Built from GI Lecture 21 (LOs 1–12). Close notes. Fill from memory. Reveal only after a genuine attempt.

LO 1 · LO 2 · LO 3

ON EXAM — NPDS top killers (SOAP), history framework (WARS), vital sign extremes, alert presentations that demand immediate intervention (AMS with focal findings, seizures, dysrhythmia, cyanosis, hyperthermia)

NPDS (National Poison Data System) — top causes of poisoning deaths

Mnemonic: SOAP — the 4 classes most responsible for fatal exposures in the US.

S — what class of medication?

O — what class of medication?

A — what single drug?

P — general category (illicit/agricultural/industrial)?

Epidemiology — age + intent patterns

Peak age of unintentional pediatric exposure?

Most common intent in adolescents/adults presenting to ED?

Most common route of exposure overall?

History framework — WARS (poisoned patient)

Letter	What It Stands For	Example Question
W
A
R
S

Vital-sign clues — each extreme suggests a different class

Vital Finding	Classic Toxin Category
Hypotension + bradycardia
Hypertension + tachycardia
Hyperthermia
Hypothermia
Bradypnea + miosis + coma

"Red-flag" alert presentations — demand immediate intervention

Altered mental status + focal neuro findings → think what?

Seizures in an undifferentiated poisoning → top 2 toxins?

Wide-complex tachycardia in overdose → top toxin?

Cyanosis that does NOT respond to O₂ → top 2 causes?

Cherry-red skin with normal SpO₂ → classic poisoning?

LO 4 · LO 5 · LO 12

ON EXAM — anion gap MUDPILES, osmolar gap toxins, UDS false pos/neg, co-oximetry, 4 classic toxidromes (anticholinergic/cholinergic/sympathomimetic/opioid)

Anion-gap metabolic acidosis — MUDPILES

Letter	Toxin
M
U
D
P
I
L
E
S

Osmolar gap — what drives it, what toxins raise it

Formula: measured osmolality − calculated osmolality; normal gap is < _______?

Gap > _______ is highly suspicious for toxic alcohol?

Name 3 toxic alcohols that raise the osmolar gap

Which toxic alcohol causes a LARGE osmolar gap but NO anion gap?

Urine drug screen (UDS) — limitations

Never trust a negative UDS to "rule out" poisoning. Know the false negatives + false positives.

False NEG — which opioids are typically missed by standard UDS?

False POS — what causes a benzo-positive UDS in non-benzo user?

False POS — what OTC nasal decongestant causes amphetamine positive?

UDS detects metabolites, not parent drug — does positive = active intoxication?

Toxidromes — side-by-side recognition (fill all cells)

Feature	Anticholinergic	Cholinergic	Sympathomimetic	Opioid
Mental status
Pupils
Skin
Bowel sounds
Temperature
Classic antidote

Anticholinergic mnemonic — fill all 4

"Hot as a ______" → what finding?

"Dry as a ______" → what finding?

"Red as a ______" → what finding?

"Mad as a ______" → what finding?

Cholinergic mnemonic — SLUDGE + DUMBELS (muscarinic)

S-L-U-D-G-E stands for?

D-U-M-B-E-L-S stands for?

Nicotinic findings (3 categories)?

LO 6 · LO 7

ON EXAM — activated charcoal (dose/window/misses = LAME Ca), MDAC indications (CPSA), urinary alkalinization targets (pH & toxins), hemodialysis criteria (SLIME), WBI indications

Activated charcoal — basics

Standard adult dose?

Ideal timing (window from ingestion)?

Main contraindication — related to airway?

Main contraindication — related to GI?

LAME Ca — what charcoal does NOT adsorb

Letter	Category/Substance
L
A
M
E
Ca

Multi-dose activated charcoal (MDAC) — CPSA indications

Letter	Drug	Reason MDAC Works
C
P
S
A

Urinary alkalinization — mechanism + targets

Agent used to alkalinize urine?

Target urine pH?

Principle (one phrase) — why does it enhance elimination?

Classic toxin #1 (carboxylic acid analgesic)?

Classic toxin #2 (long-acting barbiturate)?

Electrolyte to monitor/replace (low = treatment failure)?

