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Alcohol: use and abuse Flashcards

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1
Q

What are antidotes for alcohol intox?

A

time and fluids

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2
Q

Drugs for chronic alcoholics

A

naltrexone, acamprosate

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3
Q

Drugs for ethanol withdrawal

A

diazepam, thiamine (if deficient)

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4
Q

What are the antidotes for acute methanol and ethylene glycol intoxication

A

ethanol, fomepizole

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5
Q

Explain alcohol metabolism

A

alcohol–> alcohol dehydrogenase –> acetaldehyde –> aldehyde dehydrogenase –> acetate

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6
Q

What type of metabolism does ethanol go through?

A

zero order (as does phenytoin and high-dose of aspirin

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7
Q

Where does ethanol metabolism take place?

A

Liver

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8
Q

What is the CYP involvement in ethanol metabolism?

A

Very little CYP involvement under normal circumstances

-chronic alcoholism: may be more due to induction

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9
Q

What is the MOA of disulfiram as alcohol is concerned?

A

Used to encourage abstinence from alcohol by preventing the metabolism of acetaldehyde –> accumulation –> nausea and flushing reaction of the skin

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10
Q

what happens to asians when they drink? Why?

A

Asian flush due to decreased aldehydrogenase enzyme: build up of acetaldehyde –> skin flushing reaction

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11
Q

How can acetaldehyde affect the VTA?

A

In some patients it can act on the pleasure center in the VTA, increasing pleasure and leading to reinforcement of alcohol seeking behavior
*Maybe Native Americans

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12
Q

What CYP does ethanol affect?

A

CYP2E1

*potential for ethanol to alter metabolism of concurrent drugs – acetaminophen

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13
Q

What is significant about acetaminophen metabolism in chronic alcoholism?

A

usually only slightly metabolized to NAPQ1. When chronic alcoholics have CYP2E1 inductions more is metabolized to NAPQ1 –> depletion of glutathione (normally detoxifies NAPQ1–> hepatotoxicity

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14
Q

What antidote can be given for aspirin overdose in a chronic alcoholic

A

N-acetylcysteine (replenished glutathione store)

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15
Q

How does alcohol effect the GABA system?

A

increases GABA release and increases receptor density

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16
Q

How does alcohol effect the NMDA system?

A

inhibits postsynaptic NMDA receptors, with chronic use –> up-regulation

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17
Q

How does alcohol effect the DA system?

A

increases synaptic DA, increases effects on ventral tegmentum/ nucleus accumbens reward

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18
Q

How does alcohol effect the ACTH system?

A

increases CNS and blood levels of ACTH

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19
Q

How does alcohol effect the opioid system?

A

release of beta-endorphins and activation of mu receptors

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20
Q

How does alcohol effect the 5-HT system?

A

increases in 5-HT synaptic space

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21
Q

How does alcohol effect the cannabinoid system?

A

increases CB1 activity –> changes in DA, GABA, and glutamate activity

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22
Q

What causes “black-outs”

A

inhibition of the stimulatory actions of the glutamate system

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23
Q

How does alcohol effect the CV system?

A

CV depressant

  • HTN, anemia, dilated cardiomyopathy
  • arrhythmias with binge drinking (acutely high BAL)
  • increased HDL (modest alcohol drinking)-> protective against CHD
24
Q

How does alcohol effect smooth muscle?

A

Vascular SM: relaxtion, vasodilation –> possible hypothermia, increased gastric blood flow
Uterine SM: relaxes it, slows/stops contractions

25
Q

What determines BAL?

A

body makeup of the drinker

  • distributes within total body water
  • does not distribute into adipose tissue (more fat, higher BAC)
  • females: higher BAL than males
26
Q

What are the chronic effects of alcohol on the liver?

A
  • decreased gluconeogenesis –> hypoglycemia

- fatty liver –> hepatitis, cirrhosis, liver failure

27
Q

What are the chronic effects of alcohol on the GI tract?

A

bleeding –> scarring –> absorptive problems and nutritional deficiency

28
Q

What are the chronic effects of alcohol on the CNS?

A
  • peripheral neuropathy

- Wernicke-Korsakoff syndrome= ataxia, confusion, ocular muscle paralysis

29
Q

How is Wernike-Korsakoff treated?

A

thiamine

30
Q

What are the chronic effects of alcohol on the endocrine system?

A

-decreased synthesis of corticosteroids –> gynecomastia, testicular atrophy (steroid insuff)

31
Q

What is the result of thiamine deficiency?

