Post by pbruss on Nov 27, 2014 0:32:15 GMT -5
alsoattached in bidirectional tachycardia EKG - path-pneumonic for dig OD (not most common)
1. Answer A. Flumazenil is a benzodiazepine antagonist that is used only in selected cases to reverse benzodiazepine overdose. The only real indications for flumazenil are to speed recovery in accidental pediatric ingestions and during procedural sedation. Flumazenil can precipitate seizures in patients who are chronic benzodiazepine users, alcoholics, and those who have coingested medicines which lower the seizure threshold. The morbidity and mortality of benzodiazepine overdose is mostly from respiratory depression. Therefore, standard airway management, oxygenation, and ventilation preclude the use of flumazenil in almost all cases.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 156). Lippincot (Wolters Kluwer Health). Kindle Edition.
6. Answer C. Fluoxetine is a type of selective serotonin reuptake inhibitor (SSRI). As a class, SSRIs are generally benign in overdose, causing mild GI and CNS symptoms and rarely leading to dysrhythmias. Cyproheptadine is a serotonin antagonist that has unproven clinical efficacy in most SSRI overdoses. Its use is mainly limited to patients with serotonin syndrome, a constellation of neurologic, GI, and cardiac findings. Dysrhythmia is rare and should be treated according to current ACLS guidelines. Unlike with tricyclic antidepressant overdose, there is no indication for routine use of sodium bicarbonate to treat dysrhythmias. As in virtually all overdoses, ipecac is not recommended as a method of gastric decontamination. Hemodialysis is not indicated in patients with SSRI overdose, as the drug is highly bound to plasma proteins.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 157). Lippincot (Wolters Kluwer Health). Kindle Edition.
32. Answer B. The serotonin syndrome is classically described as a triad of cognitive abnormalities, autonomic hyperactivity, and neuromuscular problems. However, there is considerable variability in the severity of the presentation and considerable overlap of the clinical findings with neuroleptic malignant syndrome as well as the anticholinergic toxidrome. Clonus is the most important clinical finding to help differentiate the serotonin syndrome from similar clinical conditions. Clonus may be spontaneous, inducible, or isolated to the ocular muscles. Thus, physicians must perform a thorough, focused examination to specifically look for this finding.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 161). Lippincot (Wolters Kluwer Health). Kindle Edition.
51. Answer C. Isopropanol classically does not cause elevated anion gap when ingested. The osmolar gap, however, is elevated and should be calculated and measured when there is suspicion of toxic alcohol overdose. Elevation of the anion gap due to lactic acidosis can occur in cases of severe isopropanol poisoning if there is associated coma, gastrointestinal hemorrhage, or hypotension. Choices A, B, D, and E all cause an elevation in the anion gap at some point during their metabolism.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 164-165). Lippincot (Wolters Kluwer Health). Kindle Edition.
73. Answer E. Nonaspirin NSAIDs, including ibuprofen, produce generally benign and self-limited conditions in overdose. Symptoms will occur within 4 hours of ingestion, are usually mild, and resolve within 24 hours. Patients rarely have life-threatening overdoses and almost never require antidotes, decontamination, augmented renal excretion, or invasive therapies such as hemodialysis. Serum levels of nonaspirin NSAIDs are not clinically useful. Of overdoses with nonaspirin NSAIDs, phenylbutazone and mefenamic acid are more serious, potentially causing multiorgan dysfunction and seizures, respectively.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 169). Lippincot (Wolters Kluwer Health). Kindle Edition.
16. Answer C. Benzodiazepines are recommended for sedation of patients in anticholinergic crises due to their antiepileptic activity and absence of anticholinergic activity. Neuroleptic agents may exacerbate seizures and anticholinergic symptoms. Etomidate is too short acting for sedation due to agitation and may cause rapid respiratory insufficiency. Ketamine increases blood pressure and will exacerbate delirium, especially with its potential for the emergence phenomenon.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 189). Lippincot (Wolters Kluwer Health). Kindle Edition.
25. Answer E. Digitalis inhibits the membrane Na-K ATPase which normally functions to pump sodium out of the cell and potassium into it. Digitalis, therefore, increases intracellular sodium and decreases intracellular potassium. The increased intracellular sodium causes an increase in intracellular calcium, which produces a positive inotropic effect. In therapeutic doses, digitalis reduces the heart rate and can cause slight ST depression and T-wave inversions.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 191). Lippincot (Wolters Kluwer Health). Kindle Edition.
26. Answer B. Haloperidol is a high-potency antipsychotic agent whose primary therapeutic action is to block dopamine-2 receptors in the basal ganglia to cause rapid sedation and control of psychotic behavior. Haloperidol is commonly given with benzodiazepines for this use. Although haloperidol is often mistakenly considered to be part of the phenothiazine class of drugs (which lower the seizure threshold), it is actually part of the butyrophenone category, which does not affect the seizure threshold. Antipsychotics are α-1 antagonists (causing orthostatic hypotension) and antihistaminergic (causing sedation). Agranulocytosis is a side effect peculiar to clozapine, a newer generation antipsychotic.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 191). Lippincot (Wolters Kluwer Health). Kindle Edition.
30. Answer C. NAC promotes the metabolism of acetaminophen into a nontoxic compound by sulfation, through replenishment of glutathione. Prevention of hepatic injury is complete when the first dose of NAC is given within 8 hours of acute ingestion. Beneficial effects still occur as far out as 48 hours after ingestion, but efficacy in preventing hepatic injury decreases progressively starting at the 8-hour mark.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 192). Lippincot (Wolters Kluwer Health). Kindle Edition.
38. Answer B. PCP causes extreme dissociation, agitation, psychosis, and violent behavior. Superhuman strength often occurs in patients with PCP intoxication, sometimes requiring a dozen people to adequately restrain them. Vertical or rotary nystagmus is a physical examination finding characteristic of PCP intoxication. Cocaine intoxication may cause agitation, psychosis, and mydriasis but not nystagmus. LSD is a typical hallucinogen, and MDMA or ecstasy is similar to a combination of a hallucinogen and an amphetamine. Heroin causes a typical opioid toxidrome, with constricted pupils, sedation, and respiratory depression.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 193). Lippincot (Wolters Kluwer Health). Kindle Edition.
48. Answer E. Only dialysis can definitively remove ethylene glycol from the body. Ethanol and fomepizole are temporizing measures to inhibit alcohol dehydrogenase from catalyzing the conversion of toxic alcohols into their toxic metabolites. Pyridoxine and thiamine are cofactors in the conversion of glyoxylic acid, a toxic metabolite of ethylene glycol, to nontoxic compounds. They are useful as adjunctive therapies for ethylene glycol poisoning but do not constitute definitive therapy.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 194). Lippincot (Wolters Kluwer Health). Kindle Edition.
