SUMMARY TABLE p1

πŸ’€ TOX LECTURE 1 β€” ONE TABLE TO RULE THEM ALL

CATEGORY

KEY INFO (WHAT TO MEMORIZE)

EXAM TRAPS / PEARLS 😈

πŸ‘Ά WHO DIES FROM WHAT

PEDS: opioids, CV drugs (BB/CCB), sedatives, sulfonylureas
YOUTH: unregulated drugs (FENTANYL #1), antidepressants, ethanol
ADULTS: polypharmacy + CNS depressants, acetaminophen, CV drugs

πŸ‘‰ Teen + death = pick unregulated opioids
πŸ‘‰ Kids = small dose β†’ BIG effect

πŸ₯ ADMISSIONS vs DEATHS

Oral hypoglycemics = highest admission rates

πŸ‘‰ NOT most common poisonings, but high severity

πŸ’Š β€œONE PILL CAN KILL”

Bupropion β†’ seizures
BB/CCB/propafenone β†’ CV collapse
TCAs β†’ arrhythmias + seizures
Clonidine/guanfacine β†’ CNS + resp depression
Sulfonylureas β†’ hypoglycemia
Opioids β†’ resp arrest
Amphetamines β†’ hyperstimulation
Hydroxychloroquine β†’ cardiac toxicity

πŸ‘‰ Toddler + 1 pill = ASSUME DANGEROUS
πŸ‘‰ ALWAYS refer/observe

🧠 CORE TOX MECHANISMS (CAUSE OF DEATH)

CNS depression (opioids, clonidine)
Seizures (bupropion, TCAs)
Arrhythmias (CV drugs, TCAs)
Hypoglycemia (sulfonylureas)

πŸ‘‰ Most deaths fall into these 4 buckets

🧬 CLONIDINE TOXICITY

↓ HR, ↓ RR, CNS depression, MIOSIS
Central Ξ±2 agonist β†’ ↓ sympathetic activity

πŸ‘‰ Looks like opioid
❌ NOT hyperactive

🍬 SULFONYLUREA TOXICITY

Rebound hypoglycemia
Even 1 pill dangerous

❌ Dextrose alone NOT enough
βœ… OCTREOTIDE is KEY
❌ Don’t give prophylactic dextrose

⚑ BUPROPION TOXICITY

Delayed seizures (hours later)
NE + DA reuptake inhibition
QRS widening, QTc prolongation

πŸ‘‰ ❌ β€œpatient looks fine” = NOT SAFE
πŸ‘‰ still observe

πŸ‘Ά WHY KIDS GET POISONED

Environment + human error
Meds left out (grandparents!!)
Not childproof
Looks like candy
Wrong dose/med

πŸ‘‰ Grandparent meds = CLASSIC scenario

πŸ˜” YOUTH SUICIDE RISK

Previous attempt
Substance use
Mental illness
Stress/bullying
Access to meds

πŸ‘‰ High-risk groups: Indigenous youth, 2SLGBTQ+, unhoused

πŸ—£ PHARMACIST ROLE (SUICIDE)

Ask directly:
β€œThinking of hurting yourself?”
β€œDo you have a plan?”
β€œTried before?”

βœ… Asking does NOT increase risk

πŸš‘ ACTIONS

Urgent β†’ 911
Non-urgent β†’ crisis line/MD
Reduce access to meds

πŸ‘‰ Always think: refer vs manage

πŸ›‘ POISON PREVENTION

Child-resistant containers
Store out of reach
Original containers
Separate meds/chemicals
Dispose unused meds

πŸ‘‰ EASY MARKS

☎ POISON CALL STEPS (ORDER MATTERS)

1. Background: what, how much, who
2. Urgency: when, symptoms, stable?
3. Risk: toxicity, high-risk drug, child?
4. Recommendation: manage vs refer

πŸ‘‰ VERY testable sequence

🚨 WHEN TO REFER

CALL 911: unconscious, not breathing, seizing
CALL DPIC: any overdose, unknown ingestion, CV drugs, multiple meds, chemicals
CRISIS LINE: suicidal thoughts, no ingestion

