Toxicology Flashcards

1
Q

poisoning of what drug leads to uncoupling of oxidative phosphorylation, increased levels of pyruvate and lactate as well as heat production?

A

aspirin

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2
Q

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?

A

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

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3
Q

person presents with profound metabolic acidosis, seizures, and pulmonary edema leading to ARDS. They are also vomiting and are dehydrated. What toxicity is this?

A

very severe poisoning with apsirin

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4
Q

why do you see respiratory alkalosis in the initial stages of aspirin toxicity?

A

aspirin directly stimulates the respiratory center, leading to inc in resp. rate`

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5
Q

treatment for aspirin toxicity? mild/moderate/severe

A

mild: gastric lavage, activated charcoal and fluid replacement
moderate: sodium bicarb (alkalinizes the urine to promote aspirin excretion)
severe: hemodialysis

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6
Q

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?

A

acetaminophen
antidote is N-acetylcysteine that increases glutathione production as well as directly detoxes NAPQI (metabolite of acetaminophen)

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7
Q

Patient presents with dilated pupils, sweaty skin, and tachycardia. What class of drug did he take?

A

amphetamine/stimulant

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8
Q

what is important to remember when treating tachyarrhythmias of amphetamine intox?

A

dont give beta blockers without alpha blockage first!

Get unopposed alpha-1 action (vasoconstriction) and BP elevates

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9
Q

Patient presents with flushed skin, hyperthermia, dry mucous membranes, blurred vision, pupillary dilation, delirium, and tachycardia. What drug(s) are they on?

A

anticholinergics (red as a beet, hot as a hare, dry as a bone, blind as a bat, mad as a hatter)

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10
Q

How do you treat intox with anticholinergics? Under what condition should you NOT give this treatment? why?

A

physostigmine - don’t treat if TCA overdose - can aggravate cardiotoxicity and result in heart block

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11
Q

Patient presents with seizures, bradycardia, hypotension, hypoglycemia. What drug did they OD on?

A

Propranolol - most toxic B-blocker (if seizures then probably this one)

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12
Q

Patient presents with overdose of propranolol. How do you treat and why?

A

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

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13
Q

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?

A

calcium channel blockers - treat with IV calcium to restore depressed cardiac contractility

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14
Q

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?

A

TCAs - treat with Norepi for hypotension and sodium bicarb for cardiac toxicity

DON’T GIVE PHYSOSTIGMINE to overcome antimuscarinic effects!!!!!

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15
Q

Patient taking MAOIs presents with hyperthermia, muscle rigidity, myoclonus and hyperreflexia. What is the name of this condition? how do you treat it?

A

serotonin syndrome

give Cyproheptadine (5HT2 receptor antagonist) + benzos for seizures and agitation

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16
Q

Schizophrenic patient presents with muscle rigidity, hyperthermia, metabolic acidosis, and confusion. What drugs were they taking? Name of this condition? Treament?

A

antipsychotics leading to neuroleptic malignant syndrome

treat with Bromocriptine (antidote) and dantrolene (helps with profound muscle rigidity)

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17
Q

Patient presents with fever, encephalopathy, unstable vitals, elevated CPK, and rigid muscles. What drugs caused this?

A

antipsychotics - neuroleptic malignant syndrome

This is the mnemonic: FEVER (Fever, Encephalopathy, Vitals unstable, Elevated CPK, Rigid muscles)

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18
Q

Respiratory depression, apnea, and small pupils. Drug intox? treatment?

A

opiods!

Naloxone or Nalmefene

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19
Q

Patient on oral antidiabetic drugs presents with hypoglycemia. What two agents are most likely responsible? treatment?

A

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

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20
Q

Of the 5 major sources of air pollution, what accounts for over half? Name the other 4

A
Carbon monoxide (52%)
sulfur oxides
hydrocarbons
nitrogen oxides
particulate matter
21
Q

Which substance is responsible for the most deaths due to poisoning in the US?

A

carbon monoxide

22
Q

which direction does Carbon monoxide shift the oxygen saturation curve?