60. Answer B. Botulism is a neurologic syndrome caused by Clostridium botulinum, an anaerobic, gram-positive bacillus that produces botulinum toxin. Botulinum toxin is the strongest known biologic toxin, but is heat-labile, and can be inactivated by adequate preparation. Infant botulism, usually spread by honey, is the most common form of botulism, followed by food-borne botulism. Botulinum toxin blocks presynaptic acetylcholine release, causing cranial nerve palsies, parasympathetic inhibition, and descending paralysis. The diagnosis is generally made clinically, with specific toxin assays to aid in confirmation. Management involves aggressive airway evaluation and protection (due to pharyngeal muscle weakness), monitoring of vital capacity and respiratory strength, and equine antitoxin. There is little data regarding the efficacy of antibiotic therapy, and currently antibiotics are not indicated.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 196-197). Lippincot (Wolters Kluwer Health). Kindle Edition.
64. Answer B. Chelation therapy for acute lead toxicity is indicated in patients with worsening clinical course or severe CNS or GI symptoms. Several chelation therapies exist for lead. Dimercaprol (or British antilewisite) should be the first chelator given in patients with severe poisoning. It should be given before calcium disodium EDTA, as the latter, if given first, will cause chelated lead to cross the blood–brain barrier. Acute lead encephalopathy should be treated aggressively with chelation and management of attendant cerebral edema (hyperventilation and mannitol). Activated charcoal does not bind lead or other heavy metals. Patients deemed stable enough for outpatient chelation therapy should be given oral succimer. Penicillamine is a less effective alternative to succimer and should be given only if succimer is not tolerated due to GI side effects.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 197). Lippincot (Wolters Kluwer Health). Kindle Edition.
78. Answer E. Tricyclic antidepressants cause blockade of the following: α-1, muscarinic, histamine, GABA, cardiac potassium efflux, fast sodium channel, serotonin reuptake, and norepinephrine reuptake. Because of these effects and the potential for lethality in overdose, they are no longer indicated as first-line therapy for the management of major depression. 79. Answer C. The patient has nausea, vomiting, elevated anion gap, ketosis, and normal glucose in the setting of excessive alcohol use with starvation. Alcoholic ketoacidosis (AKA) is the most likely cause. Treatment of AKA is with fluid resuscitation, glucose, and thiamine. Bicarbonate is not indicated in most patients with high anion gap metabolic acidosis except in severe, life-threatening cases. Insulin is indicated in patients with DKA, who rarely present with a normal glucose level. Since alcoholic patients have adequate pancreatic endocrine function, glucose administration induces endogenous insulin release which quickly results in glucose utilization and closure of the anion gap (as the stimulus for ketogenesis is removed). Alcoholics are frequently thiamine-deficient because of poor nutrition, and thiamine is used during glucose metabolism, so supplementation should be given concurrently or before glucose administration. Potassium repletion may be indicated if hypokalemia is present or expected during the course of therapy. Magnesium supplementation is often indicated in chronic alcoholic patients, but glucose therapy is of more importance as an energy substrate in patients with alcohol ketoacidosis.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 199-200). Lippincot (Wolters Kluwer Health). Kindle Edition.
82. Answer A. Management of hydrocarbon toxicity is generally supportive. Hydrocarbons most commonly cause pulmonary toxicity and cardiac dysrhythmias. The most common scenarios are inhalation through “huffing” paint or glue cans and oral ingestion of hydrocarbons, followed by nausea, vomiting, and pulmonary aspiration. There is no evidence that antibiotics, steroids, or diuretics improve outcomes in hydrocarbon aspiration. Activated charcoal does not bind hydrocarbons and should not be used.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 200). Lippincot (Wolters Kluwer Health). Kindle Edition.
84. Answer C. H. pylori is the most common cause of gastritis. In acute H. pylori gastritis, patients commonly present with epigastric pain, nausea, and vomiting. Gastritis is a histologic diagnosis. Furthermore, although endoscopy reveals an inflamed, edematous, and friable gastric mucosa, there may be a lack of neutrophilic infiltrates in which case many authors prefer the less specific term gastropathy. In H. pylori gastritis, there is an intense infiltrate, but several of the other agents listed cause generalized inflammation of the gastric mucosa without such an infiltrate. Alcohol, aspirin or other NSAIDs, and Crohn’s disease may all cause gastritis. Caffeine is not a cause of gastritis but may predispose patients to GERD by lowering the tone of the lower esophageal sphincter muscle.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 201). Lippincot (Wolters Kluwer Health). Kindle Edition.
95. Answer A. Between 30% and 80% of alcoholics have magnesium deficiency. Patients with hypomagnesemia are frequently asymptomatic or manifest only nonspecific symptoms. The most prominent symptoms in the ED are neuromuscular and cardiovascular, and magnesium deficiency tends to mimic calcium deficiency. The mechanism of hypomagnesemia in alcoholism is thought to be a combination of malnutrition, increased renal excretion, and GI losses from vomiting and diarrhea. Diuretic therapy is also a very prevalent cause of hypomagnesemia, although the subsequent volume loss increases magnesium reabsorption in the proximal tubule. Therefore, magnesium depletion in the setting of diuretic therapy tends to be modest. Hypomagnesemia is the most common electrolyte abnormality in ambulatory diabetic patients and is also common in DKA. In these patients, magnesium is lost through the urine due to glycosuria.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 203). Lippincot (Wolters Kluwer Health). Kindle Edition.
11. Answer D. The “awake seizure” is the hallmark of strychnine poisoning. Strychnine is a glycine antagonist and its use results in disinhibition of glycine-mediated inhibitory tone at the level of the spinal motor neurons. This causes significant unopposed motor neuron activity resulting in distinctive muscle spasms called opisthotonus (arched back with a rigid trunk) as well as a unique facial appearance called risus sardonicus (sardonic smile), which is a tetanic contraction of facial muscles resulting in a persistent grimace or smile. The muscle contractions wax and wane without intervention and may be followed by flaccid periods. Ultimately, a rigid chest wall results in respiratory failure, hypoxia, and death if aggressive supportive care is not initiated (ventilation). There are no antidotes. Benzodiazepines are the class of drugs most often recommended, while barbiturates may be necessary in refractory cases. Superwarfarins are the most common agents used in rodenticides and the most common toxic exposure due to rodent poison overdose. Thallium is a heavy metal that causes hair loss and a painful neuropathy. Arsenic causes severe gastrointestinal symptoms, and patients classically present with breath that smells like garlic. In severe poisonings, the initial symptoms lead to shock, acute respiratory distress syndrome, cardiac irritability, and death. Some rodent poisons contain vitamin D (ergocalciferol) which causes hypercalcemia, but such poisons are rarely significantly toxic in humans.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 221). Lippincot (Wolters Kluwer Health). Kindle Edition.