πŸ‘‰ Know which = HUGE exam points

😈 EXAM TRAPS

❌ Most pediatric exposures severe β†’ FALSE (95% mild)
❌ Asymptomatic = safe β†’ FALSE (delayed tox!)
❌ Dextrose fixes sulfonylurea β†’ FALSE
❌ Clonidine = hyperactivity β†’ FALSE

πŸ‘‰ THESE WILL BE TESTED

⚑ 10-SECOND RECALL

Kids β†’ 1 pill can kill
Deaths β†’ opioids, CV drugs, sedatives
Bupropion β†’ delayed seizures
Sulfonylureas β†’ hypoglycemia β†’ octreotide
Clonidine β†’ CNS depression

πŸ‘‰ If panicking β†’ recall this


πŸ’€ TOX LECTURE 2 β€” ONE TABLE TO RULE THEM ALL (BASIC SCIENCE GOD MODE)

CATEGORY

KEY INFO (WHAT TO MEMORIZE)

EXAM TRAPS / PEARLS 😈

🧠 DEFINITIONS

Toxicology = study of harmful effects + mechanisms
Toxicity = harm depends on dose + exposure + patient

πŸ‘‰ NOT just overdose β†’ patient factors matter

⚠ TERMINOLOGY

Toxin = biological (venom, botulinum)
Toxicant = environmental (chemicals, metals)
Xenobiotic = foreign substance (drugs, pollutants)

πŸ‘‰ Acetaminophen = xenobiotic (NOT toxin)

πŸ‘ΆπŸ‘΅ WHO IS MORE SENSITIVE

Neonates β†’ immature metabolism (↓ glucuronidation)
Elderly β†’ ↓ clearance (↓ hepatic blood flow)
Genetics β†’ ALDH2 deficiency (↑ alcohol toxicity)
Body fat β†’ lipophilic drugs stored β†’ delayed toxicity
Liver disease β†’ ↑ acetaminophen toxicity

πŸ‘‰ Pattern: impaired clearance = ↑ toxicity

⚠ TYPES OF TOXICITY

Organ-specific β†’ one organ (acetaminophen β†’ liver)
Systemic β†’ whole body (cyanide)
Acute β†’ one exposure (methanol)
Chronic β†’ repeated (lead)
Immediate β†’ fast (methemoglobinemia)
Delayed β†’ later (benzene β†’ leukemia)
Dose-dependent β†’ predictable (aspirin)
Idiosyncratic β†’ random (sulfa allergy)

πŸ‘‰ Predictable = dose-dependent
πŸ‘‰ Random = immune/genetic

🫁 ABSORPTION (VERY TESTED)

Route risk: Inhalation > injection > oral > dermal
Lungs = huge surface area β†’ rapid absorption
Bypassing 1st pass β†’ ↑ toxicity

πŸ‘‰ inhalation = MOST dangerous

🍽 GI ABSORPTION

Small intestine = MOST absorption
Weak acids β†’ stomach (non-ionized, lipid soluble)
Weak bases β†’ intestine

πŸ‘‰ BOTH weak acids/bases matter

🫁 RESPIRATORY

Small particles β†’ go deeper β†’ worse toxicity
Alveoli = systemic absorption

πŸ‘‰ deeper = more dangerous

🧴 DERMAL

Intact skin = barrier (stratum corneum)
Damaged skin β†’ ↑ absorption

πŸ‘‰ once in dermis β†’ ↑ absorption

πŸ”„ DISTRIBUTION (Vd)

HIGH Vd β†’ drug in tissues β†’ LOW plasma levels
LOW Vd β†’ stays in blood

πŸ‘‰ β€œnormal level but toxic” = HIGH Vd

🧠 STORAGE

Fat β†’ lipophilic drugs (delayed release)
Bone β†’ metals (lead)
Liver/kidney β†’ accumulation

