DLA5- Toxicology (environment, occupational) Flashcards
(1) are the mechanisms of CO poisoning
(2) is the treatment for CO exposure
1:
- tightly binds Hb (more than O2), blocks O2 delivery
- binds Fe –> inhibits cytochrome enzymes in oxidative phosphorylation (ETC)
2- 100% O2 administration + hyperbaric chamber
ethanol:
- (1) overdose presentation
- (2) Tx
1- CNS depression, hypoglycemia (impaired gluconeogenesis)
2:
- maintain vital signs
- prevent aspiration of vomit
- IV dextrose for hypoglycemia
- Thiamine for Wernicke-Korsakoff
- electrolyte correction
describe process of methanol poisoning
- metabolized into formaldehyde + formic acid
- formic acid –> severe acidosis, retinal damage, blindness
- GI distress, SOB, LOC / coma
- death via respiratory cessation
describe methanol poisoning Tx
- fomepizol or ethanol to compete with methanol metabolism
- IV sodium bicarbinate for metabolic acidosis
- hemodialysis
Antifreeze = (1):
- (2) clinical presentation with ingestion
- (3) Tx
1- ethylene glycol
2- metabolized into toxic aldehydes / oxalate –> severe acidosis and renal damage
3:
- fomepizol or ethanol to compete with metabolism
- IV sodium bicarbonate for metabolic acidosis
- hemodialysis
(1) is used to treat insecticide poisoning
(2) may also be given if early enough, describe brief mechanism
Atropine (anti-muscarinic):
-note organophosphates and carbamate inhibit AChE
Pralidoxime- breaks bond or insecticide with AChE
(1) is a common rodenticide, (2) is Tx for ingestion
1- warfarin
2- vitK OR fresh-frozen plasma
CN has high affinity binding for (1) commonly found in (2) in the body. (3) are the resulting symptoms and mechanisms of CN poisoning.
(cyanide)
1- binds ferric iron (Fe3+)
2- heme group in cytochromes in mitochondria
3- lactic acidosis, cytotoxic hypoxia –> convulsions and death via hyperventilation
Note- acute exposure usually is survived
list the agents found in Cyanide Antidote kit
1) Amyl Nitrite Pearls + Sodium Nitrite –> Hb into methemoglobin allowing competition and upstarts ETC
2) Sodium Thiosulfate –> helps CN metabolism into thioncyanate for elimination
3) methylene blue –> methemoglobin back to Hb
4) hydroxy-cobalamin –> cyano-cobalamin –> urinary excretion
O2 therapy is not too helpful
Pb poisoning Tx:
- (1) for seizures
- (2) for cerebral edema
- (3) for chelation
(4) for organic Pb poisoning
1- diazepam
2- mannitol and dexamethasone
3- IV Edetate Calcium Disodium; IM dimercaprol, oral succimer, IV unithol
4- symptomatic, chelation only works on inorganic Pb
Arsenic poisoning Tx:
- (1) is Tx for acute inorganic poisoning
- (2) is Tx for chronic inorganic poisoning
- (3) is Tx for Arsine gas poisoning
1:
- supportive via H2O, electrolytes
- chelation via IV unithiol, IM dimercaprol, oral succimer
2- IM dimercaprol
3- n/a –> Sxs = massive hemolysis => Hb deposition and renal failure
Hg poisoning Tx:
- (1) for acute exposure
- (2) for chronic exposure
1- chelators: oral/IV unithiol, IM dimercaprol, oral succimer
2: kinda unknown
- unithiol, succimer will inc elimination but effects are unknown
- dimercaprol will redistribute Hg to CNS —- AVOID
______ is chelator of choice is acute Fe poisoning
Deferoxamine
______ is commonly effective as adsorbent for most toxins, but doesn’t bind Fe, so not used in Fe poisoning
activated charcoal
determine chelator by route of administration:
- (1) succimer
- (2) dimercaprol
- (3) unithiol
1- oral
2- IM
3- IV, oral