19. Answer D. Physostigmine is an acetylcholinesterase inhibitor that serves to antagonize the affect of anticholinergic agents. It affects both nicotinic and muscarinic receptors and crosses the blood–brain barrier. Potential toxicity may occur during rapid administration, severely limiting its clinical use. It is absolutely contraindicated in patients with tricyclic overdose due to its potential for causing seizures and asystole. Supportive care is more beneficial than physostigmine therapy in most anticholinergic crises.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 222). Lippincot (Wolters Kluwer Health). Kindle Edition.
22. Answer E. There are several “classic” contraindications in the setting of digoxin toxicity. The most commonly cited is to avoid using calcium to treat hyperkalemia that frequently accompanies digoxin toxicity (since digoxin inhibits the Na+/K+ ATPase). Interestingly, while hyperkalemia is a reliable marker of digoxin toxicity, hyperkalemia is not the cause of death in severely poisoned patients (death is caused by fatal arrhythmias induced by digoxin’s direct effects on cardiac automaticity and excessive vagal tone) and treatment of hyperkalemia has not been shown to decrease the risk of death. While there is almost no evidence to support the idea that “stone heart” (tetany of the myocardium) will result from calcium administration in the setting of hyperkalemia-associated digoxin toxicity, elevated levels of intracellular calcium are already present, and hyperkalemia is not the chief problem (but rather reflects the degree of toxicity). Therefore, intravenous calcium should not be used to treat hyperkalemia in digoxin toxicity. In addition, patients with digoxin toxicity have an exceptionally excitable myocardium, so transvenous and transthoracic pacing as well as electrical cardioversion are all classically contraindicated. Atropine can be used as a temporizing measure in patients with severe bradycardia, but Fab fragments should be given as soon as possible after the diagnosis of a digoxin-associated arrhythmia is made. While there remains scant evidence, there is a theoretical increased risk of developing more malignant arrhythmias in response to pacing and cardioversion (e.g., ventricular fibrillation and pulseless ventricular tachycardia).
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 223). Lippincot (Wolters Kluwer Health). Kindle Edition.
33. Answer B. The use of digoxin-specific Fab fragments to treat digoxin toxicity has dramatically decreased morbidity and mortality from digoxin toxicity. Fab fragments should be given to any patient presenting with hemodynamic instability, malignant or symptomatic rhythm disturbances (any ventricular arrhythmia, high-grade AV block [Mobitz type I second-degree block or third-degree heart block, as Mobitz type II almost never occurs in the setting of digoxin toxicity], symptomatic bradycardia), a potassium level >5 mEq per L (an elevated potassium level is a marker of toxicity rather than a cause of toxicity), or a digoxin level >10 ng per mL in the acute setting or >4 ng per mL in the chronic setting. The drug level can be used to determine the number of vials needed: [Digoxin ng per mL] × patient weight (kg)/100 = number of vials needed However, patients who arrive in the ED with a clear indication for Fab administration should be given Fab empirically: 10 vials in acute toxicity. 5 vials in chronic toxicity. 34. Answer C. Magnesium depresses the
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 225). Lippincot (Wolters Kluwer Health). Kindle Edition.
42. Answer B. Folate is a cofactor for the conversion of methanol’s toxic metabolite, formic acid, to carbon dioxide and water. Once formic acid is produced, significant toxicity is probably inevitable, but the addition of folate to the standard treatment of methanol overdose (bicarbonate, alcohol dehydrogenase inhibitors, and dialysis) may attenuate further injury.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 226). Lippincot (Wolters Kluwer Health). Kindle Edition.
44. Answer A. While hyperkalemia is very common in the setting of digoxin overdose, it is not a cause of digoxin toxicity but rather a manifestation of toxicity. Furthermore, the specific treatment of hyperkalemia in this setting has not been shown to reduce mortality. However, since hyperkalemia is a sign of significant toxicity in the setting of digoxin overdose, its presence is a well-defined indication for digoxin Fab administration (Digibind). Digoxin-specific Fab administration should be given to all patients with a potassium level >5.0 mEq per L. Hyperkalemia will resolve with Fab administration itself. Additional therapy with “conventional” therapies for hyperkalemia is not necessary, and may precipitate hypokalemia once Fab is given. In addition, calcium administration is a “classic” contraindication in the setting of digoxin toxicity because of the risk of “stone heart” or sudden cardiac arrest.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 227). Lippincot (Wolters Kluwer Health). Kindle Edition.
55. Answer C. Sulfonylureas fall into the “one pill can kill” category of toxic ingestions among pediatric patients. Glyburide is a commonly used second-generation sulfonylurea with a long half-life (10 hours) as well as active metabolites. Insulin release is increased within 1 hour after ingestion, and hypoglycemia rapidly follows. As with several other sulfonylureas, the peak effect does not occur for 2 to 6 hours, and because of the drug’s prolonged half-life, persistent or delayed effects both occur. Many pediatric patients are asymptomatic with euglycemia at presentation. However, most experts recommend admission to the hospital for prolonged observation, even among such patients. Patients with symptoms at presentation, such as the patient in this question, should be admitted. In contrast to adults, children should receive more dilute preparations of dextrose to manage hypoglycemia. D25W can be given to young children while D10W is typically reserved for neonates and infants, though it can also be given to older children. D50W should be reserved for older adolescents and adults. Pediatric patients should receive 0.5 to 1.0 g per kg of dextrose, which typically corresponds to 5 to 10 mL per kg of D10W or 2 to 4 mL per kg of D25W (while adolescents would receive 1 to 2 mL per kg of D50W). While some experts recommend octreotide therapy to all symptomatic patients receiving dextrose, others recommend octreotide only in settings of refractory hypoglycemia. Octreotide works by decreasing calcium influx in pancreatic beta islet cells, which results in decreased calcium-mediated insulin release.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 228-229). Lippincot (Wolters Kluwer Health). Kindle Edition.
66. Answer E. Glipizide is a sulfonylurea with a fairly long half-life (7 hours) and prolonged duration of action (12 to 24 hours). Like other sulfonylureas, the duration of action is increased further when taken in overdose. As a result, patients frequently experience prolonged and severe hypoglycemia after sulfonylurea overdose. While dextrose therapy is a critical part of treatment, its use often results in transient hyperglycemia which further increases insulin secretion causing rebound hypoglycemia. This is particularly true when it is used as a bolus injection. Octreotide works by decreasing calcium influx in pancreatic beta islet cells, which results in decreased calcium-mediated insulin release. Octreotide is continued for 24 hours, after which the patient is observed for a prolonged period for recurrent episodes of hypoglycemia. While glucagon and corticosteroids may increase blood glucose, their use does not affect insulin secretion, in contrast to octreotide. Epinephrine has no role in management.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 230-231). Lippincot (Wolters Kluwer Health). Kindle Edition.