A

inability to synthesize and replenish critical amino acids and proteins (especially in CNS)

32
Q

How is thiamine usually administered?

A

IV or IM injection, some may be treated orally

33
Q

What cancer incidence increases with alcohol consuption

A

GI cancer

34
Q

How is the immune system effected by alcohol?

A

enhanced inflammation in the liver and pancreas, but reduced immune response in other tissues
**chronic alcoholics are susceptible to infectious pneumonia

35
Q

Does alcohol cross the placenta?

A

yep

36
Q

How do fetal blood alcohol levels compare to the maternal blood alcohol levels?

A

fetal levels reflect the mother’s levels

37
Q

What does alcohol cause in the fetus?

A

apoptosis and incorrect neuronal and glial migration in the developing nervous system

38
Q

What features characterize fetal alcohol syndrome?

A
  • intrauterine growth retardation
  • microcephaly
  • poor coordination
  • midfacial underdevelopment (flattened face)
  • minor joint anomalies
  • some congenital heart defects
  • subtle neurologic deficits
39
Q

During what trimester is alcohol more damaging to the fetus?

A

1st trimester, but problems can still arise with alcohol consumption in the 3rd trimester

40
Q

What therapy is given to an intoxicated patient in the ED?

A
  • ABCs
  • dextrose (if low sugar)
  • thiamine (protect against W-K syndrome)
  • correct electrolytes
    • give thiamine before dextrose (can exacerbate W-K)
41
Q

What therapy is given to a patient suffering from alcohol withdrawal in the ED?

A
  • BNZ sedative
  • –usu long acting diazepam, with hepatic probs: lorazepam
  • thiamine
  • correct electrolytes
42
Q

What does a person with alcohol withdrawal present like?

A

insomnia, tremor, anxiety, N?V diarrhea, arrhythmias

*rarely seizures

43
Q

Why would lorazepam be used instead of diazepam in a patient with alcohol withdrawal?

A

Lorazepam is metabolized through glucuronidation and is better in patients with liver disease

44
Q

What pharmacokinetic changes can be seen when alcohol is used with other drugs?

A

increased teratogenicity, increased absorption of either or both

45
Q

What pharmacokinetic changes can be seen when alcohol is used with other drugs?

A
  • additive CNS depressive actions with drugs
  • increases toxicity of acetaminophen
  • increased risk of bleeding with NSAIDs and anticoags
  • increased risk of hypoglycemia in diabetics on medication
  • Disulfiram effects
46
Q

What are disulfiram effects, and what are some examples that cause this?

A

Have the ability to increase acetaldehyde when taken with alcohol
*sulfonylureas, cefotetan, ketoconazole, procarbazine

47
Q

What is the MOA of naltrexone?

A

mu opioid antagonist, felt to decrease drinking though decreased feelings of reward with alcohol and/or decreased craving

48
Q

What is the MOA of acamprosate?

A

weak NMDA antagonist, activator of GABA receptors, may decrease mild protracted abstinence syndroms with decreased feeling of “need” for alcohol

49
Q

What two nuclei are involved in the reward pathway effect of alcohol?

A

VTA and NA

ventral tegmental area and nucleus accumbens

50
Q

What neurotransmitters are involved in the indirect activation of the reward pathway activated by alcohol?

A

serotonin, ACh, opioids, GABA, glutamate

51
Q

What is the cause of alcohol withdrawal symptoms within the CNS?

A

with chronic use, many neurochemical systems undergo adaptations and attempt to reach homeostasis, so when alcohol is withdrawn homeostasis is effected

52
Q

How is ethylene glycol metabolized?

A

ethylene glycol –> via alcohol dehydrogenase –> oxalic acid –> acidosis and nephrotoxicity

53
Q

How is methanol metabolized?

A

methanol –> via alcohol dehydrogenase –> formaldehyde, formic acid –> severe acidosis, retinal damage

54
Q

What is the MOA of fomepizole?

A

competative inhibitor of alcohol dehydrogenase

  • IV infusion
  • can prevent optic neuropathy
55
Q

How is ethanol effective as a way to stop methanol and ethylene glycol intoxication?

A

Acts as a competitive inhibitor to saturate alcohol dehydrogenase (maintain BAL at 100 mg/dL)
**saturation of enzyme is effective because it is zero-order

56
Q

What are ways unabsorbed alcohol can be decontaminated?

A

induced emesis, gastric intubation or suction, administration of adsorbent charcoal –> reduces systemization of poison

57
Q

What is the MOA of acamprosate?

A

GABA agonist: works between the VTA and NA affecting reward pathway

Psych (12 decks)

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