The quizzes about Toxicology, Bioterrorism, and Chemical Warfare Agents

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Question 1

A patient develops status epilepticus from an unknown poisoning. Which of the following i s the most appropriate fi rst IV drug to give?

A	Carbamazepine
B	Lorazepam
C	Phenobarbital
D	Phenytoin
E	Valproic acid

Question 1 Explanation:

Intravenously administered lorazepam is the initial drug of choice for treatment of status epilepticus, especially when the cause of this life-threatening seizure (and a specific antidote) are unknown. Lorazepam, like the benzodiazepines in general, increases the apparent affinity of the inhibitory neurotransmitter GABA for binding sites on brain cell membranes. The effects of lorazepam (or diazepam) are short-lasting. Immediately after giving it either phenytoin or fos-phenytoin should be given to provide longer seizure suppression and “coverage” because the effects of lorazepam wear off in a comparatively short time. Other drugs that can be used for status epilepticus include phenobarbital (not a drug of choice) and (paradoxically) lidocaine for refractory seizures (mainly a drug of last resort). None of the other drugs listed in the question are appropriate for status epilepticus, despite their widespread use for oral therapy of seizure disorders long term.

Question 2

A fi refighter who i s trying to extinguish a car fi re has a leak in his protective air He develops cyanide poisoning from the combustion of plastic. Aside from rendering symptomatic, supportive care, which might be administered to combat the cyanide poisoning?

A	Ammonium chloride
B	Deferoxamine
C	Dimercaprol (BAL; British anti-lewisite)
D	Mannitol
E	Pralidoxime
F	Sodium thiosulfate

Question 2 Explanation:

Cyanide reacts with Fe(III) in mitochondrial cytochrome oxidase, inhibiting oxidative phosphorylation. The shift in metabolism from aerobic to glycolytic soon leads to not only ATP depletion, but also severe lactic acidosis. Cyanide normally reacts with endogenous sulfur-containing compounds, mainly thiosulfate, and under catalysis by rhodanese forms relatively less toxic thiocyanate that is formed and excreted in the urine. In cyanide poisoning, endogenous sulfur-containing substrate stores are quickly depleted. We manage this, then, by IV infusion of an aqueous sodium thiosulfate solution. (This is the same approach we use for “therapeutic cyanide poisoning,” as can arise when nitroprusside doses are too great.) Ammonium chloride would be ineffective, and may actually make matters worse by exacerbating metabolic acidosis. Deferoxamine, an iron chelator, would be of no benefit in terms of signs, symptoms, or their causes or consequences. Dimercaprol is a heavy metal (mainly lead) chelator that would be of no benefit. Mannitol and osmotic diuretic that is sometimes used to hasten the renal excretion of some toxins (via “forced diuresis”) would not alleviate or shorten signs and symptoms. Pralidoxime is a cholinesterase reactivator that is effective only for poisoning with organophosphate insecticides, nerve gases (sarin, soman), or other drugs that cause profound and largely permanent inactivation of acetylcholinesterase.

Question 3

A 28-year-old male patient i s transported to the emergency department after a massive exposure to carbon tetrachloride (CCl ₄), a solvent used at his Which one of the following best describes a characteristic of poisoning with this toxicant, or i ts cl inical management?

A	Causes a s low death due to bone marrow suppression
B	Causes widespread ATP depletion by uncoupling oxidative phosphorylation
C	Metabolized to free radicals (tri chloro radicals) that are directly cytotoxic to l iver and kidney cells
D	N-Acetylcysteine effectively scavenges carbon tetrachloride’s cytotoxic metabolite
E	Toxic consequences reduced or prevented by administration of methylene blue

Question 3 Explanation:

The primary toxic metabolite of carbon tetrachloride is a trichloro radical, and the liver and kidneys are the primary targets. Although all the biochemical mechanisms involved in CCl4 poisoning are not known, it seems clear that uncoupling of mitochondrial oxidative phosphorylation is not involved (b), as is clearly the case with, for example, cyanide. There is no antidote for poisoning with CCl 4, and so only symptomatic and supportive care are likely to help reduce the risk of death. Acetaminophen (d) is, of course, metabolized to hepatotoxic radicals, and prompt and proper administration of N-acetylcysteine can reduce the risks and consequences of hepatotoxicity. However, there is no evidence that this antidote for acetaminophen has any beneficial effects on CCl4 toxicity. Another organic solvent, benzene, is the agent that typically causes bone marrow suppression (a) and, with chronic exposure, certain leukemias. Finally, methylene blue is of no value in managing CCl4 poisoning. Recall, however, that methylene blue does have an important role in managing toxicity from a variety of drugs that tend to oxidize hemoglobin to methemoglobin: nitrites (eg, amyl nitrite), certain aniline dyes, benzocaine, nitroglycerin, primaquine, and certain sulfonamides

Question 4

A patient who has been on long-term therapy with a drug develops a lupus-like syndrome in response to i t. With which drug i s this response, probably mediated by an autoimmune reaction, most l ikely to occur?

A	Dioxin
B	Hydralazine
C	Organic mercury
D	Primaquine
E	Tricyclic antidepressants (eg, amitriptyline)

Question 4 Explanation:

Hydralazine, mainly used as an afterload-reducing drug for patients with severe heart failure and/or hypertension, induces autoantibodies against myeloperoxidase, and more so than many other drugs causes a lupus-like syndrome in some patients. Isoniazid, an element in most therapies of tuberculosis, does the same. The lupus-like syndrome from procainamide, a now seldom used antiarrhythmic drug, is also an autoimmune phenomenon, but in this case the subcellular mechanism involves autoantibodies directed against DNA. Methyldopa, an antihypertensive drug, also causes an autoimmune-mediated syndrome in some patients, but in this case the more typical consequence is hemolytic anemia, not the lupus-like problems. All the other drugs listed participate in important and often serious toxic reactions, but the mechanisms don’t involve an autoimmune response. Dioxin (a), which may be carcinogenic with long-term exposure, interacts with a cellular aryl hydrocarbon receptor and induces the cytochrome P450 system. Organic mercury compounds (c; eg, methyl or other alkyl compounds) are direct neurotoxins that additionally cause such responses as renal failure, muscle tremors, psychosis, and dementia. Primaquine (d), an antimalarial, oxidizes hemoglobin to methemoglobin. Secondary consequences of this include cyanosis, nausea, cardiac stimulation, and finally convulsions that precede death. The toxicity of tricyclic antidepressants (e) is multifaceted, and includes prolongation of the QRS complex (ie, prolonged cardiac action potentials resembling those caused by quinidine, a sodium channel-blocker), a host of other ventricular arrhythmias, and strong antimuscarinic (atropine-like) effects on the heart and elsewhere.

