9. Alcohol Toxicity Flashcards
where is alcohol rapidly absorbed
GI
true or false: ethanol is water soluble
true
when do the concentrations of alcohol peak
20-60 mins
which enzymes predominantly metabolize EtOH
cytosolic alcohol dehydrogenase and aldehyde dehydrogenase
what is a minor metabolic pathway that can be induced in the metabolism of EtOH
microsomal ethanol oxidizing system (MEOS) P450 enzyme system
what effects are typically seen if your BAC is >0.15
severe impairment, n/v, blackout, unconsciousness, resp. depression, life threatening
the enzymatic conversion of alcohol also involves the conversion of
NAD to NADH
what will happen if the body needs NAD?
NADH will be converted back to NAD by using pyruvate. this results in the depletion of pyruvate and the production of lactate
an increase in lactate which is often seen in excessive EtOH consumption may cause:
metabolic acidosis
body uses pyruvate to produce glucose when intake is low via:
gluconeogenesis
what are the three ways ethanol causes hypoglycemia
- decreased intake of glucose
- blockade of gluconeogenesis
- inhibition of glycogenolysis
patients with acute intoxication may exhibit _____________ in which dysrhythmias, especially a-fib, occur after a heavy drinking episode
holiday heart
what lab values should be measured in someone with suspected alcohol toxicity
- 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)
how should serum glucose be monitored in patients with uncomplicated alcohol toxicity vs. severe toxicity
uncomplicated toxicity = no LOC
- monitor BG q8h
severe toxicity = LOC/seizures
- monitor BG q1h
what is the treatment for ethanol toxicity
wait & watch
- fluids in patients with volume depletion
- thiamine and glucose for those who present unconscious
true or false: activated charcoal and gastric lavage are used in all patients that present with alcohol toxicity
false - need to be used within 1 hr of ingestion of alcohol therefore in most scenarios activated charcoal and gastric lavage are not helpful
which of the following are toxic
A) methanol
B) ethylene glycol
C) their metabolites
D) all of the above
C
what is the rate limiting step of the metabolism of methanol
methanol converted to formaldehyde
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
formic acid
where do ethylene glycol metabolites target?
kidney - can lead to AKI
oxalic acid can bind to serum calcium to produce ________ which can deposit in the kidneys, brain and lung tissue
calcium oxalate crystals
when do the initial symptoms appear from methanol and what do the symptoms typically look like?
12-24 hours after ingestion
often resembles ethanol intoxication and consist of drowsiness, confusion, ataxia, weakness, headache, n/v and abdominal pain
as methanol metabolism proceeds, a severe anion gap metabolic acidosis will develop due to formation of formic production. what symptoms may be seen here?
blurred or misty vision, double vision, changes in colour perception. occasionally total loss of vision.
what are the 3 phases of ethylene glycol poisoning
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
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?
anion gap
- large anion gap suggest alcohol sub
serum ethanol level
- normal suggests alcohol sub
what supportive care is done to manage methanol or ethylene glycol toxicity
- securing patients ABCs
- GI decontamination if possible
- IV sodium bicarb to correct systemic acidosis
what are antidotal therapies seen in the management of methanol or ethylene glycol toxicity
fomepizole (1st line) - blocks alcohol dehydrogenase
ethanol - alcohol dehydrogenase prefers ethanol therefore will stop making methanol or ethylene glycol metabolites
what are some cofactor therapies seen in methanol and ethylene glycol toxicity
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)