77. Answer B. The officer’s sudden collapse in the setting of a gaseous “rotten egg” smell strongly suggests the presence of hydrogen sulfide. The use of hydrogen sulfide as a relatively easy, painless means to commit suicide has gained popularity in recent years. At low concentrations, hydrogen sulfide may cause only minor irritation, cough, and a sensation of dyspnea. At higher levels, hydrogen sulfide inhibits mitochondrial cytochrome oxidase, which uncouples electron transport and terminates cellular respiration. This has profound, rapid effects on the nervous system and quickly leads to coma. Patients who remain awake will often improve after being moved to an area with uncontaminated air and with supplemental oxygen. More severely affected patients require aggressive supportive care (ventilation) and specific treatment with sodium nitrite, which induces methemoglobinemia. As in patients with cyanide intoxication, induction of methemoglobinemia is helpful by providing an alternative binding site for hydrogen sulfide. The combination of hydroxycobalamin (direct cyanide binding) and sodium thiosulfate (enhanced cyanide detoxification) is the treatment of choice for cyanide poisoning. They are not effective in treating hydrogen sulfide poisoning. Methylene blue is used to treat methemoglobinemia. Succimer (meso-2,3-dimercaptosuccinic acid) is an adjunctive treatment for lead poisoning.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 233). Lippincot (Wolters Kluwer Health). Kindle Edition.
86. Answer A. The metabolism of ethylene glycol is ethylene glycol → glycoaldehyde → glycolic acid → → → oxalic acid. Oxalic acid forms calcium oxalate crystals which can deposit in the renal tubules and cause renal insufficiency, and the other metabolites of ethylene glycol are directly nephrotoxic as well. Approximately one-fourth of ethylene glycol is directly excreted in the kidneys, but hepatic metabolism with alcohol dehydrogenase catalyzes the formation of the toxic metabolites. The goals of therapy in patients with ethylene glycol toxicity are to block the availability of alcohol dehydrogenase with either fomepizole or ethanol and to hemodialyze the unmetabolized ethylene glycol. Methanol toxicity results in the formation of formic acid, which accumulates in the brain and causes blindness and death. Isopropanol causes generalized CNS depression similar to ethanol intoxication. Salicylate overdose results in direct nephrotoxicity, metabolic acidosis, electrolyte abnormalities, and pulmonary and cerebral edema. Acetaminophen overdose causes fulminant hepatic failure.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 234). Lippincot (Wolters Kluwer Health). Kindle Edition.
88. Answer A. The patients described in this vignette are suffering from a cholinergic syndrome. The nerve agents sarin, VX, tabun, and soman are all organophosphorus compounds that strongly inhibit acetylcholinesterase resulting in symptoms of acetylcholine excess. The classic mnemonic used to recall the symptoms of a cholinergic toxidrome is SLUDGE: salivation, lacrimation, urination, defecation, gastrointestinal upset, and emesis. The “SLUDGE” mnemonic does not address the pulmonary muscarinic effects (bronchorrhea, bronchospasm), cardiac muscarinic effects (bradycardia), nor the nicotinic effects in the central nervous system (muscle weakness, fasciculations, and flaccid paralysis). For this reason, the “SLUDGE” mnemonic is sometimes appended as “SLUDGE/BBB” for bronchospasm, bronchorrhea, and bradycardia. There are several alternative mnemonics as well (e.g., DUMBELS). Since these drugs work through excessive acetylcholine action, atropine is the natural antidote and should be given immediately to any patient with evidence of moderate or more severe toxicity. The dose is titrated until the pulmonary symptoms are resolved (no shortness of breath, no wheezing, no excessive secretions). If initial doses of atropine are ineffective, the dose should be doubled every 3 to 5 minutes and repeated. 2-PAM is used to address the nicotinic effects of these agents, since atropine does not bind to nicotinic receptors. Like atropine, 2-PAM should be used liberally and should be given to any patient with evidence of toxicity. Even in the absence of significant acute toxicity, many nerve agents cause delayed neurologic effects which may be prevented by 2-PAM administration. In addition, 2-PAM should be given early because the nerve agents become irreversibly bound to acetylcholinesterase over time (called “aging”). Both atropine and 2-PAM can be given IV or IM. Since succinylcholine is metabolized by acetylcholinesterase, it should never be used for airway management in patients with organophosphate toxicity, as its use results in prolonged and excessive paralysis. Diazepam is used to treat the seizures that may occur. Sodium thiosulfate is used for cyanide intoxication while amyl and sodium nitrite are used for either cyanide or hydrogen sulfide exposure.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 234-235). Lippincot (Wolters Kluwer Health). Kindle Edition.
90. Answer D. Acetaminophen is metabolized by a variety of pathways, the most important of which is through the cytochrome P-450 system, which produces N-acetyl-p-benzoquinoneimine which is the toxic metabolite causing hepatocyte necrosis. The drug N-acetylcysteine reduces the amount of acetaminophen metabolized by this route by replenishing glutathione, the reducing agent which induces sulfation of acetaminophen to a nontoxic compound. Severity of acetaminophen overdose is measured by a 4-hour acetaminophen concentration as well as markers of liver damage, the most important of which is AST. Amylase and lipase are important indicators of pancreatic damage. Although GGT and alkaline phosphatase are present in the biliary ductal epithelium, they are less specific for hepatocellular damage than AST or ALT.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 235). Lippincot (Wolters Kluwer Health). Kindle Edition.
99. Answer C. Cyanide intoxication is treated with a three-pronged approach. The preferred approach is direct cyanide binding using hydroxycobalamin (vitamin B12), while cyanide detoxification is achieved using sodium thiosulfate (which serves as a sulfur donor to rhodanese which converts cyanide to nontoxic thiocyanate). Amyl or sodium nitrite can also be used to induce methemoglobinemia since methemoglobin binds cyanide more strongly than mitochondrial cytochrome oxidase. However, methemoglobin also more tightly binds oxygen (shifts the dissociation curve to the left), resulting in decreased tissue oxygen delivery which may have important negative effects in critically ill patients. Phosgene is a common industrial chemical that smells like freshly mown hay when aerosolized. It is a direct pulmonary irritant, like chlorine or ammonia, and causes pulmonary edema. Treatment is supportive. Sulfur mustard is a vesicant which causes redness, pain, itching, and blistering of the skin, as well as gastrointestinal, pulmonary, and ocular damage. Vesicants are slow to act and are rarely fatal, but there is no specific antidote. VX is a “nerve agent” which inhibits acetylcholinesterase resulting in a cholinergic toxidrome. PM is used along with atropine to treat victims. PM should never be used as monotherapy because of transient PM-mediated acetylcholinesterase inhibition. Hydrogen sulfide is a toxic gas that smells like rotten eggs and that decouples mitochondrial respiration like cyanide. Unlike cyanide, however, only induced methemoglobinemia is effective as an antidote, so sodium nitrite is the treatment of choice.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 236-237). Lippincot (Wolters Kluwer Health). Kindle Edition.