Question 5

A patient presents in the emergency department with a drug Among other things, the physician correctly orders IV infusion of sodium bicarbonate to alkalinize the urine, which increases the toxin’s elimination through pH-dependent inhibition of i ts tubular reabsorption, and helps correct the combined metabolic and respiratory acidosis the toxin caused. Which one of the following drugs most l ikely caused the toxicity?

A	Amphetamine
B	Aspirin (acetylsalicylic acid)
C	Cocaine
D	Morphine
E	Phencyclidine (PCP)

Question 5 Explanation:

Alkalinizing the urine interferes with the renal tubular reabsorption of organic acids (such as aspirin [salicylate] and phenobarbital) by increasing the ionized form of the drug in the urine (per the Henderson-Hasselbach equation). This increases their net renal excretion. Conversely, excretion of organic bases (such as amphetamine, cocaine, phencyclidine, and morphine) would be reduced by alkalinizing the urine. Note that other consequences of severe aspirin (salicylate) toxicity are both metabolic and respiratory acidosis. So in addition to enhancing urinary excretion of salicylate, the administration of sodium bicarbonate also tends to counteract the fall of blood pH. See the answer explanation for Question 329 (pp 369-373) for more information on the sequence of events that occur with a potentially lethal overdose of aspirin.

Question 6

A patient has taken a potentially lethal dose of The emergency department team begins administering repeated doses of N- acetylcysteine, which can be a l i fesaving antidote in many such cases. What i s the main mechanism by which this antidote exerts i ts beneficial effects?

A	Alkalinizes the urine to facilitate acetaminophen excretion
B	Causes metabolic acidosis to counteract metabolic alkalosis caused by a toxic acetaminophen metabolite
C	Inhibits P450 enzymes, thereby inhibiting formation of acetaminophen’s toxic metabolite
D	Inhibits synthesis of superoxide anion radical and hydrogen peroxide
E	Is ri ch in sulfhydryl (–SH) groups that react with and inactivate the toxic acetaminophen metabolite, sparing hepatocytes from attack by the metabolite

Question 6 Explanation:

N-acetylcysteine is used and often effective for acetaminophen poisoning because it is a sulfhydryl-rich drug that, if given soon enough and properly enough, can prevent hepatic necrosis. At safe blood levels, the major pathways of acetaminophen elimination involve glucuronidation and sulfation. When these pathways are overwhelmed, as occurs with acetaminophen poisoning, a cytochrome P450-dependent pathway attempts to handle the metabolic load. The active toxic metabolite, N-acetylbenzoquinoneimine, is formed in levels that exceed the ability of intrinsic sulfhydryl compounds to inactivate it. So long as ample hepatocyte stores of glutathione (a -SH compound) are available, cytotoxicity will not occur. However, severe poisoning depletes -SH stores, and so the hepatotoxic metabolite attacks key cellular macromolecules. That leads to hepatic necrosis. N-acetylcysteine acts as a substitute for endogenous glutathione to react with the toxic metabolite, thereby sparing -SH groups on key hepatocyte macromolecules. Alkalinization of the urine is of no benefit with acetaminophen poisoning, as it can be with severe salicylate poisoning (because raising urinepH reduces tubular reabsorption of salicylate and increases its excretion). Moreover, N-acetylcysteine does not directly change urine pH. Superoxide anion radical, or hydrogen peroxide, is not directly involved in the cytotoxicity (d). See the answer to Question 317, on pages 362-363, for a summary of the “stages” of acetaminophen poisoning

Question 7

Your patient developed acute poisoning as a result of inhaling cyanide gas in an industrial In addition to providing symptomatic, supportive care, and other appropriate interventions, administering which one of the following would be most l ikely to be effective as an adjunctive drug, in treating the cyanide poisoning?

A	Ammonium chloride
B	Deferoxamine
C	Dimercaprol (BAL; British anti-Lewisite)
D	N-acetylcysteine
E	Pralidoxime
F	Sodium thiosulfate

Question 7 Explanation:

Whether cyanide poisoning occurs from leakage of gas, the combustion of plastics, nitroprusside overdoses, or other causes, management includes many common elements. Cyanide reacts with Fe(III) in mitochondrial cytochrome oxidase, inhibiting oxidative phosphorylation. The shift in metabolism from aerobic metabolism to glycolysis soon leads not only to ATP depletion, but also to severe lactic acidosis as the glycolytic end-product accumulates. We manage cyanide poisoning first by dealing with the high reactivity of CN– with Fe(II) in hemoglobin and the subsequent formation of Fe(III) hemoglobin. We do that by administering sodium nitrite (IV) to regenerate active cytochromes and oxidize hemoglobin to the more cyanidereactive methemoglobin (forming cyanmethemoglobin). (Amyl nitrate can be administered by inhalation until venous access is established and sodium nitrite and sodium thiosulfate can be given). Once the nitrite is on board we administer sodium thiosulfate IV. Cyanide normally reacts with endogenous thiosulfate, and the hepatic enzyme rhodanese catalyzes the formation of relatively less toxic and more easily excreted thiocyanate. In cyanide poisoning endogenous thiosulfate stores are quickly depleted, so this provides the basis for infusing sodium thiosulfate (f, the correct answer) to lower cyanmethemoglobin levels. In cases of severe methemoglobinemia, we can also give methylene blue intravenously. (Note that large doses of inorganic nitrites can be intrinsically toxic as a result of methemoglobin formation. However, in the context of cyanide poisoning we can capitalize on the reactivity of otherwise toxic inorganic nitrite, in conjunction with thiosulfate administration, to help treat an otherwise fatal toxic scenario.) Ammonium chloride (a) would be ineffective and may actually make matters worse by exacerbating metabolic acidosis. Deferoxamine (b), an iron chelator, would be of no benefit, nor would dimercaprol (c), a heavy metal (mainly lead) chelator. N-acetylcysteine (d), routinely used as an antidote for acetaminophen poisoning, would not alleviate or shorten signs and symptoms in cyanide poisoning. Pralidoxime (e) is a cholinesterase “reactivator” that is used for poisoning with organophosphate insecticides, nerve gases (sarin, soman), or other drugs that cause profound and “irreversible” inactivation of acetylcholinesterase.

