Study Set Content:
Acetaminophen upon conjugation will lead to the release or the development of ()It will then be metabolized by P450 enzyme which will give the ()). The NAC react with glutathione and the NAPQI will lead to the release of sustained of () conjugates (non-toxic).
glucuronide or sulfate (non-toxic moiety). NAPQI or N-acetyl-pbenzo-quinone imine (toxic, mercapturic acid
NAPQI is normally rapidly detoxified until () is depleted
GSH
Children: more than ()mg/kg; children less than () years old are less susceptible
200, 10-12
Adults:
6-7g
APAP manifestations early stage
anorexia, NV (nausea and vomiting)
After 24-48 hours:
AST and ALT levels rise; evident hepatic necrosis
Dx
Nomogram; electrolytes (anion gap), liver enzymes NAC
Monogram to plot plasma acetaminophen levels vs time.
Rumack-Matthew Monogram
Chemical asphyxiant, blocking the aerobic utilization of oxygen by binding to cellular cytochrome oxidase.
Cyanide Poisoning
The bulk of unbound cyanide (80%) is detoxified by metabolism to (), a much less toxic compound that is excreted in the urine.
thiocyanate
HCN exposure: ()ppm; Adult ingestion of Na or K salts – ()
150-200, 200mg
Abrupt onset of profound toxic effects shortly after exposure
headache, nausea, dyspnea, and confusion
Cyanide poisoning dx
Lactic acidosis, elevated venous oxygen saturation; “bitter almond” odor
(bind and detoxify free CN) – causes red chromaturia, skin erythema
Hydroxocobalamin
Na nitrite inj. IV and Na thiosulfate IV
Nithiodote:
Universal Antidote
• 2 parts activated charcoal • 1-part tannic acid • 1-part magnesium oxide
• Forms a protective film relieving inflammation and irritation • Milk, egg albumin prevent absorption by binding with heavy metals
Demulcent
Aconitine/ Aconitum
Aconitum napellus
Tung oil tree
Aleurites fordii or Vernicia fordii
Elephant’s Ear
Alocasia macrorrhiza or Colocasia esculenta
