0071643192.pdf

(Barré) #1

TOXICOLOGY


Nonsteroidal Anti-Inflammatory Drugs

NSAIDs inhibit the enzyme cyclooxygenase, causing decreased prostaglandin
formation. Prostaglandins have a variety of functions including mediating
pain and inflammation, maintaining the gastric mucosa, and regulating blood
flow in the kidneys. Ibuprofen is the most common NSAID seen in overdose.

MECHANISM/TOXICITY
■ Gastrointestinal irritation (nausea and vomiting) caused by disruption of
the gastric mucosa
■ Large overdoses result in systemic effects from unclear mechanism.
■ Renal insufficiency and GI bleeding are rarein acute overdose.

SYMPTOMS/EXAM
■ Abdominal pain, N/V
■ Altered mental status, seizure, metabolic acidosis

DIAGNOSIS
■ Based primarily on history and physical exam

TREATMENT
■ Supportive and symptomatic therapy

Iron
■ For any given iron compound, it is the amount of elemental iron that
determines its toxicity.

MECHANISM/TOXICITY
■ Direct corrosive effecton gastrointestinal tract
■ Toxicity from free circulating iron→cellular uncoupling of oxidative
phosphorylation and production of free radicals →anaerobic metabolism
and multiorgan failure.

SYMPTOMS/EXAM
Classically described as five phases of toxicity (see Table 6.24), as follows:

TABLE 6.23. Indications for Hemodialysis in Salicylate Toxicity

Level >100 mg/dL (acute ingestions)

Altered mental status

Renal failure

Severe persistent acid-base disturbance

Pulmonary edema

Failure to respond to intensive treatment

A key feature of iron toxicity is
the uncoupling of oxidative
phosphorylation→anaerobic
metabolism.
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