Toxicology Flashcards
what is cyproheptadine used for and its mechanism
5-HT2 antagonist used for serotonin syndrome
treatment for opioid poisoning
- opioid antagonist: naloxone and nalmefene
- IV sodium bicarbonate
seen with severe acute intoxication of theophyllines
seizures
hypotension and ventricular arrhythmias
associated with chronic intoxication of theophylline
cardiac dysrhythmias
drugs given for symptomatic hypoglycemia seen with sulfonylurea and meglitinides
IV dextrose and octreotide
- octreotide: decreases calcium influx hence decreases insulin release
- giving dextrose will cause an increase in glucose which triggers insulin release so octreotide tries to prevent some insulin release so hypoglycemia isn’t triggered again
how to manage neuroleptic syndrome caused by antipsychotics
- discontinue antipsychotics
- treat with dantrolene and bromocriptine
what is methanol metabolized to
formaldehyde and formic acid
how does formic acid toxicity present
severe acidosis, retinal damage, and blindness
treatment of methanol
Fomepizole - alcohol dehydrogenase inhibitor
ethanol - higher affinity for alcohol dehydrogenase than methanol
what is ethylene glycol oxidized to
toxic aldehydes and oxalate (get calcium oxalate acid)
treatment for ethylene glycol
fomepizole and ethanol
what are the insecticides and their general mechanism
Organophosphates
Carbamates
anticholinesterase inhibitors
specific mechanism of organophosphates and how ingestion manifests
phosphorylates acetylcholinesterase therefore inhibiting it
- DUMBELS - diarrhea, urination, miosis and muscle weakness, bronchospasms, excitation, lacrimation, salivation and sweating
- also target neuropathy target esterases
treatment of organophosphate poisoning
atropine
pralidoxime: splits the phosphate-enzyme bond and can regenerate new cholinesterase
mechanism of carbamates
inhibits acetylcholinesterase by carbamoylation of its active site
how do you treat carbamates
atropine and pralidoxime
how does cyanide work in terms of its actions in the body
high affinity for iron in the ferric state –> binds to Fe3+ in heme of cytochrome a,a3 in mito –> prevents O2 from serving as final electron acceptor
treatment for cyanide poisoning
- large pool of ferric iron
- cyanide antidote kit
- cyanokit
what is in the cyanide antidote kit – explain purpose of each
amyl nitrite, sodium nitrite and sodium thiosulfate
- nitrites oxidize hemoglobin to methemoglobin –> has higher affinity for cyanide than cytochrome oxidase –> cyanmethemoglobin formed –> cytochrome oxidase restored and ETC can continue its work using O2 as final oxygen acceptor
- thiosulfate promotes conversion of cyanide to thiocyanate which is easily excreted
- methylene blue coverts methemoglobin back to hemoglobin
what is in the cyanokit
hydroxocobalamin reacts with cyanide to form cyanocobalamin which is easily excreted in urine
enzymes that lead inhibit
ALA dehydratase
ferrochetalase
all leads to reduced heme hence reduce hemoglobin hence anemia
treatment of lead poisoning
Cerebral edema - mannitol and dexamethasone
chelation therapy: SEUD Succimer Edetate calcium disodium Unithiol Dimercaprol
mechanism of toxicity of arsenic
- uncoupler of mitochondrial oxidative phosphorylation
- inhibits pyruvate dehydrogenase
clinical manifestation of acute arsenic poisoning and treatment
-rice water stool, capillary damage, dehydration and shock
- IV fluids and electrolytes
- first line: Dimercaprol
- Unithiol
- Succimer
treatment of mercury poisoning
Succimer
Unithiol
Dimercarprol
(same as lead and arsenic)
symptoms and treatment of iron toxicity
GI bleeding
Deferoxamine
