34: Toxic Alcohols Flashcards by Linda Chen

ethanol key effect

metabolic acidosis

How well did you know this?

Not at all

Perfectly

methanol key effect

metabolic acidosis, hyperosmolality, retinal damage, neuro dysfunction

How well did you know this?

Not at all

Perfectly

methanol is metabolized to 3 substances which causes toxicity

formic acid, lactic acid, ketone

How well did you know this?

Not at all

Perfectly

ethylene glycol is metabolized to 2 substances which causes toxicity

glycolic aid
calcium oxalate

How well did you know this?

Not at all

Perfectly

isopropranolol is metabolized to _____ which causes ______

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

How well did you know this?

Not at all

Perfectly

what is the tx for ketosis

no tx, just time and IV fluids

How well did you know this?

Not at all

Perfectly

3 types of exposure for methanol and ethylene glycol

suicide/ homicide
accidental
recreational

How well did you know this?

Not at all

Perfectly

T or F: methanol poisonings are often repeat pts

How well did you know this?

Not at all

Perfectly

list 2 sources of MeOH

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

How well did you know this?

Not at all

Perfectly

list 2 sources of EG

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

How well did you know this?

Not at all

Perfectly

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

formaldehyde
formic acid

How well did you know this?

Not at all

Perfectly

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

glycoaldehyde
glycolic acid
oxalic acid

How well did you know this?

Not at all

Perfectly

fomepizole and ethanol are both competitive inhibitors of

ADH

How well did you know this?

Not at all

Perfectly

EtOH becomes zero order at

1mM (DUI 17mM)

How well did you know this?

Not at all

Perfectly

what is zero order

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

How well did you know this?

Not at all

Perfectly

what is first order

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

what is the decontamination protocol for MeOH and EG

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

How well did you know this?

Not at all

Perfectly

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

F- can’t absorb alcohols

How well did you know this?

Not at all

Perfectly

hallmarks of methanol toxicity

metabolic acidosis and visual problems

How well did you know this?

Not at all

Perfectly

formic acid MOA (formed from methanol)

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

How well did you know this?

Not at all

Perfectly

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

formic acid

How well did you know this?

Not at all

Perfectly

describe stage 1 of methanol toxicity

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

How well did you know this?

Not at all

Perfectly

when does stage 2 methanol toxicity set in

6-30h

describe stage 2 methanol toxicity

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

describe stage 3 methanol toxicity

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

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

glycolic and oxalic acid

glycolic acid MOA toxicity

overwhelms HCO3- buffering ability = impairmet of celular resp

oxalic acid MOA toxicity

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

stage 1 of EG toxicity time + sx

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

stage 2 EG toxicity time + sx

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

stage 3 EG toxicity time + sx

24-72hrs renal failure stage

stage 3 EG toxiicty sx

late neurologic damage

describe anion and osmolal gap changes in alcohol intoxication

osmolal gap decreases while anion gap increases

is there osmolal gap standardization?

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

osmolal gap sensitivity and specificity?

low for both

why is there low sensitivity in measuring osmolal gap

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

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

2mOsm/L

why is there low specificity in measuring the osmolal gap

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

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

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

how is a serial anion gap done

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

EG ad MeOH poisoning can elevate lactate levels by

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

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

low <5mM

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

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

3 goals of tx in alcohol poisonings

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

what is the pref tx in alcohol poisoning

fomepizole

how to use fomepizole

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

what is 2nd line tx if fomepizole is not available

ethanol

target blood alcohol level should be ______ with ethanol

22-23mM

what is the PO alcohol LD and MD for ethanol

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

what should be monitored when giving ethanol to inhibit ADH

anion gap- if increasing = ADHi not adequate

what type of alcohol is preferred for ADHi

hard alcohol- less volume

what tx besides ADHi may be used in alcohol toxicity

dialysis bicarbonate for pH vitamins

T or F: ADHi should be continued during dialysis

bicarbonate is used in alcohol toxicity to

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

______ may cause hypocalcemia due to chelation with oxalic acid

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

T- may exacerbate precipitation of calcium oxalate

why might vitamins be used in alcohol toxicity

to facilitate metabolism- MOA not completely known

what vitamins may be used in EG toxicity

thiamine, pyridoxine (vit B6)

what vitamins may be used in MeOH toxicity

folic acid (folic acid)