Question 8

A 5-year-old boy consumed a l iquid from a container in the family He presents with central nervous system (CNS) depression, obtunded reflexes, and ventilatory depression. A blood sample indicates profound metabolic acidosis and an anion gap. A check of the urine reveals crystals that are presumed to be oxalate. What i s the most l ikely cause of the poisoning?

A	A halogenated hydrocarbon from a can of spray paint
B	An insecticide
C	Ethylene glycol
D	Gasoline
E	Paint thinner

Question 8 Explanation:

The tip-off to the correct answer should come from the metabolic acidosis, the anion gap [= (Na+) – (HCO3– + Cl–)], and the oxalate crystals in the urine. (We’ve omitted serum K+ concentration from the equation, as is common practice, because it is normally so low that it contributes little to the calculated ion gap.) Ethylene glycol (ordinary antifreeze) forms, among other metabolites, glycolic, hippuric, and oxalic acids. It is the latter that tends to crystallize in the renal tubules, which may lead to acute renal failure. Ethylene glycol is basically an alcohol, and as with an overdose of ethanol can cause CNS depression and an overall state of inebriation. None of the other agents listed tend to cause a similar poisoning syndrome. Note: The signs and symptoms of methanol poisoning reflect, in some ways (eg, CNS depression, stupor) those of ethylene glycol or ethanol. However, methanol’s main toxicity arises from its metabolism to formic acid, the consequences of which can lead to permanent blindness. Whether the poisoning is from ethylene glycol or methanol, treatment includes administration of ethanol; it will be preferentially metabolized by alcohol dehydrogenase, reducing the metabolism of the toxin to its cytotoxic products. Finally, the majority of hospitals ignore the contribution of K+ in the anion gap “equation,” which then simplifies to Na+ – (HCO3– + Cl–).

Question 9

A farm worker in California i s brought emergently, and declared dead on arrival, to a local emergency He had been exposed to an agricultural toxin. A coworker, who was not poisoned but was nearby right after the time of exposure, said, “He just started shaking bad, collapsed, and immediately stopped breathing. I didn’t see anything else happen. He looked perfectly normal one minute, then he was just dead.” What was the most l ikely cause of this man’s death?

A	Cholinesterase inhibitor insecticide, sprayed by a crop duster airplane
B	Kerosene from a barn heater, ingested
C	Long-term and cumulative cutaneous exposure to arsenic, today’s exposure proving rapidly fatal
D	Petroleum distillates used to clean grease off farm machinery, inhaled.
E	Strychnine, ingested

Question 9 Explanation:

Strychnine is a convulsant, and death from exposure is just as described in the question. The mechanism involves strychnine’s ability to antagonize the neuronal-inhibitory effects of glycine, which is an important neurotransmitter, particularly in the spinal cord. Those spinal cord receptors are sometimes called strychnine-sensitive receptors. They are coupled to a chloride channel, and in the presence of strychnine the motor neurons become hyperpolarized. The ultimate effect is a disinhibition of (primarily) skeletal motor neurons; that rapidly leads to generalized convulsions (“he just started shaking bad”) and soon thereafter ventilatory failure and death (stopped breathing, didn’t see anything else happening [to him]). There is no antidote. Cholinesterase inhibitors (a) are the most often used insecticides used in agriculture. They can cause serious harm, and sometimes death, to humans exposed to them. However, and depending on which inhibitor is involved, and depending on the exposure route (oral, cutaneous, pulmonary) the time-course leading to death can be up to several (or many) minutes or hours. Exposure is accompanied, and death is preceded, by all the expected skeletal muscle-stimulating (NM) and peripheral muscarinic activating effects (heart, gut, airways, exocrine secretions) that are consistent with what amounts to peripheral “ACh excess.” Depending on the causative agent, CNS/spinal cord manifestations may occur and be prominent too. As a generalization, kerosene (b) and other petroleum distillates (d; found in many solvents/cleaners/degreasers, including those for household use) tend to affect multiple organ systems, including: the lungs (pulmonary complications are the most common and include alveolar hemorrhage, alveolar edema and inflammation, and aspiration that contributes further to pneumonitis); heart (cardiomyopathy from chronic exposure, catecholamine-enhanced arrhythmias mainly with acute poisoning); brain (medullary stimulation, then depression; remember that most of these petroleum-based products are highly lipid soluble and enter the CNS readily); gut (typically a painful burning sensation and frequent vomiting if the toxin is ingested); liver (chronic hepatotoxicity with centrolobular necrosis, usually caused by free radical-mediated peroxidation of membrane lipids); and kidneys (renal tubular necrosis and metabolic acidosis). Long-term exposure can also cause aplastic anemia, myelomas, and leukemias (mainly acute myelogenous). Arsenic toxicity (c) and its management are described in the answer to Question 493. The clinical presentation is much different than the sudden, convulsive death described here. You should also recall that arsenic, too, is widely used as a pesticide and for other pest- and plantdisease control applications. Note: Before we appreciated the extreme toxicity of strychnine, many decades ago, the drug was used “therapeutically,” for humans, as a stimulant, a laxative, and a remedy for a host of other common but ordinarily innocuous GI maladies. Not any more, of course. However, this deadly poison is still readily available in pesticides (mainly those used to kill pesky birds). According to a quick web search, in California alone more than half a ton of strychnine was used agriculturally a mere 2 to 3 years ago

