Toxicology Flashcards
poisoning of what drug leads to uncoupling of oxidative phosphorylation, increased levels of pyruvate and lactate as well as heat production?
aspirin
person in early stages of a drug toxicity presents with hyperventilation and respiratory alkalosis. Later, an increased anion gap metabolic acidosis presents leading to a mixed response. What drug is the person on and what is causing the anion gap acidosis?
aspirin - krebs cycle is inhibited leading to an increase in glycogenolysis, gluconeogensis, lipolysis, and FA oxidation. Inc in FA oxidation leads to increased synthesis of ketone bodies responsible for inc anion gap
person presents with profound metabolic acidosis, seizures, and pulmonary edema leading to ARDS. They are also vomiting and are dehydrated. What toxicity is this?
very severe poisoning with apsirin
why do you see respiratory alkalosis in the initial stages of aspirin toxicity?
aspirin directly stimulates the respiratory center, leading to inc in resp. rate`
treatment for aspirin toxicity? mild/moderate/severe
mild: gastric lavage, activated charcoal and fluid replacement
moderate: sodium bicarb (alkalinizes the urine to promote aspirin excretion)
severe: hemodialysis
Patient has taken unknown drug in large doses, but is mostly asymptomatic with only mild GIT symptoms. 18 hours later he presents with fulminant liver failure, develops hepatic encephalopathy and dies. What did he take, what is the treatment and how does it work?
acetaminophen
antidote is N-acetylcysteine that increases glutathione production as well as directly detoxes NAPQI (metabolite of acetaminophen)
Patient presents with dilated pupils, sweaty skin, and tachycardia. What class of drug did he take?
amphetamine/stimulant
what is important to remember when treating tachyarrhythmias of amphetamine intox?
dont give beta blockers without alpha blockage first!
Get unopposed alpha-1 action (vasoconstriction) and BP elevates
Patient presents with flushed skin, hyperthermia, dry mucous membranes, blurred vision, pupillary dilation, delirium, and tachycardia. What drug(s) are they on?
anticholinergics (red as a beet, hot as a hare, dry as a bone, blind as a bat, mad as a hatter)
How do you treat intox with anticholinergics? Under what condition should you NOT give this treatment? why?
physostigmine - don’t treat if TCA overdose - can aggravate cardiotoxicity and result in heart block
Patient presents with seizures, bradycardia, hypotension, hypoglycemia. What drug did they OD on?
Propranolol - most toxic B-blocker (if seizures then probably this one)
Patient presents with overdose of propranolol. How do you treat and why?
give IV glucagon (can inc cAMP in cardiac myocytes without the beta-receptor) - normal agents used to raise BP like B-agonists and atropine generally are ineffective
Patient presents with depressed sinus node automaticity and slow AV node conduction, along with reduced CO and BP. what did they overdose on? How do you treat?
calcium channel blockers - treat with IV calcium to restore depressed cardiac contractility
Overdose of this class of drugs leads to antimuscarinic effects, vasodilation, as well as slowed conduction in the heart and depressed cardiac contractility. What is this drug? How do you treat? what is important to remember?
TCAs - treat with Norepi for hypotension and sodium bicarb for cardiac toxicity
DON’T GIVE PHYSOSTIGMINE to overcome antimuscarinic effects!!!!!
Patient taking MAOIs presents with hyperthermia, muscle rigidity, myoclonus and hyperreflexia. What is the name of this condition? how do you treat it?
serotonin syndrome
give Cyproheptadine (5HT2 receptor antagonist) + benzos for seizures and agitation
Schizophrenic patient presents with muscle rigidity, hyperthermia, metabolic acidosis, and confusion. What drugs were they taking? Name of this condition? Treament?
antipsychotics leading to neuroleptic malignant syndrome
treat with Bromocriptine (antidote) and dantrolene (helps with profound muscle rigidity)
Patient presents with fever, encephalopathy, unstable vitals, elevated CPK, and rigid muscles. What drugs caused this?
antipsychotics - neuroleptic malignant syndrome
This is the mnemonic: FEVER (Fever, Encephalopathy, Vitals unstable, Elevated CPK, Rigid muscles)
Respiratory depression, apnea, and small pupils. Drug intox? treatment?
opiods!
Naloxone or Nalmefene
Patient on oral antidiabetic drugs presents with hypoglycemia. What two agents are most likely responsible? treatment?
sulfonylureas and meglitinides (secretagogues)
give concentrated glucose bolus - if that doesn’t work give IV octreotide (antagonizes insulin release) - Diazoxide is an alternative, does the same thing
Of the 5 major sources of air pollution, what accounts for over half? Name the other 4
Carbon monoxide (52%) sulfur oxides hydrocarbons nitrogen oxides particulate matter
Which substance is responsible for the most deaths due to poisoning in the US?
carbon monoxide
which direction does Carbon monoxide shift the oxygen saturation curve?
