Toxicology Flashcards
Fomepizole
Competitive inhibitor of alcohol dehydrogenase.
Preferred antidote for overdoses of methanol or ethylene glycol.
Methanol intoxication
Is metabolized by alcohol dehydrogenase (ADH) to formaldehyde, which is then converted to formic acid by aldehyde dehydrogenase.
Formic acid is toxic to the optic nerve = blindness with as little as 30 mL ingested. Early formation of formic acid leads to metabolic acidosis.
TCA overdose
Altered mental status, dilated pupils, and wide QRS complex on ECG.
TCAs have anticholinergic properties: dry/flushed skin, decreased bowel sounds, constipation, hyperreflexia, and dilated pupils.
treatment: sodium bicarbonate.
Iron intoxication
Abdominal pain, bloody emesis, metabolic acidosis, and radiopaque tablets on radiography.
Symptoms can begin within 30-60 minutes following ingestion and escalate to circulatory shock after 48 hours.
Free iron’s toxicity to the vasculature, release of serotonin and histamine: injury to mitochondria, lipid peroxidation, and the uncoupling of oxidative phosphorylation. The treatment: stabilize the patient and administer deferoxamine.
Vitamin D toxicity
Polyuria, polydipsia, nocturia, hypercalcemia, and hypercalciuria. Abdominal pain, nausea, vomiting, and occasionally pancreatitis can be seen.
Osmolar gap
is an indication of unmeasured solute in the blood
In a patient who presents with symptoms of alcohol toxicity, an elevated anion gap and osmolar gap + calcium oxalate crystals in their urine strongly suggests?
ethylene glycol toxicity
Salicylates toxicity
Stimulates the respiratory center leading to hyperventilation= respiratory alkalosis.
Early in the presentation of aspirin overdose= isolated respiratory alkalosis. Concomitant production of endogenous acids (not the aspirin itself) leads to a metabolic acidosis.
Salicylates uncouple oxidative phosphorylation leading to numerous end-organ effects.
The diagnosis is confirmed with serum salicylate levels.
Treatment involves administration of sodium bicarbonate and dialysis.
For patients with suspected tricyclic antidepressant (TCA) overdose and widening of the QRS complex, the most appropriate next step in management is?
Administration of sodium bicarbonate.
TCAs toxicity
Have anticholinergic. anti-alpha-adrenergic, anti-histamine, and sodium channel blocking properties, which contribute to their side effects and toxicity.
3 C’s: convulsions, coma, and cardiotoxicity. Cardiotoxicity is the best predictor for TCA overdose and manifests as QRS prolongation.
Patient is presenting from a fire with evidence of smoke inhalation, and should be treated empirically for?
Both carbon monoxide and cyanide poisoning, which involves 100% oxygen and hydroxycobalamin.
Hypophosphatemia and alcoholism
Poor oral intake
Hypocalcemia from poor diet, low magnesium, and low vitamin D all lead to secondary hyperparathyroidism and increased phosphate wasting in the kidney. They are given nutrition, which leads to a refeeding syndrome————-refeeding triggers an increased release of insulin, shifting phosphate (and potassium) back into the cells.
Respiratory alkalosis during the withdrawal: facilitates phosphate (and potassium) shift into the cells via the decreased serum hydrogen concentration.
Most cases of hypophosphatemia are asymptomatic, severe or chronic cases may present with confusion, weakness, bone/muscle pain, and even rhabdomyolysis.