Question 10

Here i s an excerpt from newspaper article entitled Weed Users Chase High all the Way to the Hospital. Use i t to answer the next two questions, and note that the “weed” referred to does not include marijuana or any other plants that contain tetrahydrocannabinol or an opioid. “Teenagers seeking a hallucinogenic high from the seeds of a poisonous weed that now i s in bloom are landing in hospitals across the country, police and health officials say… “Lunatic, crazy kids,” says Dodge County, Wis., Sheriff Todd Nehls, whose deputies picked up three hallucinating teenagers in October…. “Poison centers last year recorded 975 incidents involving plants such as [the] weed…” according to the American Association of Poison Control Centers’ annual report. “[The weed has]… pods that contain seeds that when eaten or brewed in a tea can cause severe hallucinations [delirium] and other reactions, including dry mouth, overheating [fever], agitation, [and] urinary retention… Some cannot urinate and need to have a catheter inserted… [Severe] overdoses can lead to seizures, coma, or death… Most people hospitalized after eating [the] weed have hallucinations that make them so erratic they are a danger to themselves…”

A	Acetylcholine
B	Amphetamine
C	Belladonna alkaloids
D	Bethanecho
E	l e. Cocaine
F	Cyanide
G	Fluoxetine
H	Neostigmine
I	Phencyclidine (PCP)
J	Physostigmine
K	Strychnine

Question 10 Explanation:

The weed in question is Jimson Weed, also known as stinkweed, locoweed, and a few other names. The signs and symptoms described in the article are among the classic ones associated with severe atropine (or, in general, antimuscarinic drug) poisoning—the original pharmacologic source being alkaloids isolated from various species of Belladonna. No other drug listed causes responses that even come close to these in terms of the peripheral autonomic responses described above

Question 11

A mother calls to report that her 6-year-old child appears to have swallowed a large amount of an over-the-counter s leep aid about 5 hours The product contained only one active drug, and knowing your drugs you suspect the poisoning i s due to diphenhydramine. Assuming your reasoned guess about the cause of poisoning was correct, which of the following s igns or symptoms would you expect to find, upon physical exam, to confirm your hunch?

A	Fever; clear lungs; absence of bowel sounds; urinary retention, dry, flushed skin; mydriasis and photophobia; bizarre behavior
B	Bradycardia and profuse diarrhea
C	Miosis with l i ttle/no papillary response to bright l ights; spontaneous micturition; lack of response to painful stimuli
D	Hypothermia; bounding pulse; hypertension
E	Skeletal muscle weakness or paralysis; profound hypermotility of gut and bladder smooth muscle; bronchospasm

Question 11 Explanation:

ost OTC sleep aids contain a first-generation antihistamine (sedating agent, almost always an ethanolamine, usually diphenhydramine or the very similar drug, doxylamine). The preponderant signs and symptoms of toxicity arise not from any histamine receptor-blocking activity, but from intense antimuscarinic (atropine-like) effects, plus dosedependent CNS depression that ultimately (and early on, in children) can lead to seizures. The signs and symptoms of this “anticholinergic syndrome” include many, if not all, that you will see in “atropine poisoning.” Aside from symptomatic and supportive care, including the use of traditional drugs for status epilepticus, physostigmine (the nonquaternary, centrally and peripherally acting acetylcholinesterase inhibitor) may be lifesaving. It will certainly help reverse many of the central and peripheral signs and symptoms of the overdose.

Question 12

A 3-year-old girl ingests 30 tablets of aspirin, 325 mg We’ve gotten her to the emergency department within 30 minutes of the poisoning. Which one of the following drugs would be the most rational and hopefully effective to administer as part of the initial treatment plan for what otherwise could have a fatal outcome?

A	Activated charcoal
B	Deferoxamine
C	Dimercaprol
D	N-Acetylcysteine
E	Penicillamine

Question 12 Explanation:

Activated charcoal, a fine, black, powder with a high adsorptive capacity, is considered to be a valuable agent in the treatment of many kinds of oral drug poisonings—primarily if administered early on and then removed by gastric lavage. Drugs that are well adsorbed by activated charcoal include primaquine, propoxyphene, dextroamphetamine, chlorpheniramine, phenobarbital, carbamazepine, digoxin, and aspirin. Mineral acids, alkalis, tolbutamide, and other drugs that are insoluble in acidic aqueous solution are not well adsorbed. Deferoxamine (b), dimercaprol (c; also known as BAL, or British anti-Lewisite), and penicillamine (e) are polyvalent cation chelators (iron, lead, copper) and play no role in managing aspirin (salicylate) poisoning, nor poisoning with any substances other than the metals they chelate. NAcetylcysteine (d) is the preferred antidote for acetaminophen overdoses (Question 333). Notes: the term adsorb means “to bind”; it is decidedly different from the more common pharmacologic/therapeutic term absorb.

Question 13

A 50-year-old man has been consuming large amounts of ethanol on an almost daily basis for many One day, unable to find any ethanol, he ingests a large amount of methanol (wood alcohol) that he had bought for his camp lantern. Which of the following i s the most l ikely consequence of his methanol poisoning?

