Toxicology-GI Flashcards
Describe CO poisoning mechanism.
Competes avidly with oxygen for hemoglobin (200 fold greater affinity) -affinity for fetal hemoglobin even higher.
How do you treat carbon monoxide poisoning?
100% oxygen and hyperbaric oxygen
How do you determine carbon monoxide levels?
A CO-oximeter must be used to determine carboxyhemoglobin (COHb) levels. A regular pulse oximeter will misrepresent carboxyhemoglobin for oxyhemoglobin.
What are the major effects of cholinesterase inhibitors?
Muscarinic and nicotinic activators, SLUDGE (Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis).
What is the treatment for cholinesterase inhibitors?
Treatment = Atropine blocks receptor activation + Pralidoxime to regenerate cholinesterase.
What are the effects of acute lead poisoning?
Abdominal colic and CNS changes.
What are the signs of chronic lead poisoning?
Chronic lead exposure signs include peripheral neuropathy (wrist-drop), anorexia, anemia, tremor, GI symptoms.
- Lead line seen in chronic lead poisoning on gums just above teeth in 50-70% patients.
- Basophilic stippling in red blood cells.
How does lead poisoning affect children differently?
Additionally in children: growth delay, neurocognitive deficits, and developmental delay.
- Oral succimer used as preferred chelator in children.
What are the signs and symptoms of acute arsenic poisoning?
Acute arsenic poisoning severe GI discomfort, rice water stools, vomiting, capillary damage with dehydration and shock (similar to typhoid and cholera) .
What are the signs and symptoms of chronic arsenic poisoning?
Chronic arsenic exposure causes skin changes, hair loss, bone marrow depression, anemia, nausea and GI disturbances.
- Mee’s lines: Transverse white lines that run across the nail, following the shape of the nail moon.
What is the most common source of chronic arsenic poisoning?
Chronic poisoning more often environmental from ground water and soil.
What is the action/role of chelators?
- Chelators form a “chemical cage” about a metal ion sequestering it and preventing binding to cellular molecules and/or facilitating excretion.
- Chelators cannot reverse damage only prevent further damage caused by heavy metals.
What are the treatments for arsenic, mercury, or lead?
1) Dimercaprol (parenterally): acute arsenic and mercury and with EDTA for lead.
2) Succimer (oral): lead in children and adults, for acute mercury and arsenic poisoning
3) Unithiol (oral and IV): acute mercury, arsenic or lead.
What is EDTA?
EDTA (ethylenedinitrilotetraacetic acid) (IV): used before succimer for acute lead poisoning, chelates calcium so use calcium-EDTA salt to avoid hypocalcaemia.
What are the ABCDs of treating a poisoned patient?
Airway: cleared of vomitus or obstruction and oral airway or endotracheal tube inserted if necessary.
Breathing: breathing rate, pulse oximetry, arterial blood gases if doubt. Ventilation if necessary.
Circulation: continuous monitoring pulse, blood pressure, urinary output, and evaluation of peripheral perfusion. Place IV line to monitor serum glucose etc.
Dextrose: patients with altered mental status should receive dextrose challenge unless bedside glucose test indicates hypoglycemia not an issue.
How is acetaminophen metabolized?
In overdose normal metabolism is saturated and it is metabolized in the liver via the P450 system to a toxic metabolite.
How does acetaminophen cause toxicity?
The reactive metabolite covalently binds to vital proteins and the lipid bilayer of hepatocytes; this results in hepatic injury and subsequent centrilobular liver necrosis.
What should be used to treat acetaminophen poisoning?
N-acetylcysteine– increases glutathione stores, combines directly with acetaminophen’s reactive metabolite as a glutathione substitute, and enhances sulfate conjugation
- It should be started as soon as possible before liver damage starts.
What is used to treat acetaminophen emergently?
If within 1-2 hours after ingestion of acetaminophen, use activated charcoal.
What supportive therapy is suitable for acetaminophen toxicity?
Supportive therapy: IV fluids, oxygen, and cardiac monitor.
What are the physiological signs of aspirin toxicity?
- Hyperventilation causes respiratory alkalosis which then causes dehydration & a compensatory metabolic acidosis
- Increased anion gap due to the accumulation of lactate,
- Body temperature may be elevated
- Prolonged bleeding time, GI hemorrhage, nausea & vomiting
- Tinnitus & reversible hearing loss can occur & indicate ototoxicity.
What is the mechanism of aspirin toxicity?
Salicylates cause an uncoupling of oxidative phosphorylation which results in increased oxygen consumption, increased carbon dioxide production, accelerated activity of the glycolytic and lipolytic pathways, depletion of hepatic glycogen, hyperpyrexia
How should aspirin toxicity be treated?
Treatment: ABCs. Gastric lavage may be beneficial up to 60 minutes after salicylate ingestion, if longer that that administer activated charcoal.
- Sodium bicarbonate to alkalinize the urine & increase salicylate excretion and correct acidosis.
- Administer with fluids and potentially a diuretic (furosemide) with additional potassium to correct for hypokalemia which will rapidly develop
What is the best method to quickly remove aspirin and restore acid-base balance in severe poisoning?
Hemodialysis is the best method to quickly remove salicylate & restore acid-base balance & fluids in patients with severe poisoning