πŸ‘‰ low perfusion β†’ delayed toxicity + chronic effects

🧱 BARRIERS

BBB blocks polar drugs
Lipophilic drugs cross easily (opioids, ethanol)

πŸ‘‰ lipophilic = more CNS effects

πŸ”₯ METABOLISM (CORE)

Phase 1 (CYP450): oxidation, reduction, hydrolysis
β†’ can create TOXIC metabolites
Phase 2: conjugation β†’ water soluble β†’ excrete

πŸ‘‰ Phase 1 = danger
πŸ‘‰ Phase 2 = safe

☠ ACETAMINOPHEN PATHWAY

Phase 1 β†’ NAPQI (toxic)
Glutathione detoxifies NAPQI

πŸ‘‰ overdose β†’ glutathione depleted β†’ liver failure

🚨 SATURATION (BIG DEAL)

Normal β†’ safe pathway
Overdose β†’ toxic pathway activated

πŸ‘‰ β€œoverdose changes pathway” = SATURATION

🚽 ELIMINATION

Kidney = MAIN route
Lipophilic drugs β†’ must become hydrophilic first

πŸ‘‰ liver β†’ hydrophilic β†’ kidney excretion

⚑ ION TRAPPING RULE

Ionized = excreted
Non-ionized = reabsorbed

πŸ‘‰ alkalinize urine β†’ ↑ salicylate excretion

πŸ“Š DOSE RESPONSE

LD50 = lethal dose 50%
EC50 = effective dose
NOAEL = no harm
LOAEL = lowest harm

πŸ‘‰ humans set limits BELOW NOAEL

βš– THERAPEUTIC INDEX

TI = LD50 / ED50
BIG TI = safer

πŸ‘‰ classic easy mark

🀧 IMMUNE REACTIONS

NOT dose-dependent
Sensitized β†’ small dose β†’ BIG reaction

πŸ‘‰ β€œsmall dose big reaction” = immune

🧬 ALLERGY TYPES

Type I β†’ immediate (IgE, anaphylaxis)
Type II β†’ cytotoxic (IgG/IgM)
Type III β†’ immune complex
Type IV β†’ delayed (SJS)

πŸ‘‰ Immediate = Type I ALWAYS

βš– ADR vs TOXICITY

Toxicity = overdose/accumulation
ADR = harm at NORMAL dose
Side effect = expected
AE = not necessarily drug-caused

πŸ‘‰ ADR = normal dose problem

πŸ”— DRUG INTERACTIONS

Pharmacodynamic: same system (additive, synergistic, antagonistic)
Pharmacokinetic: affects ADME (CYP most common)

πŸ‘‰ opioid + alcohol = respiratory depression

πŸ§ͺ PK INTERACTIONS EXAMPLES

statin + CYP inhibitor β†’ toxicity
lithium + diuretic β†’ toxicity

πŸ‘‰ CYP interactions VERY COMMON

🧠 TOXICITY SIGNS

Hepatotoxicity β†’ ↑ ALT/AST, jaundice, dark urine
Nephrotoxicity β†’ ↑ Cr, ↓ urine, ↑ BUN, ↓ GFR

πŸ‘‰ classic exam presentation

😈 BIG EXAM PATTERNS

β€œdelayed toxicity” β†’ redistribution / metabolism / SR
β€œsmall dose big reaction” β†’ immune
β€œnormal level but toxic” β†’ HIGH Vd
β€œoverdose changes pathway” β†’ saturation

πŸ‘‰ THESE = GUARANTEED TEST

⚑ 10-SECOND RECALL

dose + patient = toxicity
inhalation = most dangerous
high Vd = hidden toxicity
acetaminophen = NAPQI
immune β‰  dose dependent
CYP interactions common

πŸ‘‰ if stuck β†’ recall this


πŸ’€ TOX LECTURE 3 β€” ONE TABLE TO RULE THEM ALL (CLINICAL GOD MODE)

CATEGORY

KEY INFO (WHAT TO MEMORIZE)

