intrauterine growth retardation
  • microcephaly
  • poor coordination
  • midfacial underdevelopment
  • minor joint anomalies
  • congential heart defects and subtle neurologic deficits
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16
Q

typical treatment of alcoholics in ED

A
  • ABCs
  • dextrose: compensate for hypoglycemia
  • thiamine - protect against wernicke-korsakoff syndrome
  • correct electrolyte issues
17
Q

EtOH withdrawal symptosm

A

insomnia, tremor, anxiety, rarely seizures

- N/V, diarrhea, arrhythmias

18
Q

treatment of EtOH withdrawal

A

BNZ sedative: diazepam but when concerned for hepatic impairment think lorazepam
Thiamine
Correct electrolytes

19
Q

Drug interactions of Alcohol

A
  • increased tertogenicity and increased absorption
  • additive CNS depressive actions w/ drugs
  • increased toxicity of acetaminophen
  • increased risk of bleeding w/ NSAIDS and anticoagulants
  • increase risk of hypglycemia in diabetics on meidcations
20
Q

what other drugs have disulfiram like effects

A
  • sulfonylureas, cefotetan, keotconazole, procarbazine
21
Q

MOA of acamprosate

A

weak NMDA blocker

  • activation of GABA receptor
  • may decreased mild protracted abstinence syndromes w/ decreased feeling of need for EtOH
22
Q

why is naltrexone used

A
  • decreased drinking through decrease feelings of reward w/ alcohol and/or decrease cravings
23
Q

Where do naltrexone, acamprosate work in the corticomesolimbia dopaminergic pathway

A
  • naltrexone at VTA

- Acamproate - glutamate at VTA and NA, GABA at VTA

24
Q

toxicity of Ethylene glycol and methanol

A
  • both use EtOH DH to form toxic metabolites
  • ethylene glycol –> oxalic acid leading to acidosis, nephrotoxicity
  • metanol –> formaldehyde and formic acid –> severe acidosis, retinal damage
  • treat w/ fomepizole or ethanol for a competitive inhibitor (give enough to maintain BAL of at least 100 to ensure E saturation)

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