Hemodialysis — SLIME mnemonic

Letter	Toxin
S
L
I
M
E

Properties that make a toxin DIALYZABLE (4 criteria)

Molecular weight?

Protein binding?

Volume of distribution?

Water solubility?

Whole-bowel irrigation (WBI)

Agent used?

Indication #1 — which toxic metal?

Indication #2 — which drug formulation type?

Indication #3 — body packer with what type of material?

LO 8 · LO 9

ON EXAM — APAP 4 clinical phases + NAPQI, Rumack-Matthew nomogram use, NAC mechanism + window; salicylate mixed acid-base + tinnitus; iron 5 phases + "quiet phase" trap

Acetaminophen (APAP) — 4 clinical phases

Phase	Time	Key Features
Phase 1
Phase 2
Phase 3
Phase 4

APAP toxicity mechanism

In overdose, APAP is metabolized to what toxic intermediate?

What enzyme generates this intermediate?

What endogenous molecule neutralizes it (depleted in overdose)?

What tissue is preferentially injured?

APAP — labs, nomogram, antidote

Draw APAP level at what time post-ingestion?

Nomogram plots level vs _______ to determine need for NAC?

Antidote + mechanism?

NAC is most effective if given within _______ hours of ingestion?

Salicylates — clinical + lab picture

Classic early symptom (ear)?

Respiratory pattern early on (direct medullary stimulation)?

Classic acid-base disturbance (mixed)?

Temperature finding — because salicylates uncouple _______?

Fatal finding indicating severity (brain edema / pulmonary)?

Salicylate treatment

Urine alkalinization rationale (in 1 phrase)?

Target serum pH for treatment?

Dialysis indications — salicylate level cutoff (mg/dL)?

Why AVOID intubation if possible?

Iron toxicity — 5 phases

Phase	Time	Hallmark
Phase 1 — GI
Phase 2 — Latent ("quiet")
Phase 3 — Shock/metabolic
Phase 4 — Hepatotoxicity
Phase 5 — Delayed

Iron — antidote + diagnostics

Antidote + MOA?

Distinctive urine color with treatment?

Imaging test that may show iron tablets?

When do you use WBI for iron? (formulation type)

LO 8 · LO 9

ON EXAM — TCA 3 receptor effects + wide QRS + NaHCO₃; naloxone reversal; CO cherry red + co-oximetry; methanol (blindness) vs ethylene glycol (renal/oxalate); fomepizole MOA

Tricyclic antidepressant (TCA) toxicity — 3 receptor effects

Receptor Blocked	Clinical Effect
Fast Na⁺ channels (cardiac)
Muscarinic (M1)
α₁-adrenergic

TCA EKG + treatment

EKG finding most associated with cardiac toxicity?

QRS width threshold (ms) predicting seizures/arrhythmia?

Antidote + mechanism (2 effects)?

Why AVOID flumazenil if coingested with a benzo?

Opioid toxicity

Classic triad?

Antidote + route?

Naloxone duration vs typical opioid duration — why does this matter?

Opioid that causes QT prolongation / torsades?

Opioid that causes seizures (via normeperidine metabolite)?

Withdrawal risk with naloxone in chronic user?

Carbon monoxide (CO)

Mechanism #1 — binds to Hb with _______× affinity vs O₂?

Mechanism #2 — inhibits mitochondrial enzyme _______?

Why does standard SpO₂ pulse oximetry FAIL in CO?

Diagnostic test of choice?

Treatment — first-line?

Treatment — severe/neurologic cases (hyperbaric) — 3 indications?

Pregnancy consideration — CO-Hb level threshold?

Methanol vs Ethylene Glycol — comparison

Feature	Methanol	Ethylene Glycol
Source
Toxic metabolite
Organ damaged
Distinctive finding
Urinalysis clue

Toxic alcohol treatment

First-line antidote (binds enzyme)?

Enzyme it blocks?

Backup antidote if fomepizole unavailable?

Role of hemodialysis?

Cofactor for methanol → folate or pyridoxine?

Cofactor for ethylene glycol → thiamine + _______?