1. Answer A. Flumazenil is a benzodiazepine antagonist that is used only in selected cases to reverse benzodiazepine overdose. The only real indications for flumazenil are to speed recovery in accidental pediatric ingestions and during procedural sedation. Flumazenil can precipitate seizures in patients who are chronic benzodiazepine users, alcoholics, and those who have coingested medicines which lower the seizure threshold. The morbidity and mortality of benzodiazepine overdose is mostly from respiratory depression. Therefore, standard airway management, oxygenation, and ventilation preclude the use of flumazenil in almost all cases.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 156). Lippincot (Wolters Kluwer Health). Kindle Edition.
6. Answer C. Fluoxetine is a type of selective serotonin reuptake inhibitor (SSRI). As a class, SSRIs are generally benign in overdose, causing mild GI and CNS symptoms and rarely leading to dysrhythmias. Cyproheptadine is a serotonin antagonist that has unproven clinical efficacy in most SSRI overdoses. Its use is mainly limited to patients with serotonin syndrome, a constellation of neurologic, GI, and cardiac findings. Dysrhythmia is rare and should be treated according to current ACLS guidelines. Unlike with tricyclic antidepressant overdose, there is no indication for routine use of sodium bicarbonate to treat dysrhythmias. As in virtually all overdoses, ipecac is not recommended as a method of gastric decontamination. Hemodialysis is not indicated in patients with SSRI overdose, as the drug is highly bound to plasma proteins.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 157). Lippincot (Wolters Kluwer Health). Kindle Edition.
32. Answer B. The serotonin syndrome is classically described as a triad of cognitive abnormalities, autonomic hyperactivity, and neuromuscular problems. However, there is considerable variability in the severity of the presentation and considerable overlap of the clinical findings with neuroleptic malignant syndrome as well as the anticholinergic toxidrome. Clonus is the most important clinical finding to help differentiate the serotonin syndrome from similar clinical conditions. Clonus may be spontaneous, inducible, or isolated to the ocular muscles. Thus, physicians must perform a thorough, focused examination to specifically look for this finding.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 161). Lippincot (Wolters Kluwer Health). Kindle Edition.
51. Answer C. Isopropanol classically does not cause elevated anion gap when ingested. The osmolar gap, however, is elevated and should be calculated and measured when there is suspicion of toxic alcohol overdose. Elevation of the anion gap due to lactic acidosis can occur in cases of severe isopropanol poisoning if there is associated coma, gastrointestinal hemorrhage, or hypotension. Choices A, B, D, and E all cause an elevation in the anion gap at some point during their metabolism.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 164-165). Lippincot (Wolters Kluwer Health). Kindle Edition.
73. Answer E. Nonaspirin NSAIDs, including ibuprofen, produce generally benign and self-limited conditions in overdose. Symptoms will occur within 4 hours of ingestion, are usually mild, and resolve within 24 hours. Patients rarely have life-threatening overdoses and almost never require antidotes, decontamination, augmented renal excretion, or invasive therapies such as hemodialysis. Serum levels of nonaspirin NSAIDs are not clinically useful. Of overdoses with nonaspirin NSAIDs, phenylbutazone and mefenamic acid are more serious, potentially causing multiorgan dysfunction and seizures, respectively.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 169). Lippincot (Wolters Kluwer Health). Kindle Edition.
16. Answer C. Benzodiazepines are recommended for sedation of patients in anticholinergic crises due to their antiepileptic activity and absence of anticholinergic activity. Neuroleptic agents may exacerbate seizures and anticholinergic symptoms. Etomidate is too short acting for sedation due to agitation and may cause rapid respiratory insufficiency. Ketamine increases blood pressure and will exacerbate delirium, especially with its potential for the emergence phenomenon.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 189). Lippincot (Wolters Kluwer Health). Kindle Edition.
25. Answer E. Digitalis inhibits the membrane Na-K ATPase which normally functions to pump sodium out of the cell and potassium into it. Digitalis, therefore, increases intracellular sodium and decreases intracellular potassium. The increased intracellular sodium causes an increase in intracellular calcium, which produces a positive inotropic effect. In therapeutic doses, digitalis reduces the heart rate and can cause slight ST depression and T-wave inversions.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 191). Lippincot (Wolters Kluwer Health). Kindle Edition.
26. Answer B. Haloperidol is a high-potency antipsychotic agent whose primary therapeutic action is to block dopamine-2 receptors in the basal ganglia to cause rapid sedation and control of psychotic behavior. Haloperidol is commonly given with benzodiazepines for this use. Although haloperidol is often mistakenly considered to be part of the phenothiazine class of drugs (which lower the seizure threshold), it is actually part of the butyrophenone category, which does not affect the seizure threshold. Antipsychotics are α-1 antagonists (causing orthostatic hypotension) and antihistaminergic (causing sedation). Agranulocytosis is a side effect peculiar to clozapine, a newer generation antipsychotic.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 191). Lippincot (Wolters Kluwer Health). Kindle Edition.
30. Answer C. NAC promotes the metabolism of acetaminophen into a nontoxic compound by sulfation, through replenishment of glutathione. Prevention of hepatic injury is complete when the first dose of NAC is given within 8 hours of acute ingestion. Beneficial effects still occur as far out as 48 hours after ingestion, but efficacy in preventing hepatic injury decreases progressively starting at the 8-hour mark.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 192). Lippincot (Wolters Kluwer Health). Kindle Edition.
38. Answer B. PCP causes extreme dissociation, agitation, psychosis, and violent behavior. Superhuman strength often occurs in patients with PCP intoxication, sometimes requiring a dozen people to adequately restrain them. Vertical or rotary nystagmus is a physical examination finding characteristic of PCP intoxication. Cocaine intoxication may cause agitation, psychosis, and mydriasis but not nystagmus. LSD is a typical hallucinogen, and MDMA or ecstasy is similar to a combination of a hallucinogen and an amphetamine. Heroin causes a typical opioid toxidrome, with constricted pupils, sedation, and respiratory depression.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 193). Lippincot (Wolters Kluwer Health). Kindle Edition.
48. Answer E. Only dialysis can definitively remove ethylene glycol from the body. Ethanol and fomepizole are temporizing measures to inhibit alcohol dehydrogenase from catalyzing the conversion of toxic alcohols into their toxic metabolites. Pyridoxine and thiamine are cofactors in the conversion of glyoxylic acid, a toxic metabolite of ethylene glycol, to nontoxic compounds. They are useful as adjunctive therapies for ethylene glycol poisoning but do not constitute definitive therapy.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 194). Lippincot (Wolters Kluwer Health). Kindle Edition.
