Toxicology-GI

Question 1

Describe CO poisoning mechanism.

Answer 1

Competes avidly with oxygen for hemoglobin (200 fold greater affinity) -affinity for fetal hemoglobin even higher.

Question 2

How do you treat carbon monoxide poisoning?

Answer 2

100% oxygen and hyperbaric oxygen

Question 3

How do you determine carbon monoxide levels?

Answer 3

A CO-oximeter must be used to determine carboxyhemoglobin (COHb) levels. A regular pulse oximeter will misrepresent carboxyhemoglobin for oxyhemoglobin.

Question 4

What are the major effects of cholinesterase inhibitors?

Answer 4

Muscarinic and nicotinic activators, SLUDGE (Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis).

Question 5

What is the treatment for cholinesterase inhibitors?

Answer 5

Treatment = Atropine blocks receptor activation + Pralidoxime to regenerate cholinesterase.

Question 6

What are the effects of acute lead poisoning?

Answer 6

Abdominal colic and CNS changes.

Question 7

What are the signs of chronic lead poisoning?

Answer 7

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.

Question 8

How does lead poisoning affect children differently?

Answer 8

Additionally in children: growth delay, neurocognitive deficits, and developmental delay.
- Oral succimer used as preferred chelator in children.

Question 9

What are the signs and symptoms of acute arsenic poisoning?

Answer 9

Acute arsenic poisoning severe GI discomfort, rice water stools, vomiting, capillary damage with dehydration and shock (similar to typhoid and cholera) .

Question 10

What are the signs and symptoms of chronic arsenic poisoning?

Answer 10

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.

Question 11

What is the most common source of chronic arsenic poisoning?

Answer 11

Chronic poisoning more often environmental from ground water and soil.

Question 12

What is the action/role of chelators?

Answer 12

• 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.

Question 13

What are the treatments for arsenic, mercury, or lead?

Answer 13

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.

Question 14

What is EDTA?

Answer 14

EDTA (ethylenedinitrilotetraacetic acid) (IV): used before succimer for acute lead poisoning, chelates calcium so use calcium-EDTA salt to avoid hypocalcaemia.

Question 15

What are the ABCDs of treating a poisoned patient?

Answer 15

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.

Question 16

How is acetaminophen metabolized?

Answer 16

In overdose normal metabolism is saturated and it is metabolized in the liver via the P450 system to a toxic metabolite.

Question 17

How does acetaminophen cause toxicity?

Answer 17

The reactive metabolite covalently binds to vital proteins and the lipid bilayer of hepatocytes; this results in hepatic injury and subsequent centrilobular liver necrosis.

Question 18

What should be used to treat acetaminophen poisoning?

Answer 18

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.

Question 19

What is used to treat acetaminophen emergently?

Answer 19

If within 1-2 hours after ingestion of acetaminophen, use activated charcoal.

Question 20

What supportive therapy is suitable for acetaminophen toxicity?

Answer 20

Supportive therapy: IV fluids, oxygen, and cardiac monitor.

Question 21

What are the physiological signs of aspirin toxicity?

Answer 21

• 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.

Question 22

What is the mechanism of aspirin toxicity?

Answer 22

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

Question 23

How should aspirin toxicity be treated?

Answer 23

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

Question 24

What is the best method to quickly remove aspirin and restore acid-base balance in severe poisoning?

Answer 24

Hemodialysis is the best method to quickly remove salicylate & restore acid-base balance & fluids in patients with severe poisoning

Question 25

What are the initial symptoms of iron poisoning?

Answer 25

Initial symptoms of acute iron overdose is vomiting, GI bleeding, lethargy and grey cyanosis. Subsequent signs of severe GI necrosis can occur, pneumonitis, jaundice, seizures and coma.

Question 26

What can’t we use charcoal in iron poisoning and what is the appropriate treatment?

Answer 26

Charcoal does not bind iron therefore use gastric lavage if within 60 minutes, if longer than an hour use whole bowel irrigation

Question 27

What is the chelator of choice in iron toxicity?

Answer 27

Deferoxamine is the chelating agent of choice.