toxicology Flashcards
(42 cards)
activated charcoal
Activated charcoal administration, whole bowel irrigation,
urinary alkalinization, and hemodialysis - Recall the indications for poison management
CHARCOAL:
-direct binding -> doesnt affect anything in blood (alcohol)
-do within 1 hour of ingestation
- useful in: acetaminophen, TCA, salicylates, barbituates, SSRIs, digoxin, warfarin/rat poison
- complication: aspiration
-CI: AMS, ileus, obstruction
-Poorly binds: Heavy Metals:
(iron, lead, mercury), Lithium, Cyanide, Hydrocarbons (pesticides), Liquids (Alcohols, Alkali / Acids, Caustics)
🦑 Activated Charcoal
📌 Mechanism
Adsorbs toxins in the GI tract, preventing absorption.
Does not enter the bloodstream — only works in the gut.
⏱️ Indication
Use within 1 hour of ingestion of a known toxic substance.
Best for:
Acetaminophen
Aspirin (salicylates)
Many prescription drugs (e.g., TCAs, antiepileptics)
❌ Does NOT bind well to:
(Memory aid: CHILLS = Charcoal Hates Iron, Lithium, Lead, Solvents)
Cyanide
Hydrocarbons (e.g., gasoline, pesticides)
Iron
Lithium
Lead
Solvents (alcohols, alkalis, acids, caustics)
🚫 Contraindications
AMS without protected airway (risk of aspiration)
GI obstruction or ileus
Caustic ingestion (can obscure endoscopy and worsen injury)
whole bowel irrigation, chelating agents
WHOLE BOWEL IRRIGATION:
-MC
-flush out GI with diarrhea
-polyethylene glycol (miralax)
-Good for sustained release like iron, lithium, lead, drug packers
-CI- ileus or obstruction
chelating agents:
* Used for heavy metal poisoning
* Combines with metallic ions to form complexes that are easily excretable
* Examples:
* Dimercaprol (BAL): Arsenic, mercury, lead
* Dimercaptosuccinic acid (DMSA): lead, arsenic, mercury
* Penicillamine: Copper toxicity, occasionally gold or arsenic
* Ethylenediaminetetraaceticacid (EDTA): Lead poisoning
* Deferoxamine: Iron poisoning*
🚽 Whole Bowel Irrigation (WBI)
📌 Mechanism:
Rapid GI cleansing by inducing diarrhea using polyethylene glycol (PEG) (e.g., GoLYTELY, MiraLAX).
✅ Indications:
Sustained-release or enteric-coated drugs
Heavy metals (iron, lithium, lead)
Body packers (drug smugglers)
Drugs poorly adsorbed by charcoal
❌ Contraindications:
Ileus
Bowel obstruction
GI bleeding
Unstable patients or compromised airway
⚛️ Chelating Agents
📌 Purpose:
Used for heavy metal poisoning
Chelators bind metals → form water-soluble complexes → excreted in urine or bile
🧪 Key Chelators & Indications:
Agent Used For Notes
Dimercaprol (BAL) Arsenic, Mercury, Lead IM injection, used with EDTA for lead
DMSA (Succimer) Lead, Arsenic, Mercury Oral; preferred in kids with lead
Penicillamine Copper toxicity (e.g., Wilson’s disease)
Also used for gold or arsenic Oral, rarely used due to side effects
EDTA (CaNa2EDTA) Lead poisoning IV or IM, often with BAL
Deferoxamine Iron poisoning IV/IM; urine turns orange (“vin rose”)
🎯 Quick Associations:
Iron → Deferoxamine
Lead → EDTA + BAL (or DMSA in mild/moderate cases)
Arsenic/Mercury → BAL or DMSA
Copper → Penicillamine
urine alkalinization and hemodialysis: indication for poison management, CI
URINE ALKALINIZAITON:
-things already been absorbed
-indications: SALICYLATES! (ASA), phenobarbital, INH**
-urine goal pH 7-8
-sodium bicarb infusion
-CI- renal failure, pulmonary edema, cerebral edema, volume overload
HEMODIALYSIS:
-good for low protein binding, low molecular wt, small volume of distribution, water solubles
-drugs that already absorbed
-works for most things
-I-STUMBLED:
-!Isopropyl alcohol, iron, INH
-!Salicylates
-Theophylline
-Uremia
-Methanol
-Barbiturates
-Lithium
-!Ethanol/ethylene glycol
-Depakote (valproic acid)
💧Urinary Alkalinization
✅ What it is:
Alkalinizing the urine with IV sodium bicarbonate to enhance renal excretion of weak acids.
