Toxicology Flashcards
siallorhea, mydriasis, diaphoresis, hyperactive bowel sounds, hyperreflexia, increased muscle tone
Serotonin Syndrome
dry muycosa, hot red dry skin, mydriasis, normal reflexes and tone
anticholinergic
Lead pipe rigidity, bradyreflexia, normal pupils, fever, diaphoresis, delirium after DA agonist
NMS
Rigor mortis type of rigidity, hyporeflexia, normal pupils and mucosa, mottled skin and diaphoresis, temp very high
Malignant Hyperthermia
inherited sarcomere disorder that is triggered by inhalational anasthesia or succ shortly after surgery
Malignant Hyperthermia
Drugs that can lead to serotonin syndrome
SSRI, MOA, analgesics, antiemetics, linezolid
treatment for severe serotonin syndrome
benzos, cyproheptadine
NMS treatment
bromocrintpine- increase CNS dopamine
dantrolene use? MOA? when to use?
reduces excitation- contraction uncoupling in muscles
- can be used to tx hyperpyrexia in SS, NMS, MH
normal metabolism of acetaminophen?
most is glucoronidation to a non toxic metabolite by the liver. A small amount is by the CYP450 system into NAPQI which is toxic
MOA of acetaminophen toxicity?
large doses depletes glutathione and overwhelms the glucoronidation pathway shifting to more NAPQI formation
MOA of NAC?
replenishes glutathione stores
what is the Rumack Mathew nomogram?
plots serum concentation vs time after ingestion to determine whether or not to treat
when should you not use the Rumack Matthew nomogram?
taking acetaminophen chronically, chronic alcohol abuse, chronic liver disease, time of overdose is not reliable
Malignant Hyperthermia presentation
it is due to hypermetabolism and releasing a large quantity of calcium from the SR after triggering agent like succ
- inc CO2 production, inc O2 consumption, combined resp and metabolic acidosis, heat production, sympathetic upregulation, hyperkalemia, can see seizures but rare
tx of MH?
cooling, stop offending agent, dantrolene
cyanide toxicity most common cause?
smoke from a building fire
MOA of cyanide poisoning?
inihibits mitochondrial oxydative phosphorylation and shift to anaerobic metabolism leading to lactic acidosis
treatment of choice for cyanide poisoning?
hydroxycobalamin- converts HCN to B12
TOC of methemoglobinemia?
methylene blue-converts the MHG to hgb
toxic metabolite of methanol?
formic acid
toxic metabolite of ethylene glycol?
oxalic acid, glycolic acid
where do you find ethylene glycol?
antifreeze, cleaning products
where do you find methanol?
anti freeze, moonshine
which toxic alcohol leads to blindness?
methanol
what happens to the osmolar gap and AGAP over time in toxic alcohol ingestion?
osmol gap decreases and AGAP increases, some recommend to just check anion gap serially because osmol gap is not reliable
when to start fomepizole?
high index of suspiscion wiht an AGAP tht continues to rise without another explanation
lactate gap in ethylene glycol ingestion, explain?
glycolate that is a toxic metabolite in EG breakdown mimics lactate. So if there is a high lactate on blood gas machine because it measures lactate differently than lab assays
reasons to start fomepizole?
ingestion history and very high anion gap without other cause
why does fomepizole dosing need to be increased over the time iots being given?
it induces its own metabolism
should you give bicarbonate to patient with toxic alcohol ingestion?
yes if they are acidotic.
- normalizing the pH can keep the toxic metabolites in their ionized state and thus less able to penetrate tissues such as brain and eye
signs and sx of lithium toxicity
GI symptoms, prolonged QT interval
- chronic toxicity can lead to nephrogenic DI or chronic neuro sx, grand mal seizures
osmol gap
calculated osmolality
measured- calculated normal <10
- (2xNa)+(glc/18)+(BUN/2.8)+(ethanol/3.7)
how is isopropyl alcohol intoxication different than methanol and ethylene glycol?
- no acidosis
- breaks down into acetone so you will see extremely high ketones in the urine
- but will still see a osmol gap