60. Answer B. Botulism is a neurologic syndrome caused by Clostridium botulinum, an anaerobic, gram-positive bacillus that produces botulinum toxin. Botulinum toxin is the strongest known biologic toxin, but is heat-labile, and can be inactivated by adequate preparation. Infant botulism, usually spread by honey, is the most common form of botulism, followed by food-borne botulism. Botulinum toxin blocks presynaptic acetylcholine release, causing cranial nerve palsies, parasympathetic inhibition, and descending paralysis. The diagnosis is generally made clinically, with specific toxin assays to aid in confirmation. Management involves aggressive airway evaluation and protection (due to pharyngeal muscle weakness), monitoring of vital capacity and respiratory strength, and equine antitoxin. There is little data regarding the efficacy of antibiotic therapy, and currently antibiotics are not indicated.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 196-197). Lippincot (Wolters Kluwer Health). Kindle Edition.
64. Answer B. Chelation therapy for acute lead toxicity is indicated in patients with worsening clinical course or severe CNS or GI symptoms. Several chelation therapies exist for lead. Dimercaprol (or British antilewisite) should be the first chelator given in patients with severe poisoning. It should be given before calcium disodium EDTA, as the latter, if given first, will cause chelated lead to cross the blood–brain barrier. Acute lead encephalopathy should be treated aggressively with chelation and management of attendant cerebral edema (hyperventilation and mannitol). Activated charcoal does not bind lead or other heavy metals. Patients deemed stable enough for outpatient chelation therapy should be given oral succimer. Penicillamine is a less effective alternative to succimer and should be given only if succimer is not tolerated due to GI side effects.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 197). Lippincot (Wolters Kluwer Health). Kindle Edition.
78. Answer E. Tricyclic antidepressants cause blockade of the following: α-1, muscarinic, histamine, GABA, cardiac potassium efflux, fast sodium channel, serotonin reuptake, and norepinephrine reuptake. Because of these effects and the potential for lethality in overdose, they are no longer indicated as first-line therapy for the management of major depression. 79. Answer C. The patient has nausea, vomiting, elevated anion gap, ketosis, and normal glucose in the setting of excessive alcohol use with starvation. Alcoholic ketoacidosis (AKA) is the most likely cause. Treatment of AKA is with fluid resuscitation, glucose, and thiamine. Bicarbonate is not indicated in most patients with high anion gap metabolic acidosis except in severe, life-threatening cases. Insulin is indicated in patients with DKA, who rarely present with a normal glucose level. Since alcoholic patients have adequate pancreatic endocrine function, glucose administration induces endogenous insulin release which quickly results in glucose utilization and closure of the anion gap (as the stimulus for ketogenesis is removed). Alcoholics are frequently thiamine-deficient because of poor nutrition, and thiamine is used during glucose metabolism, so supplementation should be given concurrently or before glucose administration. Potassium repletion may be indicated if hypokalemia is present or expected during the course of therapy. Magnesium supplementation is often indicated in chronic alcoholic patients, but glucose therapy is of more importance as an energy substrate in patients with alcohol ketoacidosis.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 199-200). Lippincot (Wolters Kluwer Health). Kindle Edition.
82. Answer A. Management of hydrocarbon toxicity is generally supportive. Hydrocarbons most commonly cause pulmonary toxicity and cardiac dysrhythmias. The most common scenarios are inhalation through “huffing” paint or glue cans and oral ingestion of hydrocarbons, followed by nausea, vomiting, and pulmonary aspiration. There is no evidence that antibiotics, steroids, or diuretics improve outcomes in hydrocarbon aspiration. Activated charcoal does not bind hydrocarbons and should not be used.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 200). Lippincot (Wolters Kluwer Health). Kindle Edition.
84. Answer C. H. pylori is the most common cause of gastritis. In acute H. pylori gastritis, patients commonly present with epigastric pain, nausea, and vomiting. Gastritis is a histologic diagnosis. Furthermore, although endoscopy reveals an inflamed, edematous, and friable gastric mucosa, there may be a lack of neutrophilic infiltrates in which case many authors prefer the less specific term gastropathy. In H. pylori gastritis, there is an intense infiltrate, but several of the other agents listed cause generalized inflammation of the gastric mucosa without such an infiltrate. Alcohol, aspirin or other NSAIDs, and Crohn’s disease may all cause gastritis. Caffeine is not a cause of gastritis but may predispose patients to GERD by lowering the tone of the lower esophageal sphincter muscle.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 201). Lippincot (Wolters Kluwer Health). Kindle Edition.
95. Answer A. Between 30% and 80% of alcoholics have magnesium deficiency. Patients with hypomagnesemia are frequently asymptomatic or manifest only nonspecific symptoms. The most prominent symptoms in the ED are neuromuscular and cardiovascular, and magnesium deficiency tends to mimic calcium deficiency. The mechanism of hypomagnesemia in alcoholism is thought to be a combination of malnutrition, increased renal excretion, and GI losses from vomiting and diarrhea. Diuretic therapy is also a very prevalent cause of hypomagnesemia, although the subsequent volume loss increases magnesium reabsorption in the proximal tubule. Therefore, magnesium depletion in the setting of diuretic therapy tends to be modest. Hypomagnesemia is the most common electrolyte abnormality in ambulatory diabetic patients and is also common in DKA. In these patients, magnesium is lost through the urine due to glycosuria.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 203). Lippincot (Wolters Kluwer Health). Kindle Edition.
11. Answer D. The “awake seizure” is the hallmark of strychnine poisoning. Strychnine is a glycine antagonist and its use results in disinhibition of glycine-mediated inhibitory tone at the level of the spinal motor neurons. This causes significant unopposed motor neuron activity resulting in distinctive muscle spasms called opisthotonus (arched back with a rigid trunk) as well as a unique facial appearance called risus sardonicus (sardonic smile), which is a tetanic contraction of facial muscles resulting in a persistent grimace or smile. The muscle contractions wax and wane without intervention and may be followed by flaccid periods. Ultimately, a rigid chest wall results in respiratory failure, hypoxia, and death if aggressive supportive care is not initiated (ventilation). There are no antidotes. Benzodiazepines are the class of drugs most often recommended, while barbiturates may be necessary in refractory cases. Superwarfarins are the most common agents used in rodenticides and the most common toxic exposure due to rodent poison overdose. Thallium is a heavy metal that causes hair loss and a painful neuropathy. Arsenic causes severe gastrointestinal symptoms, and patients classically present with breath that smells like garlic. In severe poisonings, the initial symptoms lead to shock, acute respiratory distress syndrome, cardiac irritability, and death. Some rodent poisons contain vitamin D (ergocalciferol) which causes hypercalcemia, but such poisons are rarely significantly toxic in humans.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 221). Lippincot (Wolters Kluwer Health). Kindle Edition.
19. Answer D. Physostigmine is an acetylcholinesterase inhibitor that serves to antagonize the affect of anticholinergic agents. It affects both nicotinic and muscarinic receptors and crosses the blood–brain barrier. Potential toxicity may occur during rapid administration, severely limiting its clinical use. It is absolutely contraindicated in patients with tricyclic overdose due to its potential for causing seizures and asystole. Supportive care is more beneficial than physostigmine therapy in most anticholinergic crises.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 222). Lippincot (Wolters Kluwer Health). Kindle Edition.