A	Atrioventricular conduction defect (block)
B	Blindness
C	Bronchospasm
D	Delirium tremens
E	Metabolic alkalosis

Question 13 Explanation:

Methanol is metabolized by the same enzymes that metabolize ethanol, but the products are different: formaldehyde and formic acid in the case of methanol. Headache, vertigo, vomiting, abdominal pain, dyspnea, and blurred vision can occur from accumulation of these metabolic intermediates. However, the most dangerous (or at least permanently disabling) consequence in severe cases is hyperemia of the optic disc, which can lead to blindness. The rationale for administering ethanol to treat methanol poisoning is fairly simple. Ethanol has a high affinity for alcohol and aldehyde dehydrogenases and competes as a substrate for those enzymes, reducing metabolism of methanol to its more toxic products. Important adjunctive treatments include hemodialysis to enhance removal of methanol and its products; and administration of systemic alkalinizing salts (eg, sodium bicarbonate) to counteract metabolic acidosis. Administration of systemic acidifying substances such as ascorbic acid would aggravate the condition

Question 14

A 15-year-old boy attempts suicide with a l iquid that he found in his parents’ His dad used i t to get rid of “varmints” around the yard. The toxin causes intense abdominal pain, skeletal muscle cramps, projectile vomiting, and severe diarrhea that leads to fluid and electrolyte imbalances, hypotension, and difficulty swallowing. On examination he i s found to be volume depleted and i s showing s igns of a reduced level of consciousness. His breath smells “metallic.” Which of the following probably accounts for these symptoms?

A	Arsenic
B	Cadmium
C	Iron
D	Lead.
E	Zinc

Question 14 Explanation:

Arsenic is a constituent of fungicides, herbicides, and pesticides. Symptoms of acute toxicity include tightness in the throat, difficulty in swallowing, and stomach pains. Projectile vomiting and severe diarrhea can lead to hypovolemic shock, significant electrolyte derangements, and death. Chronic poisoning may cause peripheral neuritis, anemia, skin keratosis, and capillary dilation leading to hypotension. Dimercaprol (British anti-Lewisite [BAL]) is the main antidote used for arsenic poisoning. Note: If dimercaprol is also known as anti-Lewisite, what is Lewisite? It is an obsolete organic arsenical (As-containing substance, specifically chlorovinyl dichloroarsine—don’t memorize that!) developed as a chemical warfare agent in World War II. Arsenic reacts and forms chelates with sulfhydryl moieties on various substances, including many enzymes involved in essential metabolic reactions. It is a vesicant (causes blistering) that targets many body tissues, but exerts its main toxic effects in the lungs when inhaled. Dimercaprol is a relatively simple molecule with two sulfhydryl groups in its structure. It reacts with the Lewisite, chelating it and thereby reducing attack on and inactivation of cellular –SH-rich enzymes.

Question 15

A 22-year-old i s brought to the emergency department by a They had been at a bar for about an hour, and then the patient suddenly became drowsy but was sti l l conscious. She fell and cut her head, and has l i ttle difficulty feeling the pain from the trauma. Her ventilatory rate and depth are depressed, but not to a worrisome degree. Her patellar reflexes are blunted and she i s ataxic. She responds s lowly to questions but i s unable to recall anything that happened after arriving at the bar and s ipping her fi rst (and last) adult beverage. Her friend stated that she had only one Cosmopolitan and hadn’t been drinking before they went out. With what was this patient’s drink most l ikely “spiked?”

A	A barbiturate
B	A benzodiazepine
C	An opioid
D	Chloral hydrate
E	Cocaine
F	Pure (grain) alcohol

Question 15 Explanation:

Arguably the most important tip-off in this presentation is the antegrade amnesia, which (among other things) is rather uniquely associated with benzodiazepines. The most likely benzodiazepine used in this scenario was rohypnol (flunitrazepam, better known as “roofies” on the street and by those who use it as a date-rape drug). Unless this patient were a very atypical responder, it is unlikely that any of the other CNS depressants—a barbiturate, an opioid, chloral hydrate —would cause the same responses. She’s had one drink yet still feels pain from her head gash. She apparently hasn’t had enough alcohol to be so obtunded that she doesn’t feel pain, and a barbiturate is likely to enhance the sensation of pain (hyperalgesic effect). Chloral hydrate is still used medically, mainly as a sedative for children, although its use is declining dramatically. It indeed causes powerful CNS depressants when used in combination with just a little alcohol: chloral hydrate has been known for years as “knock-out drops” and the combination with alcohol has been called a “Mickey Finn.” However, chloral hydrate is not nearly as readily available as the illicit benzodiazepines; it does not cause antegrade amnesia (important to the perpetrator, because he or she anticipates no recall of what happened by the victim), but it is not readily available, and it simply doesn’t have the “reputation” as a preferred date-rape drug among those who use such drugs.

Question 16

Let’s assume the profoundly CNS-depressed patient in the previous question indeed was overdosed with a Which drug i s most l ikely to be effective, indeed would be a preferred pharmacologic antidote, i f that were the case?

A	Amphetamine
B	Flumazenil
C	Methylphenidate
D	Naltrexone
E	Physostigmine

Question 16 Explanation:

Flumazenil is the specific benzodiazepine receptor antagonist, and it is both specific and almost always effective for excessive effects of any benzodiazepine. It’s tempting to use a CNS stimulant (a, amphetamines; or c, methylphenidate) to overcome the effects of any CNS depressant. It may help, but more likely the outcome of giving a stimulant is excessive effects manifest as seizures and unwanted cardiovascular stimulatory effects. Naltrexone, like naloxone, specifically blocks opioid receptors and will be of no benefit to this poisoned patient. Some benzodiazepines do cause anti-muscarinic effects, but weakly. For that reason, and others, physostigmine (or any other AChE inhibitor) would not at all an effective or problem-free drug to give.

Question 17

Recent occupational health studies in several heavily populated urban areas have revealed an astonishingly large number of homes that have lead-based paint and children l iving in However, a number of environmental poisons that could lead to acute or chronic poisoning have also been found there. Which s igns and symptoms would be consistent with chronic exposure to toxic levels of inorganic lead?