LEFT! - CO causes relaxed conformation causing O2 to bind with high affinity (can’t deliver O2 to tissues)
patient presents with headache, confusion, trouble seeing, tachycardia, tachypnea and soon dies from respiratory failure - what drug most likely caused this? treatment?
carbon monoxide
100% O2 for 80 min or 20 min with hyperbaric O2
Patient presents with cough, stridor, and wheezing and you suspect contact with an irritant gas (like chlorine, ammonia, nitrogen oxides etc). How do you treat?
100% oxygen
Patient presents with disinhibition, lethargy, ataxia, stupor, and impaired judgment. What substance is he taking? What is seen in blood work? How do you treat?
ethanol - increased anion gab metabolic acidosis
thiamine to prevent Wernicke-Korsakoff syndrome, IV dextrose, correction of electrolyte balance
If just acute ingestion, just maintain vitals and prevent aspiration
Patient presents with severe acidosis, retinal damage, and blindness. You find high levels of formic acid in his blood. Drug intox? Most common cause of death? treatment?
methanol (formic acid is metabolite)
death from sudden cessation of respiration
treat with ethanol (saturates alcohol dehydrogenase and reduces production of formic acid), or Fomepizole (inhibits the enzyme directly)
bicarb for acidosis and hemodialysis may be necessary
Patient presents with severe acidosis and renal damage. You find high levels of oxalate in his blood. Drug intox? treatment?
ethylene glycol (antifreeze) - metabolized to toxic aldehydes and oxalate
treat with ethanol or fomepizole
Patient with osmolar gap is most likely taking what two substances? What other substances can cause it?
methanol or ethylene glycol
also acetone, ethanol, isopropanol
What is the method of action of a drug that can be used in terrorist attack?
cholinesterase inhibitors (like insecticides)
Patient presents with diarrhea, inc urination, miosis, bradycardia, emesis, lacrimation and salivation. What drugs did he most likely take? treatment?
organophosphates (insecticides) -> muscarinic overactivation (DUMBELS)
Atropine in large doses or Pralidoxime if given before ageing
How is treatment different for carbamate insecticides vs organophosphates?
carbamates just get treated with atropine because unlike organophosphates, the inhibition of acetylcholinesterase is short lived and spontaneously reversible
Patient ate rat poison.What drug? How do you treat?
warfarin - treat with vit K unless pt is actively hemorrhaging then give fresh frozen plasma (vit K won’t work for 6+ hours with a peak affect after 24)
Patient working in the plastic and jewelry manufacturing industry presents with transient CNS stimulation with hyperpnea and headache followed by hypoxic convulsions. What were they exposed to? Most likely cause of death? treatment?
cyanide - respiratory arrest
treat with cyanide antidote kit - hydroxocobalamin which reacts with cyanide to form cyanocobalamin which can be excreted in the urine (avoid methemoglobin production like in the old kits with sodium nitrite and sodium thiosulfate)
how does cyanide poisoning work?
it has a high affinity for Fe+3 so it binds to the heme of cytochrome A and A3 in mitochondria which inhibits cellular respiration -> cytotoxic hypoxia
patient ate lots of cassava root and apricot seeds, what should you
cyanide poisoning
What compound can return methemoglobin to its ferrous form?
methylene blue
How do you treat most poisoning with heavy metals? How do they cause toxicity?
treat with chelating agents - cause toxicity by reacting with functional groups essential for normal physiological functions
Patient presents with wrist drop, anemia, and GIT symptoms. What toxin was he most likely exposed to? what type of anemia?
chronic lead poisoning - plumbism
normo/microcytic hypochromic
Treatment of lead poisoning?
diazepam for seizures
mannitol and dex for cerebral edema
chelation with edetate calcium disodium (IV), dimercaprol (IM), or succimer (oral)
Southerner comes in after drinking contaminated moonshine. What toxicity are you concerned about? treatment?
arsenic - chelation with unithiol IV or dimercaprol IM
Patient presents with ricewater diarrhea, dehydration, shock and you notice a sweet, garlicky odor in his breath and stools. What are you concerned about?
arsenic poisoning
Patient presents with raindrop pattern of hyperpigmentation and hyperkeratosis of his hands and feet. He also has hair loss and bone marrow depression. What is the cause of this? What are you worried about long term?
arsenic poisoning - cancer can appear years after exposure (lung, skin, liver, kidney, bladder)
How do you treat arsine gas poisoning?
say sorry - chelating agents for arsenic dont work
Poisoning by what compound can lead to life-threatening hemorrhagic gastroenteritis followed by renal failure?
mercury
Patient presents with tremor, neuropsychiatric disturbance, and gingivostomatitis. What toxin are you concerned about? How do you treat?
mercury - treat acute exposure with unithiol (oral or IV), dimercaprol (IM), or succimer (oral)
Child presents with painful erythema of extremities, HTN, diapohresis, anorexia, and miliarial rash. Name of this condition? what causes it?
Acrodynia - mercury poisoning
what drug should you NOT use to treat chronic mercury exposure? why?
IM dimercaprol - redistributes mercury to the CNS from other tissues
child presents with vomiting, GI bleeding, lethargy, and gray cyanosis. What happened to them? How do you treat? What treatment is ineffective?
ate a bunch of iron tablets (iron is NOT an environmental poison)
treat with deferoxamine (iron chelator)
activated charcoal does NOT work
