Foundations CBR20 – Toxicology Exam
Questions With Complete Solutions
How does activated charcoal work for decontamination and how should it be administered?
High surface area binding to toxin and preventing systemic absorption. Dose: 10:1 (10g AC per 1g
drug)
When is activated charcoal contraindicated or ineffective?
Contraindicated in AMS/obtunded patient, risk of seizure or aspiration, ileus. Ineffective for
pesticides, lithium, hydrocarbons, heavy metals, alcohols, caustics.
How does whole bowel irrigation work for decontamination and how should it be administered?
Iso-osmotic agent (e.g. Go-Lytely) taken in large volume will hasten progress through intestines and
prevent absorption; Dose: 1-2L/hr (adults) or 500mL/hr (kids), consider giving by NGT, and continue
until clear rectal effluent is produced. Think about using this for "drug packers" and also for ER beta-
blockers.
For what types of ingestion is whole bowel irrigation most effective?
Iron, lithium, sustained-release formulations, enteric-coated meds, body packers
What toxins are cleared by HD?
"I STUMBLE": Isopropyl alcohol, Salicylate (aspirin), Theophylline, Uric acid, Methanol,
Barbiturates/Beta-blockers, Lithium, Ethylene glycol
Review the general pathophysiology, Dx, and Tx of Acetaminophen (APAP) overdose
APAP normally broken down via sulfation & glucuronide conjugation. Small amount is broken down by
CYP450 enzymes → toxic NAPQI metabolite. APAP OD: overloads glutathione inactivation/metabolism
→ excess NAPQI accumulates → liver toxicity. Dx: can use acetaminophen nomogram for SINGLE,
ACUTE ingestions; get APAP level at ≥ 4 hours (< 4 hours NOT useful, unless ZERO). High risk of
toxicity: >150mg/kg (acute) or >4g/day (chronic). Rx: N-acetylcysteine (NAC) → restores glutathione,
acts as an antioxidant; best if given w/in 8 hours of ingestion; Dose PO (140mg/kg load, 70mg/kg
q4hr) or IV (150mg/kg load, 50mg/kg over 4hr, 100mg/kg over 16hr). Safe for pregnant woman and
children. Side effect: anaphylactoid reaction.
When can you use the Rumack-Matthew nomogram for acetaminophen toxicity?
For single acute ingestions, not for chronic ingestions. For chronic you treat based on acetaminophen
level or signs of acute toxicity
Review the general pathophysiology, Dx, and Tx of NSAID overdose
COX inhibitor decreases prostaglandin production. SSx: minimal toxicity but can cause GI upset (rarely
GI Bleed); large doses: AMS/ataxia, coma, metabolic acidosis, seizure. Rx: supportive.
Review the general pathophysiology, Dx, and Tx of Aspirin (ASA) overdose
Causes primary respiratory alkalosis (stimulates resp. center, EARLY, uncouples oxidative
phosphorylation (AG metabolic acidosis, hyperthermia). SSx: ↑ RR, ↑ temp, ↑ HR (sinus tach = MC
sign), tinnitus, vertigo, AMS, seizure. Rx: GI decon, urine alkalinization with bicarb (+K, +Mg) infusion
(enhances urinary excretion of salicylate, also prevents CNS distribution), HD (acute level >100,
chronic level >60, OR there is a presence of renal failure, severe acidemia, or pulmonary/cerebral
edema. *If you intubate, you must set high RR or the acidemia will worsen and the pt will arrest.*
, Review the general pathophysiology, Dx, and Tx of opioid overdose
Analgesic causing respiratory depression and impaired consciousness. SSx (TRIAD): CNS depression +
respiratory depression + miosis (pinpoint pupils). Rx: naloxone (start low dose to avoid withdrawal &
vomiting, uncomfortable but not life-threatening except in neonates)
Review unique clinical complications for meperidine, tramadol and methadone
Meperidine: seizures, serotonin syndrome, often dilated pupils. Tramadol: seizures, serotonin
syndrome, anticholinergic effects (mydirasis). Methadone: QT prolongation (& TdP), hypoglycemia.
What types of opioids are NOT seen on urine tox screen?
Synthetics. Includes fentanyl, hydromorphone, buprenorphine, methadone, meperidine. Natural
derivatives will show up (heroin, morphine, codeine, hydrocodone, oxycodone).
