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401 - Toxicology, Drug Abuse, Pharmacology > 34: Toxic Alcohols > Flashcards

34: Toxic Alcohols Flashcards

1
Q

ethanol key effect

A

metabolic acidosis

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2
Q

methanol key effect

A

metabolic acidosis, hyperosmolality, retinal damage, neuro dysfunction

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3
Q

methanol is metabolized to 3 substances which causes toxicity

A

formic acid, lactic acid, ketone

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4
Q

ethylene glycol is metabolized to 2 substances which causes toxicity

A

glycolic aid
calcium oxalate

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5
Q

isopropranolol is metabolized to _____ which causes ______

A

acetone, causes ketosis (only alcohol that deoesnt produce organic acids and therefore does not cause met acidosis).

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6
Q

what is the tx for ketosis

A

no tx, just time and IV fluids

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7
Q

3 types of exposure for methanol and ethylene glycol

A

suicide/ homicide
accidental
recreational

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8
Q

T or F: methanol poisonings are often repeat pts

A

T

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9
Q

list 2 sources of MeOH

A

windshield wiper fluid, varnish, pain thinner (huffing), fuel, industrial denaturant, moonshine

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10
Q

list 2 sources of EG

A

antifreeze, natural gas industry, liquid cooled computers, household cleaning products, pesticides, industrial solvents (for paints, plastics)

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11
Q

methanol is metabolized by ADH into _________ then metabolized by formaldehyde dehydrogenase into ________

A

formaldehyde
formic acid

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12
Q

ethylene glycol is metabolized by ADH into ________ then aldehyde dehydrogenase into _____ and later _______

A

glycoaldehyde
glycolic acid
oxalic acid

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13
Q

fomepizole and ethanol are both competitive inhibitors of

A

ADH

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14
Q

EtOH becomes zero order at

A

1mM (DUI 17mM)

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15
Q

what is zero order

A

when an enzyme is saturated and rate of metabolism is indep of drug conc

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16
Q

what is first order

A

when rate is directly proportional to substrate conc (rate dep on drug conc)

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17
Q

which of well absorbed inhalational + dermal
1. MeOH
2. EG
3. both
4. neither

A

1

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18
Q

which of not well absorbed INH and topical
1. MeOH
2. EG
3. both
4. neither

A

2

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19
Q

what is the decontamination protocol for MeOH and EG

A

use NG tube within 1hr to suction stomach
no role for AC as it does not absorb alcohols

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20
Q

T or F: AC may be used in MeOH and EG toxicity

A

F- can’t absorb alcohols

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21
Q

hallmarks of methanol toxicity

A

metabolic acidosis and visual problems

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22
Q

formic acid MOA (formed from methanol)

A

inhibits cytochrome C oxidase (mitochondrial ETC) = stops OXPHOS, ATP production = tissue hypoxia

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23
Q

________ is the metabolite of methanol responsible for photoreceptor death, decreased visual acuity, photophobia, blurred vision, abd pain

A

formic acid

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24
Q

describe stage 1 of methanol toxicity

A

mimics ethanol intoxication
inebriation, gastric irritation
absence doesn’t rule out toxic concs

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25
Q

when does stage 2 methanol toxicity set in

A

6-30h

26
Q

describe stage 2 methanol toxicity

A

latent period- critical
inebriation resolves
may be asymptomatic (coingestionof EtOH common)

27
Q

describe stage 3 methanol toxicity

A

visual sx start to appear (blurred vision, blindness)
seizures, coma, cerebral edema, herniation
cardiac failure, resp arrest`

28
Q

ethylene glycol causes metabolic acidosis and organ dysfunction primarily from ________ and _______

A

glycolic and oxalic acid

29
Q

glycolic acid MOA toxicity

A

overwhelms HCO3- buffering ability = impairmet of celular resp

30
Q

oxalic acid MOA toxicity

A

forms calcium oxalic crystals = precipitate in blood = clugs renal microcirc = tubular necrosis (oxalic acid + Ca2+)
leads to hypocalcemia = myocardial dysfxn and renal failure

31
Q

stage 1 of EG toxicity time + sx

A

30min-12hrs
mimics ethanol intoxication, early neuro CNS depression, cerebral edema, seizures

32
Q

stage 2 EG toxicity time + sx

A

12-24hrs
cardiopulmonary stage- cardiac dysfxn, shock, tachypnea, ARDs

33
Q

stage 3 EG toxicity time + sx

A

24-72hrs
renal failure stage

34
Q

stage 3 EG toxiicty sx

A

late neurologic damage

35
Q

describe anion and osmolal gap changes in alcohol intoxication

A

osmolal gap decreases while anion gap increases

36
Q

is there osmolal gap standardization?

