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TOXICOLOGY > Alcohol > Flashcards

Alcohol Flashcards

1
Q

what is the osmol gap

A

difference between the measured osmolality and calculated osmolarity

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2
Q

what is osmolarity

A

measure of the total number of particles in one litre of solution - calculated

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3
Q

what is osmolality

A

number of particles in kg of solution - measured

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4
Q

osmolarity (mmol/L) formula

A

2 x Na + glucose + BUN

all concentrations in mmol/L

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5
Q

normal BUN levels

A

3- 7.1mmol/L

8-20 mg/dL

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6
Q

other dumb formula for osmolarity

A

2 x NamEq/L + glucose mg/dL/18 + BUNmg/dL/2.8

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7
Q

measurement of osmolality

A

freezing point depression

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8
Q

why is there an osmol gap

A

serum osmolality is increased by circulating alcohols and other low MW substances that arent calculated in osmolarity

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9
Q

osmol gap =

A

measure osmolality - calculated osmolarity

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10
Q

normal osmol gap

A

10+/- 6 mOsm

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11
Q

how is ethanol eliminated

A

mostly enzymatic oxidation
unchanged
michaelis menten

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12
Q

elimination in chronic drinkers

A

increased due to enzyme induction

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13
Q

ethanol metabolism

A

first pass - ADH in gastric mucosa

liver - ADH, CYP2E1, peroxidase catalase, ALDH

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14
Q

ethanol MOA

A

membrane fluididication
enhance GABAnergic function
inhibition and upregulation of NMDA receptors and increase in dopamine release

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15
Q

what is functional tolerance

A

ppl metabolize alcohol better and can tolerate the CNS effects better so can tolerate higher doses

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16
Q

lethal ethanol dose adult

A

5-6g/kg in nontolerant

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17
Q

lethal ethanol dose child

A

3g/kg

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18
Q

stages of acute intoxication

A 
50mg/dL: mild 
100mg/dl: mild - mod 
200: moderate - NV
300: severe - hypotermia, hypoglycemia, seizure 
700: lethal - resp depression
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19
Q

metabolic derangements

A

hypoglycemia
metabolic acidosos
hypomagnesemia

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20
Q

explain ethanol induced hypoglycemia

A

hepatic glycogen is rapidly consumed
ethanol converted to acetate uses up NAD
increased lactate
thiamine deficiency impairs acetylcoA = more lactate

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21
Q

explain alcoholic ketoacidosis

A

glycogen consumed free fatty acids are mobilized
acetylcoa formed from fatty acid oxidation
forms acetoacetate or goes to fatty acid synthesis

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22
Q

management of intoxicated patient

A

glucose, oxygen, thiamine

23
Q

labs to ask for

A

alcohol levels
finger stick glucose level
electrolytes - magnesium
anion and osmol gap

24
Q

interventions

A

gastric lavage if massive ingestion
charcoal not efficient
hemodialysis

25
Q

signs of alcoholic liver disease

A

fatty liver
alcoholic hepatitis
alcoholic cirrhosis

26
Q

drug interactions in alcoholism

A

enzymatic induction results in increased clearance of phenytoin, methadone, tolbutamide, isoniazide, warfarin
but… once at cirrhosis metabolism is impaired

27
Q

acute intoxication drug interactions

A

additive effects with antihistamines, barbiturates, and sedatives
transient increase in plasma levels of other agents
increased acetaminophen hepatotoxicity
cimetidine increases levels
antabuse reaction

28
Q

what is antabuse reaction

A

inhibitors of alcohol dehydrogenase causes accumulation of acetaldehyde
tolbutamide, carbamates, metronidazole

29
Q

why does alcohol wihtdrawal occur

A

hbituation of the organism to the cns depressant effects - uncompensated state of overstimulation due to upregulation of NMDA receptors

30
Q

interventions for alcoholic patient

A 
serotonin uptake inhibitors 
naltrexone
campral
bromocriptine
lithium
disulfiram
31
Q

absorption of methanol

A

rapid from oral route
inhalation
skin

32
Q

Vd of methanol

A

small, in the blood

33
Q

elimination of methanol

A

primarily liver
zero order at high conc and first order at low
unchanges in urine and by lungs

34
Q

methanol metabolized into

A

formaldehyde and formic acid

very toxic

35
Q

how is ethanol an antidote for methanol

A

affinity of ADH for ethanol is 4x greater than its affinity for methanol, prevent the metabolism into toxic metabolites

36
Q

formation of formic acid

A

conversion of formaldehyde to formic acid is rapid so there is no accumulation of formaldehyde

37
Q

metabolic effect of methanol

A

direct effect on metbaolic acidosis from formic acid and indirect effect due to lactate produciton, mitochondria toxicity, etc

38
Q

how does ocular toxicity occur

A

directly by formic acid
acidosis increases toxicity by favoring diffusion
inhibition of retinal and optic nerve mitochondrial function

39
Q

signs of ocular toxicity

A

blurred vision
snow field vision
fundoscopic exam shows hyperemia of the optic disc and retinal edema
reduced pupillary response to light

40
Q

permanent ocular damage due to methanol

A 
optic atrophy 
perpheral constriction of visual fields
central scotoma
reduced visual acuity
loss of color vision
blindness
41
Q

treatment of methanol od

A 
supportive care
correction of acidemia (sodium bicarb)
fomepizole or ethanol 
iv folinic acid
hemodialysis
42
Q

when would you use hemodialysis in methanol od

A

> 25mg/dL

>7.8mmol/L

43
Q

methanol od levels we want to determine

A

evaluate acidosis
osmol gap - check if all accounted for by ethanol
ethanol and methanol levels
anion gap

44
Q

action level for hemodialysis in ethylene glycol

A

> 25mg/dL or >4.03mmol/L with acidosis or renal insufficiency

45
Q

fomepizole moa

A

competitive inhibitor of ADH

46
Q

fomepizole dosing

A

loading dose 15mg/kg
10mg/kg q12hr for 4 doses
15mg/kg q12hr

47
Q

treatment for ethylene glycol od

A 
ethanol 
fomepizole 
thiamine and pyridoxine to min oxalic acid formation
folates 
hemodialysis
48
Q

dose of thiamine and pyridoxine

A

100mg and 50mg iv every 6hr

49
Q

methanol change in osm

A

31

50
Q

ethanol change in osm

A

22

51
Q

isopropanol change in osm

A

17

52
Q

ethylene glycol change in osm

A

16

53
Q

acetone change in osm

A

18

TOXICOLOGY (24 decks)

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