A	Anorexia and weight loss; weakness, especially of extensor muscles (eg, wrist drop); recurrent abdominal pain
B	Gingivitis, discolored gums, loosened teeth, or stomatitis; tremor of the extremities; swollen parotid or other salivary glands
C	Hallucinations, insomnia, headache, generalized CNS i rri tability
D	Hyperventilation in response to metabolic acidosis; hypotension; abdominal pain, diarrhea, brown or bloody vomitus; pallor or cyanosis
E	Severe, watery diarrhea; garlicky or metallic breath; encephalopathy, hypovolemia and hypotension

Question 17 Explanation:

The presentation of chronic lead exposure, as from being exposed to (or even eating) older lead-based paints, differs from the typical presentation of acute organic lead poisoning (answer c), which usually arises fromsniffing leaded gasoline (and just about all gasolines nowadays are organic lead-enriched). Answer b, with the predominant gingival/head/neck signs and symptoms, is typical of chronic or acute mercury intoxication. Answer d, with the hyperventilation, GI disturbances (including discolored vomitus) and pallor, is what you are likely to encounter in acute iron poisoning (as from a consuming ferrous sulfate supplements in large doses). A characteristic breath (garlicky or metallic), profuse diarrhea, encephalopathy, and hypotension (answer e) are typical of acute inorganic arsenic poisoning. Knowing more about the patient’s history and environment will help immensely in sorting out what the “most likely” cause of intoxication is.

Question 18

Lab tests conducted by the local health department are positive for chronic lead exposure in a Lead levels are s ignificantly elevated, but symptoms fortunately are mild and not at all imminently l i fe-threatening. What i s the most appropriate antidote for reducing the child’s body load of lead?

A	Ca-Na 2-EDTA
B	Deferoxamine
C	Dimercaprol
D	N-Acetylcysteine
E	Penicillamine
F	Succimer

Question 18 Explanation:

Succimer (a more polar salt of dimercaprol; British anti-Lewisite; BAL) would be the choice, given the proof of lead poisoning, the lack of acute symptoms, and the fact that our patient is a child. Succimer is easy to give orally and is tolerated far better than the alternatives: Ca-Na2-EDTA (a), penicillamine (e; traditionally viewed as a copper chelator, but it also chelates lead), or dimercaprol (c) itself. Although the heavy metal chelation profiles for succimer are not drastically different from those of dimercaprol, the fact that succimer is more polar (and, therefore, less likely to enter cells) seems to account for far fewer and milder side effects than those of dimercaprol (especially with respect to risks of tachycardia and hypertension). N-Acetylcysteine (d), as noted elsewhere, is the drug of choice for acetaminophen poisoning. It has no ability to chelate lead or other cations.

Question 19

Not long ago, several patients (and a rather shady health care “provider” who i s now incarcerated) seeking “relief” from facial wrinkles nearly died because they received injections of botulinum toxin that was improperly obtained and inadequately Which i s a correct characteristic, finding, or mechanism associated with this toxin?

A	Complete failure of all cholinergic neurotransmission
B	Favorable response to administration of pralidoxime
C	Impairment of parasympathetic, but not sympathetic, nervous system activation
D	Massive overstimulation of all structures having muscarinic cholinergic receptors
E	Selective paralysis of skeletal muscle

Question 19 Explanation:

Botulinus (botulinum) toxin prevents release of acetylcholine (from storage vesicles) by virtually all cholinergic nerves. Thus, there is no activation of any cholinergic receptors, whether nicotinic or muscarinic. Noteworthy findings, then, include an inability to activate all postganglionic neurons (sympathetic and parasympathetic), no physiologic release of epinephrine from the adrenal medulla, and flaccid skeletal muscle paralysis due to failure of ACh release from motor nerves. The cause of death is ventilatory failure because the intercostal muscles and diaphragm are nonfunctional. Pralidoxime is a cholinesterase reactivator, an antidote and adjunct (along with atropine) for poisonings with “irreversible” cholinesterase inhibitors such as soman, sarin, VX (“nerve gases”), and many organo-phosphorus insecticides. Because no ACh is being released in botulinus poisoning, “reactivation” of the enzyme that normally metabolizes the neurotransmitter is irrelevant (and ineffective).

Question 20

A terrorist drops a vial of “nerve gas” into a crowded subway at rush The patients are brought to the nearest emergency centers and are given atropine. Which effect of the nerve gas will persist after giving the atropine?

A	Bradycardia
B	Bronchospasm
C	Excessive lacrimal, mucus, sweat, and salivary secretions
D	GI hypermotility, fluid and electrolyte loss from profuse diarrhea
E	Skeletal muscle hyperfunction or paralysis

Question 20 Explanation:

Most of the adverse responses to nerve gases (irreversible ACh esterase inhibitors such as soman and sarin) are due to a build-up of ACh at muscarinic receptors (ie, ACh released from postganglionic parasympathetic nerves or sympathetic/cholinergic nerves innervating sweat glands). Those responses will be attenuated by atropine, because it is a highly specific competitive muscarinic antagonist. However, skeletal muscle stimulation (or eventual paralysis) involves nicotinic receptor activation. That will not be affected by atropine, and unless other supportive measures are provided, the patient is likely to die from ventilatory arrest/apnea.

Question 21

A neighbor calls you for advice and She knows you are not a veterinary student, but s ince you’re going to be a physician soon she figures you know everything. Her pet puppy, Pookie, a Pekingese, has eaten a large amount of rodent (rat and mouse) poison. She’s panicked and pleads to know i f the precious pooch i s poisoned. The rodenticide indeed contains a powerful poison intended to ki l l rats and mice, but i t can do the same to any other animals that have ingested i t too, including humans. What i s the most l ikely toxic ingredient in these rodenticides, and probably will cause poor Pookie pronounced problems?

A	Amphetamine-cocaine combination
B	Morphine
C	Succinylcholine
D	Vecuronium (or a s imilar neuromuscular blocker)
E	Warfarin

Question 21 Explanation:

No, this is not a frivolous question. Someday you may be working in an emergency department or a poison center, so you need to know. The critters that eat the rodenticide ultimately bleed to death from a warfarin overdose. When treating such poisonings in humans or poisoned pets, the approach is the same as with therapeutic warfarin: administer vitamin K (orally or parenterally, whichever is indicated), and provide other symptomatic and supportive measures. Amphetamine or cocaine, alone or in combination (a), as well as morphine (b), are controlled substances with high potential for dependence and abuse. Such substances simply wouldn’t be permitted in products that virtually anyone could obtain at their local home care or hardware store. What about succinylcholine (c)? It’s ineffective when ingested; it has to be injected. The same applies the nondepolarizing blockers (d), vecuronium, and the other “curoniums” or “curines.” (You’ll remember that some peoples indigenous to the Amazon killed their prey with curare-tipped darts. And they ate that curare-laced meat with absolutely no ill effects from the drug.)

