Tox Flashcards
Stages of Ethylene Glycol Tox
1) Acute Neuro Stage <12h (intoxication, cranial neuropathies)
2) Cardiopulmonary stage 12-24h (myocardial dysfunction and pulmonary edema, longQT)
3) Renal Stage 1-3d
4) Delayed Neuro sequelae (1-3w)
Ethylene Glycol : toxic metabolite
Oxalic Acid
Glycolic Acid
Calcium Oxylate
Ethylene Glycol: lab findings
HAGMA
Osmolar Gap
Hypocalcemia
ARF
Ethylene Glycol: management/meds
□ Fomepizole 15mg/kg IV or ethanol
□ Thiamine 100mg IV; 0.25 to 0.5 mg/kg, ie 10-50mg
□ Pyroxidine 1 to 2 mg/kg
□ Calcium (e.g., 10% calcium gluconate, 0.3 to 0.6 mL/kg)
- Hemodialysis
Methanol: metabolism and enzymes
Methanol (ETOH dehydrogenase) –> Formaldehyde
Formaldehyde (Aldehyde dehydrogenase) –> Formic acid
Formic acid (folate) –> CO2 and H20
Methanol: intox clinical
CNS: Putamen Crisis = Leads to parkinsoniasm
Optic Neuropathy = Blindness (snowstorm vision)
GI: after latent period can see massive UGIB
Methanol intox: labs
HAGMA
Methanol intox: management/meds
❏ Fomepizole 15mg/kg IV or ethanol
❏ Folic acid 50mg IV (1mg/kg peds)
❏ Hemodialysis
Acetaminophen : toxic dose
150mg/kg
NAC: mechanism
- APAP –> NAPQI (TOXIC)
- NAC:
○ Precursor to glutathione (which binds NAPQI make nontoxic)
○ Directly binds NAPQI
○ Is a Glutathione substitute
○ Increases non toxic sulfation metabolism
Reduces NAPQI to APAP
APAP/Acetaminophen: tox stages
o Stage 1: 30 min - 24 hours asymptomatic, or nausea, vomiting, diaphoresis, pallor
o Stage 2: 24 – 48 hours asymptomatic OR nausea, vomiting, RUQ tenderness, with elevation of liver enzymes and jaundice
o Stage 3: 72 hours – 96 hours fulminant hepatic failure with jaundice, thrombocytopenia, prolonged PTT, hepatic encephalopathy. Renal failure, cardiomyopathy
o Stage 4: Recovery
ASA toxicity:
Indications for haemodialysis
Altered mental status,,
Renal failure
Liver failure
Pulmonary edema
Severe acidosis
Failure of urine alkalization
ASA level >3 acute and >7 chronic
ASA toxicity
Stages
0 to 4 hours: respiratory alkalosis, tachypnea, tinnitus, GI
4 to 12 hours: respiratory alkalosis with acidosis, Could be normal pH, severe tachypnea, AMS: Lethargy/agitation
12 to 24 hours: Acidosis, Severe tachypnoea, delirium, pulmonary oedema, Seizure,,
ASA toxicity:
Indications for your an alkalinization
ASA level >2.8
Signs of severe toxicity
Acidosis
Increasing ASA levels
Indications of MDAC vs single dose
ABCD
- Antimalrrheals: Quinone, Amanita (mushroom Cyclopeptide), ASA
- Barbs: AED: phenobarb, b-blocker (some)
- Carbamazipine
- D: Dilantin,dapsone
Activated Charcoal PHAILS at treating what?
- Common electrolytes
- Metals—iron, lead, arsenic, lithium
- Mineral acids or bases
- Alcohols
- Cyanide
- Most solvents
- Most water-insoluble compounds (e.g., hydrocarbons)
- Pesticides
- Hydrocarbons
- Acids/Alkali/Alcohols
- Iron
- Lithium, Lead
- Solvents
How to calculate
OSMOLAR GAP
{Osmolarity} = 2Na + gluc + BUN (2 salts+ sticky + bun)
OSM GAP = Measured Osmol - {Calc Osmolarity}
(<10)
How to calculate
ANION GAP
AG= Na - (Cl+Bicarb)
AG= Na- Cl- HCO3
<12
HAGMA
causes
MUDPILES
- C- cyanide (lact acidosis), carbon monoxide,
- A- alcoholic ketoacidosis
- T - toluene (glue sniffing)
- M — Methanol
- U — Uremia- CKD
- D — DKA
- P — Paracetamol, Propylene glycol
- I — Infection, Iron, Isoniazid, IEM
- L — Lactic acidosis
- E — Ethylene glycol
- Ethanol–> lactic acidosis, ketoacidosis
- S — Salicylates
Toxic alcohols and
AG and OG
- Initial: Anion Gap HIGH
-
Later: Anion gap low — Osmolar Gap HIGH
- (as the alcohol is metabolized over time)
Exceptions:
- Coingestion with EtOH: Osmolar gap not high due to lack of metabolism (self-treated) – therefore delay in OG…
Anticholinergics
- give examples
- mechanism of action of toxicity and presentation
- AntiDote
Examples:
- Jimson Weed
- Scopolamine. • Glycopyrrolate
- Atropine
- Benztropine (Cogentin)
- Diphenhydramine and dimenhydrinate (benadryl/Gravol)
- Olanzapin
Mechanism:
- Antagonism of muscarinic receptors
- Antagonism of central muscarinic:
- delirium, agitation, or seizures
- Antagonism of peripheral muscarinic receptors:
- tachycardia, decreased GI motility, urinary retention, and flushed skin
Presentation:
- Mad, Hot, Dry, tachy , mydriasis
AntiDote
- Physostigmine
- Use: if no TCA
- Dont: if TCA used, wide QRS ! or ASA allergy
- Monitor for: bradycardia / cholinergic s/s
Toxicity of halogenated/chlorinated HydroCarbons?
- Myocardial pre-sensitization:
- more sensistive to Catecholamines, VTACH!
- Sudden sniffing death
- Surge in NE/Epi (bec of anything straining or seizing) –> VT
- Rx:
- Beta Blocker! As rx for Vtach! (only time when would come first in ACLS)
8 groups of mushrooms - main toxicity - antidote?
-
Cyclopeptide - DEATH/Liver failure - NAC, pen G
- MDAC, lytes, Dialysis , liver tx
- (amanita phalloide)
- *DELAY s/s
-
Gyromitrin (brain) - Seizures - Pyridoxine (Vit B6)
- AC, benzo
-
Muscarine - SLUDGEBBB- Atropine
- AC
- GI Irritant - N/V/hypovol shock- Nil
- Coprine - Disulf like, post EtOH - Nil
-
Ibotenic Acid - CNS s/s (halluc, sz)- Nil
- amanita muscaria
- Psyolcybin - LSD like- Nil
-
Orellinine- nephrotox - Nil
- Dialysis , lytes
- *DELAY s/s
NAME 1 PILL KILLERS
- TCA ( imipramine)
- Ca channel blockers ( Verapamil, diltiazam)
- Clonidine
- Antimalarials ( quinine, chloroquine)
- Sulfonylureas (glyburide)
- Opioids (long acting?)
- Theophylline
- Camphor
- B blockers( propanolol- MAYBE)
- Diphenoxylate/atropine ( Lomotil)