LO 10 · LO 11

ON EXAM — full antidote master table, delayed-toxicity agents, supportive care priorities (ABCs + glucose/thiamine + intubation thresholds)

Antidote master table — fill all rows

Toxin	Antidote
Acetaminophen
Opioids
Benzodiazepines
Iron
TCA (cardiac)
Salicylates
Methanol / ethylene glycol
Carbon monoxide
Cyanide
Methemoglobinemia
Organophosphates (cholinergic)
Anticholinergic (severe)
Beta-blocker
Calcium channel blocker
Digoxin
Heparin
Warfarin
Lead (severe)
Isoniazid overdose (seizures)

Delayed-toxicity trap — agents where symptoms lag behind ingestion

Agent	Delay Before Symptoms	Why Delayed?
Acetaminophen
Iron (phase 2)
Sustained-release opioid
Methanol / ethylene glycol
Warfarin

Rapid-onset toxicity — these kill fast

Agent	Time-to-lethality	Key Intervention
Cyanide
Organophosphate (large exposure)
TCA (massive OD)
Calcium channel blocker

Supportive care priorities — the core of every tox case

First priority always?

In AMS of unknown cause — give what 3 empiric agents?

Thiamine before dextrose — why?

GCS threshold for intubation consideration?

Supportive care — seizures + hyperthermia

First-line seizure control in poisoning?

AVOID which anticonvulsant in TCA/INH/theophylline toxicity?

Hyperthermia from sympathomimetic/serotonergic — treatment?

AVOID which agent for tox hyperthermia (ineffective)?

Practice Questions

Q1: APAP overdose timing

A 22-year-old woman arrives 6 hours after ingesting ~30 extra-strength acetaminophen tablets. She is currently asymptomatic. What is the BEST next step?

A) Observe and discharge — she is asymptomatic
B) Draw a 4-hour level and plot on the Rumack-Matthew nomogram; start NAC if above treatment line
C) Begin NAC empirically now without labs
D) Give activated charcoal and discharge
E) Order LFTs only; if normal, no treatment needed

Correct Answer: B

A 4-hour post-ingestion APAP level plotted on the Rumack-Matthew nomogram is the standard. Phase 1 patients are classically asymptomatic — a normal exam does NOT rule out toxicity. NAC is most effective within 8 hours, so draw the level NOW (she's at 6h) and decide. If the level is above treatment line or timing uncertain (e.g., >8–10h), start NAC empirically without waiting. LFTs are normal in Phase 1.

Q2: Mixed acid-base in overdose

A 45-year-old man presents tachypneic with tinnitus, confusion, and vomiting. ABG shows pH 7.48, pCO₂ 22, HCO₃ 16. Anion gap is 22. What is the most likely intoxication?

A) Acetaminophen
B) Ethylene glycol
C) Salicylates (aspirin)
D) Tricyclic antidepressant
E) Opioid

Correct Answer: C

Classic salicylate presentation: mixed primary respiratory alkalosis (direct medullary stimulation → tachypnea) + anion gap metabolic acidosis (uncoupling of oxidative phosphorylation → lactate, ketones). Tinnitus is the pathognomonic early symptom. Treatment: urine alkalinization (NaHCO₃) → target serum pH ~7.5, urine pH >7.5. Dialyze if level >100 mg/dL, AMS, renal failure, or pulmonary edema. Ethylene glycol is anion gap only, no respiratory alkalosis.

Q3: Wide-complex tachycardia

A 30-year-old woman is brought in after a suicide attempt. She is somnolent, tachycardic (HR 130), hypotensive, with dry warm skin and mydriasis. ECG shows QRS 130 ms with a terminal R wave in aVR. What is the best immediate treatment?

A) Amiodarone IV
B) Sodium bicarbonate IV bolus
C) Cardioversion
D) Flumazenil IV
E) Lidocaine infusion

Correct Answer: B

TCA toxicity: anticholinergic features (mydriasis, dry skin, tachycardia) + Na-channel blockade (wide QRS, terminal R wave in aVR, right axis deviation). NaHCO₃ IV provides two benefits: (1) alkalinization reduces drug binding to Na channel, (2) sodium load overcomes the block. A/E worsen conduction. Flumazenil is contraindicated (seizure risk + could unmask TCA if coingested). QRS >100 ms = seizure risk; >160 ms = arrhythmia risk.

Q4: Hemodialysis indications

Which of the following toxins is MOST effectively removed by hemodialysis?