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1.A patient develops status epilepticus from an unknown poisoning. Which of the following i s the most appropriate fi rst IV drug to give?

Carbamazepine
Lorazepam
Phenobarbital
Phenytoin
Valproic acid

2. A fi refighter who i s trying to extinguish a car fi re has a leak in his protective air He develops cyanide poisoning from the combustion of plastic. Aside from rendering symptomatic, supportive care, which might be administered to combat the cyanide poisoning?

Ammonium chloride
Deferoxamine
Dimercaprol (BAL; British anti-lewisite)
Mannitol
Pralidoxime
Sodium thiosulfate

3. A 28-year-old male patient i s transported to the emergency department after a massive exposure to carbon tetrachloride (CCl ₄), a solvent used at his Which one of the following best describes a characteristic of poisoning with this toxicant, or i ts cl inical management?

Causes a s low death due to bone marrow suppression
Causes widespread ATP depletion by uncoupling oxidative phosphorylation
Metabolized to free radicals (tri chloro radicals) that are directly cytotoxic to l iver and kidney cells
N-Acetylcysteine effectively scavenges carbon tetrachloride’s cytotoxic metabolite
Toxic consequences reduced or prevented by administration of methylene blue

4. A patient who has been on long-term therapy with a drug develops a lupus-like syndrome in response to i t. With which drug i s this response, probably mediated by an autoimmune reaction, most l ikely to occur?

Dioxin
Hydralazine
Organic mercury
Primaquine
Tricyclic antidepressants (eg, amitriptyline)

5. A patient presents in the emergency department with a drug Among other things, the physician correctly orders IV infusion of sodium bicarbonate to alkalinize the urine, which increases the toxin’s elimination through pH-dependent inhibition of i ts tubular reabsorption, and helps correct the combined metabolic and respiratory acidosis the toxin caused. Which one of the following drugs most l ikely caused the toxicity?

Amphetamine
Aspirin (acetylsalicylic acid)
Cocaine
Morphine
Phencyclidine (PCP)

6. A patient has taken a potentially lethal dose of The emergency department team begins administering repeated doses of N– acetylcysteine, which can be a l i fesaving antidote in many such cases. What i s the main mechanism by which this antidote exerts i ts beneficial effects?

Alkalinizes the urine to facilitate acetaminophen excretion
Causes metabolic acidosis to counteract metabolic alkalosis caused by a toxic acetaminophen metabolite
Inhibits P450 enzymes, thereby inhibiting formation of acetaminophen’s toxic metabolite
Inhibits synthesis of superoxide anion radical and hydrogen peroxide
Is ri ch in sulfhydryl (–SH) groups that react with and inactivate the toxic acetaminophen metabolite, sparing hepatocytes from attack by the metabolite

7. Your patient developed acute poisoning as a result of inhaling cyanide gas in an industrial In addition to providing symptomatic, supportive care, and other appropriate interventions, administering which one of the following would be most l ikely to be effective as an adjunctive drug, in treating the cyanide poisoning?

Ammonium chloride
Deferoxamine
Dimercaprol (BAL; British anti-Lewisite)
N-acetylcysteine Pralidoxime
Sodium thiosulfate

8. A 5-year-old boy consumed a l iquid from a container in the family He presents with central nervous system (CNS) depression, obtunded reflexes, and ventilatory depression. A blood sample indicates profound metabolic acidosis and an anion gap. A check of the urine reveals crystals that are presumed to be oxalate. What i s the most l ikely cause of the poisoning?

A halogenated hydrocarbon from a can of spray paint
An insecticide
Ethylene glycol
Gasoline
Paint thinner

9. A farm worker in California i s brought emergently, and declared dead on arrival, to a local emergency He had been exposed to an agricultural toxin. A coworker, who was not poisoned but was nearby right after the time of exposure, said, “He just started shaking bad, collapsed, and immediately stopped breathing. I didn’t see anything else happen. He looked perfectly normal one minute, then he was just dead.” What was the most l ikely cause of this man’s death?

Cholinesterase inhibitor insecticide, sprayed by a crop duster airplane
Kerosene from a barn heater, ingested
Long-term and cumulative cutaneous exposure to arsenic, today’s exposure proving rapidly fatal
Petroleum distillates used to clean grease off farm machinery, inhaled.
Strychnine, ingested

10. Here i s an excerpt from newspaper article entitled Weed Users Chase High all the Way to the Hospital. Use i t to answer the next two questions, and note that the “weed” referred to does not include marijuana or any other plants that contain tetrahydrocannabinol or an opioid.

“Teenagers seeking a hallucinogenic high from the seeds of a poisonous weed that now i s in bloom are landing in hospitals across the country, police and health officials say… “Lunatic, crazy kids,” says Dodge County, Wis., Sheriff Todd Nehls, whose deputies picked up three hallucinating teenagers in October….

“Poison centers last year recorded 975 incidents involving plants such as [the] weed…” according to the American Association of Poison Control Centers’ annual report.

“[The weed has]… pods that contain seeds that when eaten or brewed in a tea can cause severe hallucinations [delirium] and other reactions, including dry mouth, overheating [fever], agitation, [and] urinary retention… Some cannot urinate and need to have a catheter inserted… [Severe] overdoses can lead to seizures, coma, or death… Most people hospitalized after eating [the] weed have hallucinations that make them so erratic they are a danger to themselves…”

Acetylcholine
Amphetamine
Belladonna alkaloids
Bethanechol e. Cocaine
Cyanide
Fluoxetine
Neostigmine
. Phencyclidine (PCP)
Physostigmine
Strychnine

Which drug l i sted above causes s igns and symptoms that are most s imilar to—indeed, vi rtually identical to—those described in the scenario?