📌 Indications (Best for weak acids):
Mnemonic: “PI-S”
Phenobarbital
Isoniazid (some sources)
Salicylates (most important – aspirin)
🎯 Goal urine pH: 7.5–8.0
❌ Contraindications:
Renal failure – can’t excrete bicarbonate
Pulmonary edema or volume overload
Cerebral edema – alkalosis can worsen swelling
🩸 Hemodialysis
✅ When to use it:
For drugs that are:
Low molecular weight
Low protein binding
Small volume of distribution (Vd)
Water-soluble
💡 These characteristics make toxins easier to remove from the blood.
📌 Mnemonic: I STUMBLED
Letter Toxin
I Isopropanol, Iron, INH (Isoniazid)
S Salicylates
T Theophylline
U Uremia (ESRD, not poison but indication)
M Methanol
B Barbiturates
L Lithium
E Ethylene glycol, Ethanol
D Depakote (Valproic acid)
These are all absorbed poisons — dialysis removes them from blood, unlike charcoal.
❌ Hemodialysis Contraindications (relative):
Hemodynamic instability (though sometimes tolerated)
Severe coagulopathy (bleeding risk from HD access)
High protein-binding or large Vd toxins (e.g., TCAs, digoxin)
gastric decontamination - Recall the indications for poison management
Gastric decontamination = functionally removing an ingested toxin from the GI tract in order to decrease its absorption
May be beneficial in the following patients:
* Early ingestion ( <1 hour from ingestion benefit the most)
* Delayed release products
* Not fully absorbed yet
Most patients will not benefit from gastric decontamination:
* Time of presentation is past the window of potential benefit
* Ingestion of non-toxic substances
* Ingestion of non-toxic amounts of toxic substances
options:
- activated charcoal
- whole bowel irrigation: good for sustained release products
- chelating agents: heavy metal poisoning (BAL - dimercaprol; (DMSA))
- urine alkalinization: enhances elimination
- hemodialysis: good for low protein binding drugs, LMW, small volume distribution, water soluble
Anticholinergics overdose signs and sx, EKG findings and their tx
- [ ] Recognize the signs and symptoms of anticholinergic toxicity
- [ ] Recognize the medications or exposures that can cause anticholinergic toxicity
- [ ] What are the ECG findings in TCA toxicity and its treatment? If refractory?
-MCC- ANTIHISTAMINES, antidepressants (TCAs), anti-psychotics
-atropine, phenothiazines, parkinsonian drugs, scopolamine, jimsonweed
-!Blind as a bat, mad as a hatter, red as beet, dry as a bone, hot as Hades”
-Blurry vision, delirium, FLUSHED BUT DRY SKIN, hyperthermia, dry mucus membranes
-mydriasis (dilated pupils!), hypoactive bowel, URINARY RETENTION, agitation, seizures
ECG:
- sinus tachy (common)
- wide complex tachycardias: tx = SODIUM BICARB**
- ventricular dysrhythmias: tx = lidocaine,amiodarone
- torsades de pointes: MAGNESIUM
-Wide QRS >100ms, terminal R wave, right axis deviation
anticholinergics OD tx and EKG finding tx
- [ ] Be able to determine when first- and second-line medications for anticholinergic toxicity are required, and what those medications are.
-supportive- fluids and COOLING
-mainstay of tx = BENZODIAZEPINES
-second line: physostigmine!! for refractory sx of seizures, hyperthermia, dysrhythmias
-> CI in heart block and TCA overdose
ekg:
-ventricular dysrhythmias -> lidocaine, amiodarone
-torsades -> Mg
-wide complex tachy -> sodium bicarb!!!
Tricyclic antidepressants (TCA): MOA, drug names, sx
-self poisoning ANTICHOLINERGIC
-drugs: Amitriptyline, nortriptyline, cyclobenzaprine
-MOA: Inhibits reuptake of norepinephrine and serotonin, sodium, histamine, muscuarinic, alpha 1, potassium, GABA
-Blood or urine TCA
->5mg/kg – average toxic dose
->10-20mg/kg- severe
Anticholinergic effects
-!!3 C’s = Cardiac abnormalities, Convulsions, Coma*
-CV effects: hypotension, tachy, wide QRS, V-tach, torsade’s
-!!!!ECG - most useful in determining severity
-!sinus tachy
-!wide QRS >100ms (seizures)
-prolonged QT
-!Wide terminal R wave in aVR
-hypotension
tca od tx
-ABCs
-intubation bc LOC
-NG tube -> charcoal!