A

LEFT! - CO causes relaxed conformation causing O2 to bind with high affinity (can’t deliver O2 to tissues)

23
Q

patient presents with headache, confusion, trouble seeing, tachycardia, tachypnea and soon dies from respiratory failure - what drug most likely caused this? treatment?

A

carbon monoxide

100% O2 for 80 min or 20 min with hyperbaric O2

24
Q

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?

A

100% oxygen

25
Q

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?

A

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

26
Q

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?

A

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

27
Q

Patient presents with severe acidosis and renal damage. You find high levels of oxalate in his blood. Drug intox? treatment?

A

ethylene glycol (antifreeze) - metabolized to toxic aldehydes and oxalate

treat with ethanol or fomepizole

28
Q

Patient with osmolar gap is most likely taking what two substances? What other substances can cause it?

A

methanol or ethylene glycol

also acetone, ethanol, isopropanol

29
Q

What is the method of action of a drug that can be used in terrorist attack?

A

cholinesterase inhibitors (like insecticides)

30
Q

Patient presents with diarrhea, inc urination, miosis, bradycardia, emesis, lacrimation and salivation. What drugs did he most likely take? treatment?

A

organophosphates (insecticides) -> muscarinic overactivation (DUMBELS)

Atropine in large doses or Pralidoxime if given before ageing

31
Q

How is treatment different for carbamate insecticides vs organophosphates?

A

carbamates just get treated with atropine because unlike organophosphates, the inhibition of acetylcholinesterase is short lived and spontaneously reversible

32
Q

Patient ate rat poison.What drug? How do you treat?

A

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)

33
Q

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?

A

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)

34
Q

how does cyanide poisoning work?

A

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

35
Q

patient ate lots of cassava root and apricot seeds, what should you

A

cyanide poisoning

36
Q

What compound can return methemoglobin to its ferrous form?

A

methylene blue

37
Q

How do you treat most poisoning with heavy metals? How do they cause toxicity?

A

treat with chelating agents - cause toxicity by reacting with functional groups essential for normal physiological functions

38
Q

Patient presents with wrist drop, anemia, and GIT symptoms. What toxin was he most likely exposed to? what type of anemia?

A

chronic lead poisoning - plumbism

normo/microcytic hypochromic

39
Q

Treatment of lead poisoning?

A

diazepam for seizures
mannitol and dex for cerebral edema
chelation with edetate calcium disodium (IV), dimercaprol (IM), or succimer (oral)

40
Q

Southerner comes in after drinking contaminated moonshine. What toxicity are you concerned about? treatment?

A

arsenic - chelation with unithiol IV or dimercaprol IM

41
Q

Patient presents with ricewater diarrhea, dehydration, shock and you notice a sweet, garlicky odor in his breath and stools. What are you concerned about?

A

arsenic poisoning

42
Q

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?

A

arsenic poisoning - cancer can appear years after exposure (lung, skin, liver, kidney, bladder)

43
Q

How do you treat arsine gas poisoning?

A

say sorry - chelating agents for arsenic dont work

44
Q

Poisoning by what compound can lead to life-threatening hemorrhagic gastroenteritis followed by renal failure?

A

mercury

45
Q

Patient presents with tremor, neuropsychiatric disturbance, and gingivostomatitis. What toxin are you concerned about? How do you treat?

A

mercury - treat acute exposure with unithiol (oral or IV), dimercaprol (IM), or succimer (oral)

46
Q

Child presents with painful erythema of extremities, HTN, diapohresis, anorexia, and miliarial rash. Name of this condition? what causes it?

A

Acrodynia - mercury poisoning

47
Q

what drug should you NOT use to treat chronic mercury exposure? why?

A

IM dimercaprol - redistributes mercury to the CNS from other tissues

48
Q

child presents with vomiting, GI bleeding, lethargy, and gray cyanosis. What happened to them? How do you treat? What treatment is ineffective?

A

ate a bunch of iron tablets (iron is NOT an environmental poison)

treat with deferoxamine (iron chelator)

activated charcoal does NOT work