A) Digoxin
B) Tricyclic antidepressant
C) Lithium
D) Iron
E) Calcium channel blocker

Correct Answer: C

SLIME — Salicylates, Lithium, Isopropanol, Methanol/Metformin, Ethylene glycol. Dialyzable toxins: low MW, low protein binding, low Vd, water soluble. Lithium meets all criteria perfectly. Digoxin has huge Vd (bound to tissue), TCAs are highly protein bound + high Vd, iron is too large/complexed, CCBs have high Vd.

Q5: Cherry-red skin

A family of 4 is found obtunded in their home one morning in winter. The furnace has been malfunctioning. SpO₂ on pulse oximetry reads 99% but all members have cherry-red mucosa and lactic acidosis. What test confirms the diagnosis?

A) Arterial blood gas PaO₂
B) Standard pulse oximetry
C) Co-oximetry (carboxyhemoglobin level)
D) Methemoglobin level
E) Cyanide level

Correct Answer: C

Co-oximetry directly measures carboxyhemoglobin (CO-Hb), distinguishing it from O₂-Hb — which standard pulse oximetry CANNOT do (CO-Hb and O₂-Hb absorb light similarly at 660/940 nm). PaO₂ is normal in CO poisoning because dissolved O₂ is unchanged; the problem is Hb can't carry it. Treatment: 100% O₂; HBO for severe CNS symptoms, LOC, pregnancy, or CO-Hb >25% (>15% if pregnant since fetal Hb has even higher CO affinity).

Q6: Toxic alcohol

A 52-year-old man presents intoxicated but the ED smells no alcohol on his breath. He is acidotic with a HIGH anion gap (AG 28) and HIGH osmolar gap (25 mOsm/kg). Urinalysis shows calcium oxalate crystals. What is the best immediate treatment?

A) Ethanol infusion
B) Fomepizole IV
C) Naloxone IV
D) Activated charcoal
E) Pyridoxine IV

Correct Answer: B

Ethylene glycol poisoning: AG metabolic acidosis + elevated osmolar gap + calcium oxalate crystals on UA. Fomepizole is first-line (competitive alcohol dehydrogenase inhibitor) — prevents conversion to toxic glycolate/oxalate. Ethanol (A) is backup if fomepizole unavailable. Adjuncts: thiamine + pyridoxine (shunts to non-toxic metabolites). Hemodialysis if severe acidosis, renal failure, or high level. Methanol would give visual symptoms (blindness) + no oxalate crystals.

Q7: Charcoal contraindication

Activated charcoal is LEAST effective for which of the following ingestions?

A) Acetaminophen 1 hour ago
B) Aspirin 30 minutes ago
C) Tricyclic antidepressant 45 minutes ago
D) Lithium carbonate 1 hour ago
E) Phenytoin 30 minutes ago

Correct Answer: D

LAME Ca — Lithium, Alcohols, Metals (iron), Electrolytes, Caustics — are NOT effectively adsorbed by activated charcoal. Lithium is an ion (not organic) and doesn't bind well. Whole-bowel irrigation with PEG is preferred for lithium (especially sustained-release). Charcoal works best for organic, low-polarity compounds and is ideally given within 1 hour.

Q8: Cholinergic toxidrome

A 40-year-old farmworker is brought in after being sprayed with an unknown pesticide. He has copious oral secretions, miosis, bradycardia, bronchoconstriction, and fasciculations. What is the FIRST-line treatment?

A) Atropine IV titrated to dry secretions
B) Pralidoxime (2-PAM) IM only
C) Naloxone IV
D) Physostigmine
E) Activated charcoal

Correct Answer: A

Organophosphate poisoning (AChE inhibition) = cholinergic crisis (DUMBELS + SLUDGE). Atropine IV is first-line, titrated aggressively to DRY PULMONARY SECRETIONS (not HR/pupils). Pralidoxime (2-PAM) regenerates AChE and should be given WITH atropine, especially for nicotinic effects (muscle weakness/fasciculations) — but NOT as sole therapy. Give pralidoxime within 24–48h before "aging" of enzyme occurs. Physostigmine (D) is the WRONG direction — would worsen cholinergic excess; it's the antidote for ANTIcholinergic toxicity.

Poisoning Conference — Active Recall