-QRS >100ms, ventricular dysrhythmia -> !!!Sodium bicarb IV bolus -> infusion! -> lidocaine! if refractory + arryhthmia
-hypotension -> crystalloids! + norepinephrine (reverse alpha1 blockage)
-seizures -> (GABA-A inhibition) -> BENZOS!! (diazepam, phenobarbital) -> !!!physostigmine!!! if refractory
Cholinergic: sx
- [ ] Recognize the signs and symptoms of cholinergic toxicity
- [ ] Recognize the exposures or medications that can cause cholinergic crisis
- [ ] Order the correct treatment for cholinergic crisis
sx:
-!!!Killer Bs: BRADYCARDIA, Bronchospasm, and BRONCHORHEA (frothy mouth)
-weakness, fasciculations, resp failure, wheezing
-people that work with chemicals or landscapers (insecticides)
-VERY WET PTS
-SLUDGE- saliva, lacrimation, urinartion, diarrhea, GI dysmotility, emesis
-DUMBBELLS- DIAPHORESIS, urine, miosis, bradycardia, emesis, lacrimation, lethargy, salivation
-nictoinic effects- FASCICULTIONS, weakness, paralysis
-Causes: !Organophosphate poisoning (insecticides)!, chemical warfare agents (nerve gas like sarin)
Tx:
-!Decontamination -> use PPE
-ABCs
-elevate head of the bed
-Antidotes: ATROPINE! and 2-PAM (PRALIDOXIME)!
-Atropine -> reduce muscarinic effects
-2-5 mg q 5-10 min until !secretions are dry!
-Increases HR
-Pralidoxime or 2-PAM -> reverse paralysis and fasciculations
cholinergics: causes and tx
- [ ] Recognize the signs and symptoms of cholinergic toxicity
- [ ] Recognize the exposures or medications that can cause cholinergic crisis
- [ ] Order the correct treatment for cholinergic crisis
-Causes: !Organophosphate poisoning (insecticides)!, chemical warfare agents (nerve gas like sarin)
Tx:
-!Decontamination -> use PPE
-ABCs
-elevate HOB
-Antidotes: ATROPINE! and 2-PAM (PRALIDOXIME)!
Atropine -> reduce muscarinic effects
-2-5 mg q 5-10 min until !secretions are dry!
-Increases HR
Pralidoxime or 2-PAM -> reverse paralysis and fasciculations
sx:
-!!!Killer Bs: Bradycardia, Bronchospasm, and Bronchorrhea
-weakness, fasciculations, resp failure, wheezing
-people that work with chemicals or landscapers (insecticides)
-VERY WET PTS
-SLUDGE- saliva, lacrimation, urine, diarrhea, GI dysmotility, emesis
-DUMBBELLS- diaphoresis, urine, miosis, bradycardia, emesis, lacrimation, lethargy, salivation
-nictoinic effects- fasciculations, weakness, paralysis
Opioids oD: cause, sxs
Causes: morphine, heroin, fentanyl, Demerol, codeine, diphenoxylate (Lomotil), propoxyphene (Darvon), hydrocodone (Vicodin), Percocet (careful of Tylenol addition), etc.
-Caution: Clonidine can mimic opioid overdose (pinpoint pupils and hypoventilation) -> also reversed with high dose naloxone (10mg)
sx:
-PINPOINT pupils + not breathing = opioids
-Resp depression! (<12) -> respiratory arrest!!!
- BRADYCARDIA*
- miosis
- lethargy
- hypotension
- coma
- noncardiogenic pulmonary edema
- N/V in opioid naïve patients
- ileus
-some cause agitation and dilated pupils such as dilaudid, Demerol, diphenoxylate
-Death by apnea!