22. Answer E. There are several “classic” contraindications in the setting of digoxin toxicity. The most commonly cited is to avoid using calcium to treat hyperkalemia that frequently accompanies digoxin toxicity (since digoxin inhibits the Na+/K+ ATPase). Interestingly, while hyperkalemia is a reliable marker of digoxin toxicity, hyperkalemia is not the cause of death in severely poisoned patients (death is caused by fatal arrhythmias induced by digoxin’s direct effects on cardiac automaticity and excessive vagal tone) and treatment of hyperkalemia has not been shown to decrease the risk of death. While there is almost no evidence to support the idea that “stone heart” (tetany of the myocardium) will result from calcium administration in the setting of hyperkalemia-associated digoxin toxicity, elevated levels of intracellular calcium are already present, and hyperkalemia is not the chief problem (but rather reflects the degree of toxicity). Therefore, intravenous calcium should not be used to treat hyperkalemia in digoxin toxicity. In addition, patients with digoxin toxicity have an exceptionally excitable myocardium, so transvenous and transthoracic pacing as well as electrical cardioversion are all classically contraindicated. Atropine can be used as a temporizing measure in patients with severe bradycardia, but Fab fragments should be given as soon as possible after the diagnosis of a digoxin-associated arrhythmia is made. While there remains scant evidence, there is a theoretical increased risk of developing more malignant arrhythmias in response to pacing and cardioversion (e.g., ventricular fibrillation and pulseless ventricular tachycardia).
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 223). Lippincot (Wolters Kluwer Health). Kindle Edition.
33. Answer B. The use of digoxin-specific Fab fragments to treat digoxin toxicity has dramatically decreased morbidity and mortality from digoxin toxicity. Fab fragments should be given to any patient presenting with hemodynamic instability, malignant or symptomatic rhythm disturbances (any ventricular arrhythmia, high-grade AV block [Mobitz type I second-degree block or third-degree heart block, as Mobitz type II almost never occurs in the setting of digoxin toxicity], symptomatic bradycardia), a potassium level >5 mEq per L (an elevated potassium level is a marker of toxicity rather than a cause of toxicity), or a digoxin level >10 ng per mL in the acute setting or >4 ng per mL in the chronic setting. The drug level can be used to determine the number of vials needed: [Digoxin ng per mL] × patient weight (kg)/100 = number of vials needed However, patients who arrive in the ED with a clear indication for Fab administration should be given Fab empirically: 10 vials in acute toxicity. 5 vials in chronic toxicity. 34. Answer C. Magnesium depresses the
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 225). Lippincot (Wolters Kluwer Health). Kindle Edition.
42. Answer B. Folate is a cofactor for the conversion of methanol’s toxic metabolite, formic acid, to carbon dioxide and water. Once formic acid is produced, significant toxicity is probably inevitable, but the addition of folate to the standard treatment of methanol overdose (bicarbonate, alcohol dehydrogenase inhibitors, and dialysis) may attenuate further injury.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 226). Lippincot (Wolters Kluwer Health). Kindle Edition.
44. Answer A. While hyperkalemia is very common in the setting of digoxin overdose, it is not a cause of digoxin toxicity but rather a manifestation of toxicity. Furthermore, the specific treatment of hyperkalemia in this setting has not been shown to reduce mortality. However, since hyperkalemia is a sign of significant toxicity in the setting of digoxin overdose, its presence is a well-defined indication for digoxin Fab administration (Digibind). Digoxin-specific Fab administration should be given to all patients with a potassium level >5.0 mEq per L. Hyperkalemia will resolve with Fab administration itself. Additional therapy with “conventional” therapies for hyperkalemia is not necessary, and may precipitate hypokalemia once Fab is given. In addition, calcium administration is a “classic” contraindication in the setting of digoxin toxicity because of the risk of “stone heart” or sudden cardiac arrest.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 227). Lippincot (Wolters Kluwer Health). Kindle Edition.
55. Answer C. Sulfonylureas fall into the “one pill can kill” category of toxic ingestions among pediatric patients. Glyburide is a commonly used second-generation sulfonylurea with a long half-life (10 hours) as well as active metabolites. Insulin release is increased within 1 hour after ingestion, and hypoglycemia rapidly follows. As with several other sulfonylureas, the peak effect does not occur for 2 to 6 hours, and because of the drug’s prolonged half-life, persistent or delayed effects both occur. Many pediatric patients are asymptomatic with euglycemia at presentation. However, most experts recommend admission to the hospital for prolonged observation, even among such patients. Patients with symptoms at presentation, such as the patient in this question, should be admitted. In contrast to adults, children should receive more dilute preparations of dextrose to manage hypoglycemia. D25W can be given to young children while D10W is typically reserved for neonates and infants, though it can also be given to older children. D50W should be reserved for older adolescents and adults. Pediatric patients should receive 0.5 to 1.0 g per kg of dextrose, which typically corresponds to 5 to 10 mL per kg of D10W or 2 to 4 mL per kg of D25W (while adolescents would receive 1 to 2 mL per kg of D50W). While some experts recommend octreotide therapy to all symptomatic patients receiving dextrose, others recommend octreotide only in settings of refractory hypoglycemia. Octreotide works by decreasing calcium influx in pancreatic beta islet cells, which results in decreased calcium-mediated insulin release.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 228-229). Lippincot (Wolters Kluwer Health). Kindle Edition.
66. Answer E. Glipizide is a sulfonylurea with a fairly long half-life (7 hours) and prolonged duration of action (12 to 24 hours). Like other sulfonylureas, the duration of action is increased further when taken in overdose. As a result, patients frequently experience prolonged and severe hypoglycemia after sulfonylurea overdose. While dextrose therapy is a critical part of treatment, its use often results in transient hyperglycemia which further increases insulin secretion causing rebound hypoglycemia. This is particularly true when it is used as a bolus injection. Octreotide works by decreasing calcium influx in pancreatic beta islet cells, which results in decreased calcium-mediated insulin release. Octreotide is continued for 24 hours, after which the patient is observed for a prolonged period for recurrent episodes of hypoglycemia. While glucagon and corticosteroids may increase blood glucose, their use does not affect insulin secretion, in contrast to octreotide. Epinephrine has no role in management.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 230-231). Lippincot (Wolters Kluwer Health). Kindle Edition.