What is the potential risk of using meperidine, tramadol, or dextromethorphan in the setting of
antidepressant use?
Serotonin syndrome
Review the general pathophysiology, Dx, and Tx of clonidine intoxication
Alpha-2 agonist. In OD appears similar to opioid toxidrome but causes bradycardia. SSx: AMS + miosis
+ respiratory depression. Others: bradycardia, hypotension. Rx: supportive, atropine, pressors,
naloxone.
What common substances are associated with methanol, ethylene glycol, and isopropyl alcohol
ingestions?
Methanol: wood alcohol, moonshine, windshield washer fluid, paint solvent, perfume, antifreeze.
Ethylene glycol: antifreeze & other automotive fluids, radiator coolant, aircraft de-icing. Isopropyl
alcohol: rubbing alcohol, hand sanitizer.
Clinical manifestations of an ethylene glycol and methanol intoxication?
Comatose pt with slight hypothermia, tachypnea and a blood gas that shows metabolic acidosis with
normal respiratory compensation. **remember metabolic acidosis w/ respiratory compensation = last
two numbers of pH roughly equal the PCO2 (pH 7.23 —> PCO ~ 23)
What are the potential clinical consequences and clues to diagnosis of methanol, ethylene glycol, and
isopropyl alcohol ingestions?
Methanol: metabolized to formic acid → optic neuropathy ("snowy" field of vision, blindness) and
basal gangliar injury; Labs: + AG metabolic acidosis, ↑ osmolar gap. Ethylene glycol: metabolized to
glycolic acid & oxalic acid (binds Ca → low Ca + renal failure); Labs: hypoCa, calcium oxylate crystals in
urine, +AG metabolic acidosis, ↑ osmolar gap. Isopropyl alcohol: metabolized to acetone (uncharged
ketone), no significant pathology other than CNS depression; similar to ethanol overdose, ketosis
WITHOUT acidosis, NO anion gap.
Biggest lab difference btw ethylene glycol and methanol ingestions when compared to isopropanol
(isopropyl alcohol) ingestion?
Ethylene glycol and methanol will lead to an AG metabolic acidosis with ↑ osmolar gap. Isopropanol
will lead to ketosis, no acidosis
Questions With Complete Solutions
How does activated charcoal work for decontamination and how should it be administered?
High surface area binding to toxin and preventing systemic absorption. Dose: 10:1 (10g AC per 1g
drug)
When is activated charcoal contraindicated or ineffective?
Contraindicated in AMS/obtunded patient, risk of seizure or aspiration, ileus. Ineffective for
pesticides, lithium, hydrocarbons, heavy metals, alcohols, caustics.
How does whole bowel irrigation work for decontamination and how should it be administered?
Iso-osmotic agent (e.g. Go-Lytely) taken in large volume will hasten progress through intestines and
prevent absorption; Dose: 1-2L/hr (adults) or 500mL/hr (kids), consider giving by NGT, and continue
until clear rectal effluent is produced. Think about using this for "drug packers" and also for ER beta-
blockers.
For what types of ingestion is whole bowel irrigation most effective?
Iron, lithium, sustained-release formulations, enteric-coated meds, body packers
What toxins are cleared by HD?
"I STUMBLE": Isopropyl alcohol, Salicylate (aspirin), Theophylline, Uric acid, Methanol,
Barbiturates/Beta-blockers, Lithium, Ethylene glycol
Review the general pathophysiology, Dx, and Tx of Acetaminophen (APAP) overdose
APAP normally broken down via sulfation & glucuronide conjugation. Small amount is broken down by
CYP450 enzymes → toxic NAPQI metabolite. APAP OD: overloads glutathione inactivation/metabolism
→ excess NAPQI accumulates → liver toxicity. Dx: can use acetaminophen nomogram for SINGLE,
ACUTE ingestions; get APAP level at ≥ 4 hours (< 4 hours NOT useful, unless ZERO). High risk of
toxicity: >150mg/kg (acute) or >4g/day (chronic). Rx: N-acetylcysteine (NAC) → restores glutathione,
acts as an antioxidant; best if given w/in 8 hours of ingestion; Dose PO (140mg/kg load, 70mg/kg
q4hr) or IV (150mg/kg load, 50mg/kg over 4hr, 100mg/kg over 16hr). Safe for pregnant woman and
children. Side effect: anaphylactoid reaction.