opiods OD: PE, dx, tx
PE:
- Pinpoint pupils, lethargy, RR<12 breaths/min
- Look for circumstantial evidence of opioid use: needle marks, drug paraphernalia (undress), tourniquets, fentanyl patches (mucus membranes), witnesses
Dx- urine can be positive 2-4 days after
Tx:
-NALOXONE (opiod antagonist)
-Intranasal: 1mg each nostril (total 2mg)
-IV start with 0.4mg if mild-moderate depression, 2mg if apneic
-repeat q 2-3 mins up to 10mg due to opioid longer half life
- may cause an ALI that resolves within 24 hrs
discharging someone with opiod use disorder:
Addiction medicine referral
Fentanyl test strips
Naloxone
Buprenorphine
Suboxone
Methadone
opiod withdrawal
toxidrome chart summary:
- sympathomimetic
- anticholinergic
- cholinergic
- sedative/hynotic
- opiod
full toxidrome charts: opiods and sympathomimetics and cholinergics
full toxidrome charts: anticholinergics and salicylates
hypoglycemia and serotonin syndrome toxidrome chart
toxic alcohol: METHANOL
causes, sx, tx
Anion gap metabolic acidosis + increased osmolal gap
-paint thinner, car window wash, wood alcohol, gas tank additive
-sx delayed 12-18 hrs
-!BLINDNESS from disc hyperemia!, seizures, resp failure, N/S, pancreatitis, visual changes, ataxia, AMS
Tx:
-1. !!Fomepizole (4-methylpyrazole)
-excretes via kidneys
-temporizing until dialysis
-2. !Ethanol- competitive inhibition
-!!Dialysis and bicarbonate if severe acidosis + refractory to 4-MP or ethanol therapy
-ETHYLENE GLYCOL:
-ANTIFREEZE, moonshine, paints, solvents, windshield wiper fluid
-will have NO SMELL BUT APPEAR INTOXICATED
-oxalic acid -> forms calcium oxalate crystals! -> acidosis and kidney injury
-<12 hrs: Intox + CNS depression!! w/o odor
-12-24 hrs: Tachy, HF/pulm edema
-24-72 hrs: ATN, anuria, flank pain, hypocalcemia, hematuria
-Wood’s lamp - green glowing urine, d/t calcium oxalate crystals
Tx:
-FOMEPIZOLE - inhibits alcohol dehydrogenase
-HEMODIALYSIS if severe
-THIAMINE & PYRIDOXINE
-Both are consumed in the metabolism of ethylene glycol and need supplementation
-ISOPROPYL ALCOHOL:
-Rubbing alcohol (mouthwash, ginseng shots, NyQuil)
-CNS depression worse than ethanol
- Hallmark: Normal anion gap, increased osmolar gap , Ketosis with normal glucose**
-!Hemorrhagic gastritis, pulmonary edema, hypoglycemia
-Severe hypotension
tx:
-Supportive care, don’t give alcohol
-Hemodialysis (if severe)
flowchart of toxic alcohol ingestion
toxic alcohol overview: when to consider it and how to calculate the osmolol gap
Toxic metabolites produced by alcohol dehydrogenase which can be inhibited by ethanol or fomepizole. These all cause inebriation.
Consider toxic alcohol if there is an unexplained anion gap or ↑ osmolar gap
Methanol and Ethylene glycol will produce an anion gap. Isopropyl alcohol will NOT.
-Ethanol < isopropyl alcohol < ethylene glycol < methanol (order of increasing alcohol toxicity)
- Drunk + Anion gap metabolic acidosis + osmolol gap = ethylene glycol or methanol poisoning
- Drunk + osmol gap = isopropyl
acetaminophen (paracetamol) overdose overview pathophys and labs to order, when can you use the normogram
pathophysiology of acetaminophen toxicity
-!toxic dose = >150mg/kg
-Hepatic metabolism via CYP450 to NAPQI –> highly toxin that damages liver
-Normally, NAPQI combines with thiols to produce non-toxic metabolites
-In overdose -> thiol stores are depleted -> NAPQI accumulates
Dx:
-!LFTs (serial)
-Coagulation profile (PT/PTT/INR)
-CBC
-anion gap, ABG
-Renal study
-APAP LEVEL
-!>140u/mL 4 hours after ingestion is TOXIC -> tx with NAC
-Rumack-Mathew normogram -> for !Acute SINGLE ingestion ONLY within 4-24hrs and NON-extended release product -> need to know exact timing
acetaminophen 4 stages of injury - what sx
-NO characteristic PE findings
-stage 1- first 24hrs -> N/V, abdominal pain
-stage 2 (latent)- 24-48hrs, GI sx resolve (asymptomatic!), hepatic/renal dysfunction begins (high AST/ALT bilirubin INR)
-stage 3- 3-4 days, LFTs peak, coagulopathy, renal failure, fulminant hepatic failure, encephalopathy, sepsis, coma, death
-stage 4: 4 days-2wks, recovery if survive stage 3