77. Answer B. The officer’s sudden collapse in the setting of a gaseous “rotten egg” smell strongly suggests the presence of hydrogen sulfide. The use of hydrogen sulfide as a relatively easy, painless means to commit suicide has gained popularity in recent years. At low concentrations, hydrogen sulfide may cause only minor irritation, cough, and a sensation of dyspnea. At higher levels, hydrogen sulfide inhibits mitochondrial cytochrome oxidase, which uncouples electron transport and terminates cellular respiration. This has profound, rapid effects on the nervous system and quickly leads to coma. Patients who remain awake will often improve after being moved to an area with uncontaminated air and with supplemental oxygen. More severely affected patients require aggressive supportive care (ventilation) and specific treatment with sodium nitrite, which induces methemoglobinemia. As in patients with cyanide intoxication, induction of methemoglobinemia is helpful by providing an alternative binding site for hydrogen sulfide. The combination of hydroxycobalamin (direct cyanide binding) and sodium thiosulfate (enhanced cyanide detoxification) is the treatment of choice for cyanide poisoning. They are not effective in treating hydrogen sulfide poisoning. Methylene blue is used to treat methemoglobinemia. Succimer (meso-2,3-dimercaptosuccinic acid) is an adjunctive treatment for lead poisoning.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 233). Lippincot (Wolters Kluwer Health). Kindle Edition.
86. Answer A. The metabolism of ethylene glycol is ethylene glycol → glycoaldehyde → glycolic acid → → → oxalic acid. Oxalic acid forms calcium oxalate crystals which can deposit in the renal tubules and cause renal insufficiency, and the other metabolites of ethylene glycol are directly nephrotoxic as well. Approximately one-fourth of ethylene glycol is directly excreted in the kidneys, but hepatic metabolism with alcohol dehydrogenase catalyzes the formation of the toxic metabolites. The goals of therapy in patients with ethylene glycol toxicity are to block the availability of alcohol dehydrogenase with either fomepizole or ethanol and to hemodialyze the unmetabolized ethylene glycol. Methanol toxicity results in the formation of formic acid, which accumulates in the brain and causes blindness and death. Isopropanol causes generalized CNS depression similar to ethanol intoxication. Salicylate overdose results in direct nephrotoxicity, metabolic acidosis, electrolyte abnormalities, and pulmonary and cerebral edema. Acetaminophen overdose causes fulminant hepatic failure.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 234). Lippincot (Wolters Kluwer Health). Kindle Edition.
88. Answer A. The patients described in this vignette are suffering from a cholinergic syndrome. The nerve agents sarin, VX, tabun, and soman are all organophosphorus compounds that strongly inhibit acetylcholinesterase resulting in symptoms of acetylcholine excess. The classic mnemonic used to recall the symptoms of a cholinergic toxidrome is SLUDGE: salivation, lacrimation, urination, defecation, gastrointestinal upset, and emesis. The “SLUDGE” mnemonic does not address the pulmonary muscarinic effects (bronchorrhea, bronchospasm), cardiac muscarinic effects (bradycardia), nor the nicotinic effects in the central nervous system (muscle weakness, fasciculations, and flaccid paralysis). For this reason, the “SLUDGE” mnemonic is sometimes appended as “SLUDGE/BBB” for bronchospasm, bronchorrhea, and bradycardia. There are several alternative mnemonics as well (e.g., DUMBELS). Since these drugs work through excessive acetylcholine action, atropine is the natural antidote and should be given immediately to any patient with evidence of moderate or more severe toxicity. The dose is titrated until the pulmonary symptoms are resolved (no shortness of breath, no wheezing, no excessive secretions). If initial doses of atropine are ineffective, the dose should be doubled every 3 to 5 minutes and repeated. 2-PAM is used to address the nicotinic effects of these agents, since atropine does not bind to nicotinic receptors. Like atropine, 2-PAM should be used liberally and should be given to any patient with evidence of toxicity. Even in the absence of significant acute toxicity, many nerve agents cause delayed neurologic effects which may be prevented by 2-PAM administration. In addition, 2-PAM should be given early because the nerve agents become irreversibly bound to acetylcholinesterase over time (called “aging”). Both atropine and 2-PAM can be given IV or IM. Since succinylcholine is metabolized by acetylcholinesterase, it should never be used for airway management in patients with organophosphate toxicity, as its use results in prolonged and excessive paralysis. Diazepam is used to treat the seizures that may occur. Sodium thiosulfate is used for cyanide intoxication while amyl and sodium nitrite are used for either cyanide or hydrogen sulfide exposure.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 234-235). Lippincot (Wolters Kluwer Health). Kindle Edition.
90. Answer D. Acetaminophen is metabolized by a variety of pathways, the most important of which is through the cytochrome P-450 system, which produces N-acetyl-p-benzoquinoneimine which is the toxic metabolite causing hepatocyte necrosis. The drug N-acetylcysteine reduces the amount of acetaminophen metabolized by this route by replenishing glutathione, the reducing agent which induces sulfation of acetaminophen to a nontoxic compound. Severity of acetaminophen overdose is measured by a 4-hour acetaminophen concentration as well as markers of liver damage, the most important of which is AST. Amylase and lipase are important indicators of pancreatic damage. Although GGT and alkaline phosphatase are present in the biliary ductal epithelium, they are less specific for hepatocellular damage than AST or ALT.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (p. 235). Lippincot (Wolters Kluwer Health). Kindle Edition.
99. Answer C. Cyanide intoxication is treated with a three-pronged approach. The preferred approach is direct cyanide binding using hydroxycobalamin (vitamin B12), while cyanide detoxification is achieved using sodium thiosulfate (which serves as a sulfur donor to rhodanese which converts cyanide to nontoxic thiocyanate). Amyl or sodium nitrite can also be used to induce methemoglobinemia since methemoglobin binds cyanide more strongly than mitochondrial cytochrome oxidase. However, methemoglobin also more tightly binds oxygen (shifts the dissociation curve to the left), resulting in decreased tissue oxygen delivery which may have important negative effects in critically ill patients. Phosgene is a common industrial chemical that smells like freshly mown hay when aerosolized. It is a direct pulmonary irritant, like chlorine or ammonia, and causes pulmonary edema. Treatment is supportive. Sulfur mustard is a vesicant which causes redness, pain, itching, and blistering of the skin, as well as gastrointestinal, pulmonary, and ocular damage. Vesicants are slow to act and are rarely fatal, but there is no specific antidote. VX is a “nerve agent” which inhibits acetylcholinesterase resulting in a cholinergic toxidrome. PM is used along with atropine to treat victims. PM should never be used as monotherapy because of transient PM-mediated acetylcholinesterase inhibition. Hydrogen sulfide is a toxic gas that smells like rotten eggs and that decouples mitochondrial respiration like cyanide. Unlike cyanide, however, only induced methemoglobinemia is effective as an antidote, so sodium nitrite is the treatment of choice.
Aldeen, Amer Z.; Rosenbaum, David H. (2012-07-12). 1200 Questions to Help You Pass the Emergency Medicine Boards (pp. 236-237). Lippincot (Wolters Kluwer Health). Kindle Edition.