EXAM TRAPS / PEARLS 😈

🧠 MASTER ALGORITHM (MOST IMPORTANT)

1. Stabilize
2. History
3. Diagnosis (toxidrome)
4. GI decontamination
5. Enhanced elimination
6. Antidotes
7. Disposition

πŸ‘‰ If you blank β†’ WRITE THIS ORDER = free marks

🚨 STABILIZATION (ABCDE)

A airway β†’ intubate if needed
B breathing:
↓RR β†’ opioids β†’ naloxone
↑RR β†’ salicylates/stimulants
C circulation:
↓BP β†’ CCB/BB
↑BP β†’ stimulants

πŸ‘‰ ALWAYS FIRST STEP = stabilization

🧠 D = DISABILITY (SUPER TESTED)

Seizures β†’ BENZOS ONLY
❌ NOT phenytoin

πŸ‘‰ toxin seizures β‰  regular seizures

😡 AGITATION

BENZOS FIRST

❌ avoid antipsychotics (↓ seizure threshold, ↑ toxicity)

🍬 HYPOGLYCEMIA

D50
Β± glucagon
Β± octreotide (if sulfonylurea)

πŸ‘‰ sulfonylurea = always think octreotide

🌑 HYPERTHERMIA

DEADLY (>40.5Β°C brain damage risk)
Goal: <39Β°C FAST (30–60 min)

πŸ‘‰ BEST = ICE BATH
πŸ‘‰ sedation to prevent shivering

⚑ TOX-SPECIFIC INTERVENTIONS

Seizures β†’ benzos
Agitation β†’ benzos
Wide QRS β†’ sodium bicarbonate
CCB/BB shock β†’ insulin + glucose

πŸ‘‰ these are literally exam answers

❌ FLUMAZENIL (BIG TRAP)

DO NOT USE in overdose

πŸ‘‰ causes withdrawal seizures + unmasks co-ingestions

🧾 HISTORY

Kids β†’ accidental
Adults β†’ intentional (may lie)
AMS β†’ EMS, family, pill bottles

πŸ‘‰ LOW effort marks

🧠 TOXIDROMES (CORE)

OPIOID: ↓LOC, ↓RR, miosis β†’ naloxone
CHOLINERGIC: SLUDGE/DUMBELS β†’ atropine Β± pralidoxime
SYMPATHOMIMETIC: ↑HR, ↑BP, sweating β†’ benzos + cooling
ANTICHOLINERGIC: dry, hot, confused β†’ benzos Β± physostigmine/rivastigmine
SEROTONIN: hyperreflexia, clonus β†’ benzos + cyproheptadine

πŸ‘‰ Sweaty = sympathomimetic
πŸ‘‰ Dry = anticholinergic

πŸ§ͺ LABS (MUST KNOW)

Chem-7 (lytes, glucose, renal)
LFTs
ASA level
Acetaminophen level

πŸ‘‰ ALWAYS check acetaminophen

🧠 ANION GAP

Na - (Cl + HCO₃)
Normal: 6–14
↑ = metabolic acidosis

πŸ‘‰ β€œextra acids?”

☠ MUDPILES CAT (CAUSES)

methanol, ethylene glycol, salicylates, metformin, iron, INH, etc.

πŸ‘‰ memorize BIG ones

🍷 OSMOL GAP

detects toxic alcohols
(methanol, ethylene glycol, isopropanol)

πŸ‘‰ anion gap = acids
πŸ‘‰ osmol gap = alcohols

🧽 ACTIVATED CHARCOAL

Use within 1–2 hrs
life-threatening ingestion

❌ does NOT bind: lithium, iron, alcohols, cyanide

❌ IPECAC

NO LONGER USED

πŸ‘‰ delays charcoal

🚫 GASTRIC LAVAGE

Rare
only if VERY early + life-threatening

πŸ‘‰ not routine

🚿 WHOLE BOWEL IRRIGATION

sustained-release
lithium, iron
body packers

πŸ‘‰ when charcoal doesn’t work

πŸ§ͺ ENHANCED ELIMINATION

HEMODIALYSIS removes:
methanol, ethylene glycol, lithium, salicylates, valproate

πŸ‘‰ works best for small, water-soluble, low Vd

πŸ’§ URINE ALKALINIZATION

↑ salicylate excretion

πŸ‘‰ ion trapping concept

πŸ’Š ANTIDOTES (FREE MARKS)