11. A mother calls to report that her 6-year-old child appears to have swallowed a large amount of an over-the-counter s leep aid about 5 hours The product contained only one active drug, and knowing your drugs you suspect the poisoning i s due to diphenhydramine. Assuming your reasoned guess about the cause of poisoning was correct, which of the following s igns or symptoms would you expect to find, upon physical exam, to confirm your hunch?

Fever; clear lungs; absence of bowel sounds; urinary retention, dry, flushed skin; mydriasis and photophobia; bizarre behavior
Bradycardia and profuse diarrhea
Miosis with l i ttle/no papillary response to bright l ights; spontaneous micturition; lack of response to painful stimuli
Hypothermia; bounding pulse; hypertension
Skeletal muscle weakness or paralysis; profound hypermotility of gut and bladder smooth muscle; bronchospasm

12. A 3-year-old girl ingests 30 tablets of aspirin, 325 mg We’ve gotten her to the emergency department within 30 minutes of the poisoning. Which one of the following drugs would be the most rational and hopefully effective to administer as part of the initial treatment plan for what otherwise could have a fatal outcome?

Activated charcoal
Deferoxamine
Dimercaprol
N-Acetylcysteine
Penicillamine

13.. A 50-year-old man has been consuming large amounts of ethanol on an almost daily basis for many One day, unable to find any ethanol, he ingests a large amount of methanol (wood alcohol) that he had bought for his camp lantern. Which of the following i s the most l ikely consequence of his methanol poisoning?

Atrioventricular conduction defect (block)
Blindness
Bronchospasm
Delirium tremens
Metabolic alkalosis

14. A 15-year-old boy attempts suicide with a l iquid that he found in his parents’ His dad used i t to get rid of “varmints” around the yard. The toxin causes intense abdominal pain, skeletal muscle cramps, projectile vomiting, and severe diarrhea that leads to fluid and electrolyte imbalances, hypotension, and difficulty swallowing. On examination he i s found to be volume depleted and i s showing s igns of a reduced level of consciousness. His breath smells “metallic.” Which of the following probably accounts for these symptoms?

Arsenic
Cadmium
Iron
Lead.
Zinc

15. A 22-year-old i s brought to the emergency department by a They had been at a bar for about an hour, and then the patient suddenly became drowsy but was sti l l conscious. She fell and cut her head, and has l i ttle difficulty feeling the pain from the trauma. Her ventilatory rate

and depth are depressed, but not to a worrisome degree. Her patellar reflexes are blunted and she i s ataxic. She responds s lowly to questions but i s unable to recall anything that happened after arriving at the bar and s ipping her fi rst (and last) adult beverage. Her friend stated that she had only one Cosmopolitan and hadn’t been drinking before they went out. With what was this patient’s drink most l ikely “spiked?”

A barbiturate
A benzodiazepine
An opioid
Chloral hydrate Cocaine
Pure (grain) alcohol

`16. Let’s assume the profoundly CNS-depressed patient in the previous question indeed was overdosed with a Which drug i s most l ikely to be effective, indeed would be a preferred pharmacologic antidote, i f that were the case?

Amphetamine
Flumazenil
Methylphenidate
Naltrexone
Physostigmine

17. Recent occupational health studies in several heavily populated urban areas have revealed an astonishingly large number of homes that have lead-based paint and children l iving in However, a number of environmental poisons that could lead to acute or chronic poisoning have also been found there. Which s igns and symptoms would be consistent with chronic exposure to toxic levels of inorganic lead?

Anorexia and weight loss; weakness, especially of extensor muscles (eg, wrist drop); recurrent abdominal pain
Gingivitis, discolored gums, loosened teeth, or stomatitis; tremor of the extremities; swollen parotid or other salivary glands
Hallucinations, insomnia, headache, generalized CNS i rri tability
Hyperventilation in response to metabolic acidosis; hypotension; abdominal pain, diarrhea, brown or bloody vomitus; pallor or cyanosis Severe, watery diarrhea; garlicky or metallic breath; encephalopathy, hypovolemia and hypotension

18. Lab tests conducted by the local health department are positive for chronic lead exposure in a Lead levels are s ignificantly elevated, but symptoms fortunately are mild and not at all imminently l i fe-threatening. What i s the most appropriate antidote for reducing the child’s body load of lead?

Ca-Na ₂-EDTA
Deferoxamine
Dimercaprol
N-Acetylcysteine Penicillamine
. Succimer

19. Not long ago, several patients (and a rather shady health care “provider” who i s now incarcerated) seeking “relief” from facial wrinkles nearly died because they received injections of botulinum toxin that was improperly obtained and inadequately Which i s a correct characteristic, finding, or mechanism associated with this toxin?

Complete failure of all cholinergic neurotransmission
Favorable response to administration of pralidoxime
Impairment of parasympathetic, but not sympathetic, nervous system activation
Massive overstimulation of all structures having muscarinic cholinergic receptors
Selective paralysis of skeletal muscle

20. A terrorist drops a vial of “nerve gas” into a crowded subway at rush The patients are brought to the nearest emergency centers and are given atropine. Which effect of the nerve gas will persist after giving the atropine?

Bradycardia
Bronchospasm
Excessive lacrimal, mucus, sweat, and salivary secretions
GI hypermotility, fluid and electrolyte loss from profuse diarrhea
Skeletal muscle hyperfunction or paralysis

21. A neighbor calls you for advice and She knows you are not a veterinary student, but s ince you’re going to be a physician soon she figures you know everything. Her pet puppy, Pookie, a Pekingese, has eaten a large amount of rodent (rat and mouse) poison. She’s panicked and pleads to know i f the precious pooch i s poisoned. The rodenticide indeed contains a powerful poison intended to ki l l rats and mice, but i t can do the same to any other animals that have ingested i t too, including humans. What i s the most l ikely toxic ingredient in these rodenticides, and probably will cause poor Pookie pronounced problems?

Amphetamine-cocaine combination
Morphine
Succinylcholine
Vecuronium (or a s imilar neuromuscular blocker)
Warfarin

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