Toxicology of Alcohol Flashcards
1
Q
ADH pathway
A
- located mainly in the liver
- activated at lower concentrations of alcohol
- polymorphism especially in Asians
2
Q
MEOS pathway
A
- consists of P450, 3A4 most important isozyme
- inducible in chronic intoxication
- NAD+ independent, higher threshold than ADH
3
Q
MOA of fomepizole
A
- inhibits ADH
4
Q
MOA of disulfiram
A
- inhibits aldehyde dehydrogenase
5
Q
drugs that potentiate disulfirams effects
A
- metronidazole
- cefotetan
- trimethoprim
6
Q
GABA-A drugs and the effects of alchol
A
- GABA-A mimetic (benzos, barbiturates) exacerbate the effects of ethanol
- GABA-A antagonists decreases the effects
7
Q
ethanol effect on NMDA receptors
A
- decreases the ability of glutamate to open the cation channel associated the the NMDA receptor
8
Q
symptoms of mild alcohol withdrawal
A
- tremors
- anxiety
- insomnia
- starts 6-8 hours after consumption stops
9
Q
symptoms of severe alcohol withdrawal
A
- visual hallucinations
- total disorientations
- marked abnormality of vital signs
10
Q
treatment of mild withdrawal cases
A
- PO4, K, an Mg balance should be restored as soon as possible
- thiamine therapy is initiated in all cases
11
Q
treatment of severe withdrawal cases
A
- thiamine therapy
- hemodialysis and drug therapy
- long acting sedative hypnotic is administered and then tapered off (benzos are preferred)
- short acting benzos (lorazepam and oxazepam) are recommended in patients with liver problems
12
Q
three available drug therapies for alcoholism
A
- naltrexone
- acamprosate
- disulfiram
13
Q
naltrexone
A
- mu antagonist that reduces cravings and reduces relapses to either drinking or alcohol dependence
- should not be administered concurrently with disulfiram because of risk of hepatic toxicity
- patients must be opioid free before taking naltrexone
14
Q
acamprosate
A
- weak NMDA receptor antagonist
- C.I. in patients with serious renal impairment
15
Q
disulfiram
A
- causes severe discomfort in drinkers
16
Q
metabolism of methanol
A
- methanol to formaldehyde to formate
17
Q
symptoms of methanol poisoning
A
- visual disturbances (blurred vision with clear sensorium is a giveaway)
- metabolic acidosis
- ## smell of formaldehyde on the breath and in urine
18
Q
lab finds in methanol poisoning
A
- metabolic acidosis with elevated anion gap and osmolal gap
19
Q
treatment of methanol poisoning
A
- suppression of metabolism (FA may increase metabolism of formate)
- hemodialysis
- alkalinization
- ethanol IV to compete for ADH to reduce formaldehyde buildup
20
Q
indications of fomeprizole
A
- methanol and ethylene glycol poisoning
21
Q
three stages of ethylene glycol overdose
A
- transient CNS excitation followed by CNS depression within the first few hours
- severe metabolic acidosis
- deposition of oxalate in the renal tubules leads to delayed renal insufficiency (CK, BUN, K all increase)
22
Q
lab findings of ethylene glycol poisoning
A
- acidosis with anion gap, osmolal gap and oxalate cystals in the urine without visual symptoms
23
Q
treatment of ethylene glycol
A
- hemodialysis and ethanol IV