acetaminophen β†’ NAC
opioids β†’ naloxone
sulfonylurea β†’ octreotide
digoxin β†’ digoxin immune Fab
iron β†’ deferoxamine
toxic alcohols β†’ fomepizole
cyanide β†’ hydroxocobalamin
methemoglobinemia β†’ methylene blue
INH β†’ pyridoxine

πŸ‘‰ THESE ARE STRAIGHT TEST QUESTIONS

πŸ₯ DISPOSITION

SUPPORTIVE CARE = MOST IMPORTANT
fluids, airway, monitoring, ICU if needed

πŸ‘‰ antidotes β‰  everything

😈 EXAM PATTERNS

seizure β†’ benzos
agitation β†’ benzos
wide QRS β†’ sodium bicarb
low BP + CCB β†’ insulin + glucose
pinpoint + ↓RR β†’ opioid
sweaty + tachy β†’ sympathomimetic
dry + hot β†’ anticholinergic
hidden acids β†’ anion gap
hidden alcohols β†’ osmol gap

πŸ‘‰ THIS SECTION = EXAM KEY

⚑ 10-SECOND RECALL

ABCDE FIRST ALWAYS
benzos = seizures + agitation
charcoal early (not Li/iron/alcohols)
dialysis = lithium/salicylates/toxic alcohols
memorize antidotes
supportive care > everything

πŸ‘‰ if panicking β†’ recall this


πŸ’€ TOX LECTURE 4 β€” ONE BIG ULTRA TABLE (TOXIC ALCOHOLS)

CATEGORY

KEY INFO (WHAT TO MEMORIZE)

COMPARE / PATTERN / TRAPS 😈

🧠 CORE IDEA

Toxicity = ACID METABOLITES (NOT alcohol itself)
Methanol β†’ formic acid β†’ blindness
Ethylene glycol β†’ glycolic/oxalic acid β†’ kidney failure
Both β†’ anion gap metabolic acidosis

πŸ‘‰ They will try to trick you with β€œalcohol level”
πŸ‘‰ ALWAYS think acids

⚑ KEY PATHWAY

MeOH/EG β†’ ADH β†’ toxic acids β†’ death

πŸ‘‰ BLOCK ADH = life-saving

πŸ’Š FIRST-LINE TREATMENT

Fomepizole (preferred)
Ethanol (backup)

πŸ‘‰ DO NOT WAIT for labs
πŸ‘‰ β€œif thinking about it β†’ give it”

🎯 WHY BLOCK ADH

Stops formation of toxic acids
Buys time for elimination

πŸ‘‰ doesn’t remove toxin, just prevents damage

πŸ§ͺ DOUBLE GAP (MOST TESTED PATTERN)

↑ Osmol gap + ↑ Anion gap = TOXIC ALCOHOL

πŸ‘‰ THIS = diagnosis clue

⏳ TIME COURSE (VERY HIGH YIELD)

EARLY: ↑ OG, normal AG, mild symptoms
LATE: ↓ OG, ↑ AG, severe acidosis

πŸ‘‰ ❌ Normal OG β‰  safe
β†’ could be late presentation

🚨 WHEN TO SUSPECT

Unexplained acidosis
Altered LOC
↑ AG + ↑ OG
Alcohol use / suicide

πŸ‘‰ If unclear β†’ assume toxic alcohol

🚫 DO NOT WAIT

Start treatment BEFORE confirmation

πŸ‘‰ VERY COMMON EXAM TRAP

πŸ§ͺ TREATMENT ALGORITHM

1. Block ADH (fomepizole)
2. Fix acidosis (NaHCO₃ if pH <7.25)
3. Remove toxin (dialysis)
4. Supportive

πŸ‘‰ MUST know order

πŸ’‰ DIALYSIS INDICATIONS

Severe acidosis
High levels
Renal failure
Very sick patient

πŸ‘‰ ALSO helps correct acidosis

πŸ‘ CLINICAL DIFFERENCES

Methanol β†’ vision loss
Ethylene glycol β†’ kidney failure
Both β†’ metabolic acidosis

