9. Alcohol Toxicity Flashcards

1
Q

where is alcohol rapidly absorbed

A

GI

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2
Q

true or false: ethanol is water soluble

A

true

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3
Q

when do the concentrations of alcohol peak

A

20-60 mins

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4
Q

which enzymes predominantly metabolize EtOH

A

cytosolic alcohol dehydrogenase and aldehyde dehydrogenase

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5
Q

what is a minor metabolic pathway that can be induced in the metabolism of EtOH

A

microsomal ethanol oxidizing system (MEOS) P450 enzyme system

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6
Q

what effects are typically seen if your BAC is >0.15

A

severe impairment, n/v, blackout, unconsciousness, resp. depression, life threatening

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7
Q

the enzymatic conversion of alcohol also involves the conversion of

A

NAD to NADH

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8
Q

what will happen if the body needs NAD?

A

NADH will be converted back to NAD by using pyruvate. this results in the depletion of pyruvate and the production of lactate

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9
Q

an increase in lactate which is often seen in excessive EtOH consumption may cause:

A

metabolic acidosis

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10
Q

body uses pyruvate to produce glucose when intake is low via:

A

gluconeogenesis

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11
Q

what are the three ways ethanol causes hypoglycemia

A
  1. decreased intake of glucose
  2. blockade of gluconeogenesis
  3. inhibition of glycogenolysis
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12
Q

patients with acute intoxication may exhibit _____________ in which dysrhythmias, especially a-fib, occur after a heavy drinking episode

A

holiday heart

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13
Q

what lab values should be measured in someone with suspected alcohol toxicity

A
  • serum ethanol concentrations
  • liver and kidney function
  • electrolyte levels (anion gap - presence of a large anion gap should suggest the ingestion of an alcohol substitute)
  • serum glocsue (most imp. test) *make sure they are not in severe hypoglycemia)
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14
Q

how should serum glucose be monitored in patients with uncomplicated alcohol toxicity vs. severe toxicity

A

uncomplicated toxicity = no LOC
- monitor BG q8h

severe toxicity = LOC/seizures
- monitor BG q1h

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15
Q

what is the treatment for ethanol toxicity

A

wait & watch
- fluids in patients with volume depletion
- thiamine and glucose for those who present unconscious

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16
Q

true or false: activated charcoal and gastric lavage are used in all patients that present with alcohol toxicity

A

false - need to be used within 1 hr of ingestion of alcohol therefore in most scenarios activated charcoal and gastric lavage are not helpful

17
Q

which of the following are toxic
A) methanol
B) ethylene glycol
C) their metabolites
D) all of the above

A

C

18
Q

what is the rate limiting step of the metabolism of methanol

A

methanol converted to formaldehyde

19
Q

this is the metabolite of methanol. it can eventually cause permanent blindness. the metabolism of this metabolite is very slow therefore it often accumulates in the body which can result in metabolic acidosis

A

formic acid

20
Q

where do ethylene glycol metabolites target?

A

kidney - can lead to AKI

21
Q

oxalic acid can bind to serum calcium to produce ________ which can deposit in the kidneys, brain and lung tissue

A

calcium oxalate crystals

22
Q

when do the initial symptoms appear from methanol and what do the symptoms typically look like?

A

12-24 hours after ingestion

often resembles ethanol intoxication and consist of drowsiness, confusion, ataxia, weakness, headache, n/v and abdominal pain

23
Q

as methanol metabolism proceeds, a severe anion gap metabolic acidosis will develop due to formation of formic production. what symptoms may be seen here?

A

blurred or misty vision, double vision, changes in colour perception. occasionally total loss of vision.

24
Q

what are the 3 phases of ethylene glycol poisoning

A

phase 1 (mins-12 hrs) : CNS toxicity + GI symptoms

phase 2 (12-24 hrs): cardiopulmonary symptoms

phase 3 (> 24 hrs): tubular necrosis and renal failure

25
Q

if a patient presents with alcohol toxicity but it is not evident which type of alcohol they may be intoxicated with, what lab values will reveal the type of alcohol?

A

anion gap
- large anion gap suggest alcohol sub

serum ethanol level
- normal suggests alcohol sub

26
Q

what supportive care is done to manage methanol or ethylene glycol toxicity

A
  • securing patients ABCs
  • GI decontamination if possible
  • IV sodium bicarb to correct systemic acidosis
27
Q

what are antidotal therapies seen in the management of methanol or ethylene glycol toxicity

A

fomepizole (1st line) - blocks alcohol dehydrogenase

ethanol - alcohol dehydrogenase prefers ethanol therefore will stop making methanol or ethylene glycol metabolites

28
Q

what are some cofactor therapies seen in methanol and ethylene glycol toxicity

A

eliminiation of formate (toxic metabolite of methanol) is sped up by administration of folic acid; thus all patients treated with an ADH blocker should also receive folinic acid (either leucovorin or folic acid IV)

ethylene glycol patients are treated with pyridoxine and thiamine (cofactors of metabolism therefore they speed up metabolism)