Alcohol Flashcards
what is the osmol gap
difference between the measured osmolality and calculated osmolarity
what is osmolarity
measure of the total number of particles in one litre of solution - calculated
what is osmolality
number of particles in kg of solution - measured
osmolarity (mmol/L) formula
2 x Na + glucose + BUN
all concentrations in mmol/L
normal BUN levels
3- 7.1mmol/L
8-20 mg/dL
other dumb formula for osmolarity
2 x NamEq/L + glucose mg/dL/18 + BUNmg/dL/2.8
measurement of osmolality
freezing point depression
why is there an osmol gap
serum osmolality is increased by circulating alcohols and other low MW substances that arent calculated in osmolarity
osmol gap =
measure osmolality - calculated osmolarity
normal osmol gap
10+/- 6 mOsm
how is ethanol eliminated
mostly enzymatic oxidation
unchanged
michaelis menten
elimination in chronic drinkers
increased due to enzyme induction
ethanol metabolism
first pass - ADH in gastric mucosa
liver - ADH, CYP2E1, peroxidase catalase, ALDH
ethanol MOA
membrane fluididication
enhance GABAnergic function
inhibition and upregulation of NMDA receptors and increase in dopamine release
what is functional tolerance
ppl metabolize alcohol better and can tolerate the CNS effects better so can tolerate higher doses
lethal ethanol dose adult
5-6g/kg in nontolerant
lethal ethanol dose child
3g/kg
stages of acute intoxication
50mg/dL: mild 100mg/dl: mild - mod 200: moderate - NV 300: severe - hypotermia, hypoglycemia, seizure 700: lethal - resp depression
metabolic derangements
hypoglycemia
metabolic acidosos
hypomagnesemia
explain ethanol induced hypoglycemia
hepatic glycogen is rapidly consumed
ethanol converted to acetate uses up NAD
increased lactate
thiamine deficiency impairs acetylcoA = more lactate
explain alcoholic ketoacidosis
glycogen consumed free fatty acids are mobilized
acetylcoa formed from fatty acid oxidation
forms acetoacetate or goes to fatty acid synthesis
management of intoxicated patient
glucose, oxygen, thiamine
labs to ask for
alcohol levels
finger stick glucose level
electrolytes - magnesium
anion and osmol gap
interventions
gastric lavage if massive ingestion
charcoal not efficient
hemodialysis
signs of alcoholic liver disease
fatty liver
alcoholic hepatitis
alcoholic cirrhosis
drug interactions in alcoholism
enzymatic induction results in increased clearance of phenytoin, methadone, tolbutamide, isoniazide, warfarin
but… once at cirrhosis metabolism is impaired
acute intoxication drug interactions
additive effects with antihistamines, barbiturates, and sedatives
transient increase in plasma levels of other agents
increased acetaminophen hepatotoxicity
cimetidine increases levels
antabuse reaction
what is antabuse reaction
inhibitors of alcohol dehydrogenase causes accumulation of acetaldehyde
tolbutamide, carbamates, metronidazole
why does alcohol wihtdrawal occur
hbituation of the organism to the cns depressant effects - uncompensated state of overstimulation due to upregulation of NMDA receptors
interventions for alcoholic patient
serotonin uptake inhibitors naltrexone campral bromocriptine lithium disulfiram
absorption of methanol
rapid from oral route
inhalation
skin
Vd of methanol
small, in the blood
elimination of methanol
primarily liver
zero order at high conc and first order at low
unchanges in urine and by lungs
methanol metabolized into
formaldehyde and formic acid
very toxic
how is ethanol an antidote for methanol
affinity of ADH for ethanol is 4x greater than its affinity for methanol, prevent the metabolism into toxic metabolites
formation of formic acid
conversion of formaldehyde to formic acid is rapid so there is no accumulation of formaldehyde
metabolic effect of methanol
direct effect on metbaolic acidosis from formic acid and indirect effect due to lactate produciton, mitochondria toxicity, etc
how does ocular toxicity occur
directly by formic acid
acidosis increases toxicity by favoring diffusion
inhibition of retinal and optic nerve mitochondrial function
signs of ocular toxicity
blurred vision
snow field vision
fundoscopic exam shows hyperemia of the optic disc and retinal edema
reduced pupillary response to light
permanent ocular damage due to methanol
optic atrophy perpheral constriction of visual fields central scotoma reduced visual acuity loss of color vision blindness
treatment of methanol od
supportive care correction of acidemia (sodium bicarb) fomepizole or ethanol iv folinic acid hemodialysis
when would you use hemodialysis in methanol od
> 25mg/dL
>7.8mmol/L
methanol od levels we want to determine
evaluate acidosis
osmol gap - check if all accounted for by ethanol
ethanol and methanol levels
anion gap
action level for hemodialysis in ethylene glycol
> 25mg/dL or >4.03mmol/L with acidosis or renal insufficiency
fomepizole moa
competitive inhibitor of ADH
fomepizole dosing
loading dose 15mg/kg
10mg/kg q12hr for 4 doses
15mg/kg q12hr
treatment for ethylene glycol od
ethanol fomepizole thiamine and pyridoxine to min oxalic acid formation folates hemodialysis
dose of thiamine and pyridoxine
100mg and 50mg iv every 6hr
methanol change in osm
31
ethanol change in osm
22
isopropanol change in osm
17
ethylene glycol change in osm
16
acetone change in osm
18
