Toxicology Flashcards
Cholinergic toxidrome Cause Mnemonic Most dangerous aspect Treatment
- Caused by pesticides (AchE inhibitors such as organophosphates and carbamates) and mushrooms (muscarine agonists). Sarin nerve gas is also an organophosphate.
- Leaky from all orafaces
- DUMBBELSS: diarrhea, urination, miosis, bradycardia, bronchosecretions, emesis, lacrimation, salivation, sweating
- Bronchosecretions is most dangerous complication
- Treat with atropine (muscarinic receptor antagonist) + pralidoxime (2PAM; regenerates poisoned AchE) if due to pesticide
Anticholinergic toxidrome Cause Problems (8) Most dangerous aspect Treatment
- Inhibition of muscarinic receptors → knocks out parasympathetics
- Caused by Anti’s (anti-histamines, anti-psychotics, anti-depressants, anti-parkinsonians) and Atropine. Classic is a Benadryl overdose.
- Hot as a hare, Red as a beet, Dry as a bone, Blind as a bat, Mad as a hatter
- Hyperthermia, Dry skin (not sweating), Mydriasis, Delirium / hallucinations, tachycardia, urinary retention, seizure, lack of bowel sounds
- # 1 lethal thing is seizures
- Treat w/ physostigmine (reversible inhibitor of AchE)
Sympathomimetic Toxidrome Characteristics (7) Comparison to anticholinergic 2 most dangerous aspects Treatment
- Hyperthermia, sweating, mydriasis, tachycardia, HTN, seizure, active bowel sounds.
- Similar to anticholinergic but w/ sweating and no urinary retention. Agitated instead of delirium / hallucinations.
- 2 most dangerous parts are seizures and HTN
- No antidote. Treat seizures, HTN, and hyperthermia.
What does activated charcoal not remove?
When is it indicated / contraindicated?
PHAILS to remove: pesticides, hydrocarbons, acid / alkali, iron, lithium, and solvents
Only give if ingestion is less than 1 hour ago.
Do NOT give to somnolent pas due to risk of vomiting / aspirations.
Multiple dose activated charcoal
How does it work?
What does it remove?
Interrupts enterohepatic circulation Used to remove ABCD: • Antimalarials / Aminophylline (theophylline) • Barbiturates / Beta blockers • Carbamazepine • Dapsone
When is urinary alkalization useful?
Aspirin and phenobarbital
Hemodialysis
3 main uses
Mnemonic
Types of things dialysis can remove
- Mainly used for aspirin, toxic alcohols, and lithium
- I STUMBLE: isopropryl alcohol, salicylate, theophylline, uremia, methanol, barbiturates, lithium, ethylene glycol
- Hemodialysis only works for agents that are: not protein bound, low MW, small volume of distribution, and water-soluble.
Causes of osmolar gap
ME DIE
Methanol, ethylene glycol, diuretic (osmotic mannitol), isopropyl alcohol, ethanol
Metabolism and toxicities of methanol, ethylene glycol, and isopropyl alcohol
- Methanol → formaldehyde → blindness (snowstorm blindness due to retinal epithelium falling off) and damage to basal ganglia
- Ethylene glycol → glycol aldehyde → Ca-oxalate crystals in urine → renal damage.
- Isopropyl alcohol → hemorrhagic gastritis (from acetone)
MUDPILES
Methanol, uremia, diabetic ketoacidosis (or alcoholic), propylene glycol, iron / isoniazid, lactic acid, ethylene glycol, salicylates
Sxs of aspirin toxicity (4)
Tinnitus, sweating, N/V, acid/base disturbance
Treating aspirin toxicity
Treat w/ urinary alkalization.
Hemodialysis if severe / refractory or CNS sxs are present
4 stages of acetaminophen toxicity
- Stage 1 = 0.5-24 hrs: asymptomatic or N/V
- Stage 2 = 24-72 hrs: RUQ pain, elevated LFTs
- Stage 3 = 72-96 hrs: hepatic phase w/ necrosis, coagulopathies, and multiple organ failure. This is when people die. May need liver transplant.
- Stage 4 = 4-21 days: recovery / no chronic disease
3 side effects of NAC
Allergic rxn (flushing / pruritis / rash; counteract w/ anthistamine), anaphylactoid rxn (bronchospasm / hypotension; use oral instead), vomiting (33%; give anti-emetic or give IV)
When to stop NAC (3)
Stop NAC w/ resolution of sxs, undetectable acetaminophen, and normalization of LFTs
Lead levels correlated to degree of sxs
- Levels up to 50 mcg/dL may be “asymptomatic”
- Levels from 50-70 mcg/dL mild to moderate sxs
- Levels of 70-100 mcg/dL with severe toxicity
Clinical findings of lead poisoning
- CNS: cognitive delay, headache, encephalopathy (coma) if severe
- GI: “lead colic” w/ severe / obscure abdominal pain, nausea, vomiting, spasms of bowel.
- Neuromuscular: WRIST DROP (peripheral neuropathy), weakness, paralysis. NO sensory loss.
- Renal: dysfunction → cellular necrosis w/ glucose, phosphate, and AA’s in urine. May get gout.
- Blood: microcytic hypochromic anemia w/ basophilic stippling. Lead inhibits aminolevulinate dehdratase and final stage of heme synthesis.
- Bone: radiodense metaphyseal lines called “lead lines”
- Vit D increases level of lead in the bone. PTH decreases lead in the bone.
- Dental: dental carries, gingival lead lines, metallic taste.
At what lead level is treatment mandated?
> 45 mcg/dL
3 chelators and problems w/ 2 of them.
- Succimer (oral)
- BAL (British antilewisite). Formulated in peanut oil, so can’t use in pxs w/ peanut allergy
- CaNa2EDTA (IV). May cause renal toxicity. Do not use alone due to risk of redistribution of lead to CNS
Lead levels and treatment
- Toxicity, Sxs or Level >69: BAL + CaNa2EDTA
- Asymptomatic at 45-69: succimer or Parenteral (CaNa2EDTA + BAL)
- 20-44: Chelation controversial
- Less than 20: No chelation
- Stop chelating when lead is
Things that cause sweating (4)
SOAP: sympathomimetic, organophosphate, aspirin, PCP.
Wash sweat w/ soap.
Things that cause horizontal nystagmus (3)
Alcohols, barbiturates, antiepileptics (phenytoin, carbamazepine).
Things that cause vertical / rotary nystagmus (1)
PCP
What is used to reverse a heparin overdose?
Protamine sulfate