πŸ‘‰ vision vs kidney = classic

πŸ’Š BONUS TREATMENT

Methanol β†’ folic acid (helps metabolize formate)

πŸ‘‰ low yield but testable

🧠 WHEN TO GIVE FOMEPIZOLE

OG >10 + history
OR suspicion + β‰₯2:
↓HCO₃ (<20)
↑AG (>16)
↓pH (<7.3)
↑OG (>10)
OR levels: EG >3, MeOH >6

πŸ‘‰ LOW THRESHOLD β†’ GIVE IT ANYWAY

🍺 AKA (ALCOHOLIC KETOACIDOSIS)

↑ AG + mild OG
↑ beta-hydroxybutyrate
low/absent ethanol
improves with glucose + fluids

πŸ‘‰ GETS BETTER with treatment

πŸ”₯ AKA VS TOXIC ALCOHOL

AKA β†’ improves
Toxic alcohol β†’ worsens

πŸ‘‰ HUGE differentiation question

πŸ§ͺ KETONE PEARL

Beta-hydroxybutyrate ↑
Ketone tests NOT sensitive

πŸ‘‰ test limitation = exam trap

πŸ§ƒ ISOPROPYL ALCOHOL (IPA)

↑ OG ONLY
❌ NO anion gap
❌ NO acidosis
causes ketosis (acetone)
fruity breath

πŸ‘‰ ↑ OG without acidosis = IPA

πŸ’Š IPA TREATMENT

Supportive only

πŸ‘‰ NO fomepizole

⚠ EXAM TRAPS

❌ β€œNormal OG = no toxic alcohol” β†’ FALSE
❌ β€œWait for labs” β†’ FALSE
❌ β€œAll alcohols cause acidosis” β†’ FALSE (IPA doesn’t)
❌ β€œAll ↑ OG = toxic alcohol” β†’ FALSE (AKA, DKA etc.)

πŸ‘‰ THESE ARE GUARANTEED TEST QUESTIONS

πŸ§ͺ ANION GAP (AG)

AG = Na - (Cl + HCO₃)
Normal: 6–14
↑ AG β†’ metabolic acidosis

πŸ‘‰ β€œextra acids in blood?”
πŸ‘‰ toxic alcohols β†’ ↑ AG

πŸ§ͺ OSMOL GAP (OG)

OG = measured – calculated
Calculated β‰ˆ 2(Na) + glucose + urea + 1.25Γ—EtOH
Normal: <10

πŸ‘‰ detects toxic alcohols
πŸ‘‰ ↑ OG = alcohols

⏳ TIME COURSE (LABS)

EARLY: ↑ OG, normal AG
LATE: ↓ OG, ↑ AG

πŸ‘‰ ❌ normal OG β‰  safe

πŸ§ͺ pH (ABG)

Normal: 7.35–7.45
↓ pH = acidosis

πŸ‘‰ toxic alcohol β†’ ↓ pH

πŸ§ͺ HCO₃ (BICARB)

Normal: 22–26
↓ HCO₃ = metabolic acidosis

πŸ‘‰ <20 β†’ concerning
πŸ‘‰ <7.25 β†’ treat (NaHCO₃)

πŸ§ͺ WHEN TO TREAT (CUT-OFFS)

pH < 7.3 (suspect)
pH < 7.25 β†’ give bicarbonate
AG > 16
OG > 10

πŸ‘‰ helps decide fomepizole

πŸ§ͺ FOMEPIZOLE THRESHOLDS

EG > 3
MeOH > 6

πŸ‘‰ BUT don’t wait for levels 😈


πŸ’€ TOX LECTURE 5 β€” ONE ULTRA COMPARISON TABLE (APAP vs SALICYLATES vs NSAIDs)