When can you use the Rumack-Matthew nomogram for acetaminophen toxicity?
For single acute ingestions, not for chronic ingestions. For chronic you treat based on acetaminophen
level or signs of acute toxicity
Review the general pathophysiology, Dx, and Tx of NSAID overdose
COX inhibitor decreases prostaglandin production. SSx: minimal toxicity but can cause GI upset (rarely
GI Bleed); large doses: AMS/ataxia, coma, metabolic acidosis, seizure. Rx: supportive.
Review the general pathophysiology, Dx, and Tx of Aspirin (ASA) overdose
Causes primary respiratory alkalosis (stimulates resp. center, EARLY, uncouples oxidative
phosphorylation (AG metabolic acidosis, hyperthermia). SSx: ↑ RR, ↑ temp, ↑ HR (sinus tach = MC
sign), tinnitus, vertigo, AMS, seizure. Rx: GI decon, urine alkalinization with bicarb (+K, +Mg) infusion
(enhances urinary excretion of salicylate, also prevents CNS distribution), HD (acute level >100,
chronic level >60, OR there is a presence of renal failure, severe acidemia, or pulmonary/cerebral
edema. *If you intubate, you must set high RR or the acidemia will worsen and the pt will arrest.*
, Review the general pathophysiology, Dx, and Tx of opioid overdose
Analgesic causing respiratory depression and impaired consciousness. SSx (TRIAD): CNS depression +
respiratory depression + miosis (pinpoint pupils). Rx: naloxone (start low dose to avoid withdrawal &
vomiting, uncomfortable but not life-threatening except in neonates)
Review unique clinical complications for meperidine, tramadol and methadone
Meperidine: seizures, serotonin syndrome, often dilated pupils. Tramadol: seizures, serotonin
syndrome, anticholinergic effects (mydirasis). Methadone: QT prolongation (& TdP), hypoglycemia.
What types of opioids are NOT seen on urine tox screen?
Synthetics. Includes fentanyl, hydromorphone, buprenorphine, methadone, meperidine. Natural
derivatives will show up (heroin, morphine, codeine, hydrocodone, oxycodone).
What is the potential risk of using meperidine, tramadol, or dextromethorphan in the setting of
antidepressant use?
Serotonin syndrome
Review the general pathophysiology, Dx, and Tx of clonidine intoxication
Alpha-2 agonist. In OD appears similar to opioid toxidrome but causes bradycardia. SSx: AMS + miosis
+ respiratory depression. Others: bradycardia, hypotension. Rx: supportive, atropine, pressors,
naloxone.
What common substances are associated with methanol, ethylene glycol, and isopropyl alcohol
ingestions?
Methanol: wood alcohol, moonshine, windshield washer fluid, paint solvent, perfume, antifreeze.
Ethylene glycol: antifreeze & other automotive fluids, radiator coolant, aircraft de-icing. Isopropyl
alcohol: rubbing alcohol, hand sanitizer.
Clinical manifestations of an ethylene glycol and methanol intoxication?
Comatose pt with slight hypothermia, tachypnea and a blood gas that shows metabolic acidosis with
normal respiratory compensation. **remember metabolic acidosis w/ respiratory compensation = last
two numbers of pH roughly equal the PCO2 (pH 7.23 —> PCO ~ 23)
What are the potential clinical consequences and clues to diagnosis of methanol, ethylene glycol, and
isopropyl alcohol ingestions?
Methanol: metabolized to formic acid → optic neuropathy ("snowy" field of vision, blindness) and
basal gangliar injury; Labs: + AG metabolic acidosis, ↑ osmolar gap. Ethylene glycol: metabolized to
glycolic acid & oxalic acid (binds Ca → low Ca + renal failure); Labs: hypoCa, calcium oxylate crystals in
urine, +AG metabolic acidosis, ↑ osmolar gap. Isopropyl alcohol: metabolized to acetone (uncharged
ketone), no significant pathology other than CNS depression; similar to ethanol overdose, ketosis
WITHOUT acidosis, NO anion gap.
Biggest lab difference btw ethylene glycol and methanol ingestions when compared to isopropanol
(isopropyl alcohol) ingestion?
Ethylene glycol and methanol will lead to an AG metabolic acidosis with ↑ osmolar gap. Isopropanol
will lead to ketosis, no acidosis