A

no- many different equations and no consensus on upper limit (between 10-20 mOsm)
ranges may vary between labs

37
Q

osmolal gap sensitivity and specificity?

A

low for both

38
Q

why is there low sensitivity in measuring osmolal gap

A

values range ~20mOsm
EG level >20mg/dL shift in osmolal gap only 3mOsm/L
baseline is at lower end of normal- clinically sig intoxication within normal gap
later stages of intoxication as EG or meOH are metabolized = osmolal gap may eb absent

39
Q

EG lvl >20mg/dL shifts the osmolal gap _______

A

2mOsm/L

40
Q

why is there low specificity in measuring the osmolal gap

A

elevated osmolal gap may be caused by any uncharged molecule (ex- EG, MeOH, EtOH, ketoacidosis, renal failure, shock) = doesn’t prove EG or MeOH intoxication

41
Q

why is a serial anion gap sometimes used in determining EG and MeOH toxicity?

A

clinically significant poisoning will elevate anion gap
MeoH and EG metabolized to acidic metabolites = rise anion gap

42
Q

how is a serial anion gap done

A

measured at baseline then repeated q2-4hrs for 6-12h passed ingestion

43
Q

EG ad MeOH poisoning can elevate lactate levels by

A

mitochondrial poison, pts often have low thiamine levels, stress response

44
Q

generally in EG and MeOH poisoning, lactate is ______ and does not fully account for elevated anion gap (attributed to formate and glyoxylate)

A

low <5mM

45
Q

what are the issues with sensitivity of assays used (2)

A

portable blood gas (lactate oxidase) can’t differentiate
lab assay (GC specific) uses lactate dehydrogenase

46
Q

3 goals of tx in alcohol poisonings

A

block toxic metabolite formation (inhibit ADH with fomepizole, EtOH)
correct pH to 7.2 (with bicarb)
eliminate toxic metabolites with dialysis

47
Q

what is the pref tx in alcohol poisoning

A

fomepizole

48
Q

how to use fomepizole

A

initial dose 15mg/kg IV, then 10mg/kg IV q12h for 4 doses (2 days, then 15mg/kg IV q12h until toxic alcohol levels were safe (can take a long time as elimination is slow)
- dialysis may be req to clear parent alcohol

49
Q

what is 2nd line tx if fomepizole is not available

A

ethanol

50
Q

target blood alcohol level should be ______ with ethanol

A

22-23mM

51
Q

what is the PO alcohol LD and MD for ethanol

A

17mmol/kg LD
1.4-2.8mmol/kg/hr MD (~1/2 standard drink perhr)

52
Q

what should be monitored when giving ethanol to inhibit ADH

A

anion gap- if increasing = ADHi not adequate

53
Q

what type of alcohol is preferred for ADHi

A

hard alcohol- less volume

54
Q

what tx besides ADHi may be used in alcohol toxicity

A

dialysis
bicarbonate for pH
vitamins

55
Q

T or F: ADHi should be continued during dialysis

A

T

56
Q

bicarbonate is used in alcohol toxicity to

A

normalize pH to keep metabolites in ionized state = prevent penetration into tissues + increase urinary excretion

57
Q

______ may cause hypocalcemia due to chelation with oxalic acid

A

EG

58
Q

T or F; in hypocalcemia caused by EG, avoid giving Ca

A

T- may exacerbate precipitation of calcium oxalate

59
Q

why might vitamins be used in alcohol toxicity

A

to facilitate metabolism- MOA not completely known

60
Q

what vitamins may be used in EG toxicity

A

thiamine, pyridoxine (vit B6)

61
Q

what vitamins may be used in MeOH toxicity

A

folic acid (folic acid)

401 - Toxicology, Drug Abuse, Pharmacology (32 decks)

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