CATEGORY

ACETAMINOPHEN (APAP)

SALICYLATES (ASA)

NSAIDs

🎯 MAIN TOXICITY

Liver failure

Mixed acid-base disorder

Usually mild (GI), severe = CNS + renal

⚑ MECHANISM

CYP2E1 β†’ NAPQI (toxic) β†’ covalent binding + mitochondrial damage

1. Stimulate resp center β†’ resp alkalosis
2. Uncouple oxidative phosphorylation β†’ metabolic acidosis

COX inhibition β†’ ↓ prostaglandins

πŸ’€ CORE PROBLEM

Glutathione depletion β†’ NAPQI damage

Mixed disorder + CNS effects + metabolic stress

Usually supportive, severe rare

⏳ EARLY PRESENTATION

😈 ASYMPTOMATIC (BIG TRAP)

Hyperventilation

Nausea, vomiting, drowsiness

⏳ MID (24–30 hr)

↑ AST/ALT

progressing acid-base issues

usually still mild

⏳ LATE

↑ INR β†’ liver failure

Metabolic acidosis dominates

coma, hypotension (rare)

πŸ§ͺ LAB PATTERN

↑ AST/ALT

Mixed: resp alkalosis + metabolic acidosis

usually normal unless severe

πŸ“Š ACID-BASE

metabolic acidosis (late)

MIXED DISORDER ALWAYS

metabolic acidosis (severe only)

πŸ’Š TOXIC DOSE

10 g OR 200 mg/kg

Mild: 150–200 mg/kg
Severe: 300–500 mg/kg

<200 mg/kg mild
>400 mg/kg severe

πŸ§ͺ KEY LAB TEST

4-hour APAP level (nomogram)

Serial salicylate levels

usually none needed

❌ TRAP (LABS)

❌ cannot check before 4 hrs

❌ single level NOT enough

β€”

πŸ’Š FIRST STEP (EARLY)

Activated charcoal (if early)

Activated charcoal (if not vomiting)

usually none

πŸ’‰ ANTIDOTE

NAC (LIFE SAVER)

❌ none

❌ none

πŸ”₯ TREATMENT CORE

NAC (replenishes glutathione)

GASP:
G = glucose
A = alkali (MOST IMPORTANT)
S = saline
P = potassium

Supportive only

⚑ MOST IMPORTANT TX

NAC ASAP (best <8 hrs but works late)

Sodium bicarbonate (alkalinization)

Supportive

🧠 KEY PEARL

β€œNAPQI = nuclear bomb to liver”

β€œMixed disorder ALWAYS”

β€œUsually mild”

🧠 GLUCOSE PEARL

β€”

Give glucose EVEN if normal (brain starving)

β€”

⚑ ION TRAPPING

β€”

Alkalinize urine β†’ keeps salicylate OUT of brain

β€”

🎯 GOAL pH

β€”

7.45–7.55 (serum)
urine pH 7.5–8

β€”

⚠ POTASSIUM

β€”

MUST correct K⁺ to alkalinize urine

β€”

🚨 DIALYSIS

massive overdose

Severe acidosis, seizures, renal failure, very sick

rarely needed

πŸ’€ MASSIVE OD

Early lactic acidosis + coma

severe CNS toxicity

severe CNS depression

🚫 BIGGEST TRAP

❌ patient looks fine early

❌ DO NOT INTUBATE lightly

❌ assume severe

⚠ INTUBATION DANGER

β€”

↓ RR β†’ acidosis β†’ drug enters brain β†’ death

β€”

🧠 PATTERN RECOGNITION

Initially well β†’ later liver failure β†’ NAC

Hyperventilation + mixed disorder β†’ bicarb

Mild symptoms β†’ supportive

❌ EXAM TRAPS

❌ early normal = safe

❌ normal glucose = no glucose
❌ single level enough

❌ all behave same