"Bad" Alcohols Flashcards
lab investigation - if looking to see if there is alcohol consumption what do we test?
1st - osmolality and osmolal gap
2nd- pH = acid/base disorder?
3rd - pCO2, HCO3 = helps physician determine if acidosis coming from organic molecule or resp in nature?
4th - anion gap (Na, K, Cl, HCO3) = CATMUDPILES
5 - toxic alcohol identification = GC-FID, headspace or serum analysis)
6 - ethanol enzymatic assay (is it a contributing osmol?)
acidosis
pH <7.35
is the acidosis metabolic or respiratory?
decrease in HCO3 = metabolic
increase in CO2 = respiratory
is there an anion gap?
AG = Na - HCO3 - Cl
> 12 mmol/L
CATMUDPILES
cyanide, Co2
aminoglycosides
theophylline
methanol
uremia
diabetic ketoacidosis
paraldehyde
isoniazid
lactate
ethylene glycol
salicylic acid
pathophysiology of methanol poisoning
- formic acid production => metabolic acidosis
- formic acid destruction of optic nerve/retina => blindness; unique!!
- irritation of GI lining => nausea and abdominal pain
in addition to alcohol mediated CNs depression
competitive inhibitor of alcohol dehydrogenase
Fomepizole
- 8000x greater affinity than ethanol
Fomepizole
diluted in total body water
elimination:
- 97% hep metabolism (<3% unchanged in urine)
- induces own metabolism (dose increased after 5th)
- zero order pre-induction; 1st order post-induction
- t1/2 =16-17h
T or F. Alcohols can freely traverse cell membranes (small, uncharged, organic properties)
T!
the number and location of hydroxyl group is relevant to metabolism and toxicity of each alc
methanol clinical presentation
CNS: headache, vertigo, lethargy, confusion, coma, seizures, NO BUZZ
GI: nausea, vomiting, ab pain
acid/base balance: met acidosis
ocular: blurred vision -> blindness
cardiac: bradycardia
renal: myoglobiunria, possible renal failure
ethylene glycol clinical presentation
CNS: depression (1-12 hr), coma, seizures, transient exhiliration
GI: nausea, vomiting
acid/base balance: met acidosis
ocular: nystagmus
cardiac: tachycardia, mild hypertension
renal: oligouria, acute tubular necrosis, renal failure, oxalate crystals (24-72 hr)
pathophysiology of ethylene glycol poisoning
- 0.5-2 hrs = cute CNS depression
- 12-24 hrs = glycolic, glyoxylic and oxalic acid => met acidosis
- 24-72 hrs = CaOxalate formation => AKI with oliguria
these impact the PCT of the nephron
calcium oxalate monohydrate and dihydrate crystals
(ethylene glycol)
treatment for methanol
folic acid
to turn formate to CO2
treatment for ethylene glycol
thiamine, pyridoxine
treatment for BOTH methanol and ethylene glycol
supportive
ethanol
- methanol = 1/10 ADH affinity
- eth glycol = 1/100 ADH affinity
correct acidosis with NaHCO3
hemodialysis
Fomepizole
folic acid
vit B9
vit B6
pyridoxine
thiamine
vitamin B1
progressive ethylene glycol and methanol testing
- perform initial diagnosis and treatment = supportive care focus; assess for toxic syndromes
- request eth glycol &/or methanol, Na, urea, glucose, osm, ethanol
- lab performs all except eth glyc and methanol
- determine: calc osm, osm gap, unaccounted osm gap
- is unaccounted osm gap greater than or equal tp decision level???
> eth glyc = 2
methanol = 5
if yes, performed eth glyc and methanol analysis
if not, cancel tests
T or F. MeOH elimination during hemodialysis is zero order
F! first order
T or F. Fomepizole prolongs methanol and ethylene glycol half-life
T! patient may need several infusions to adequately eliminate the alcohol; fomepizole to stop metabolism and dialysis to get rid of everything
T or F. Ethylene glycol is volatile
F! methanol is but not ethylene glycol
- not excreted in lungs unchanged
exclusions to cancelling toxic alc request if does not fall lower than threshold (<2 eth glycol; <5 methanol)
if stat request subsequent to an initial pos result
if ped patient <11y/o
does presence of ethanol affect Kd of methanol hemodialysis?
no, there is a generally flat line; Kd is not changing even if there is ethanol (no matter how much)
antizol
fomepizole brand name in Canada
T or F. Fomepizole induces its own metabolism
T; causes CYP enzymes to be induced … then zero -> first = will have constant half-life so constant dosing
