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Prerequisite basic sciences
Environmental and chemical toxicities: Pathology review
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Kristen is a 47 year old female who showed up at the ER due to vomiting and diarrhea. Kristen works as a farmer, and tells you that her symptoms started right after she sprayed her crops with insecticides using her bare hands. On clinical examination, her pupils appear constricted. And a few minutes later, Kristen has a seizure.
Next comes Federico, a 9 year old boy who is brought to the ER by his parents after accidentally consuming a bottle of insecticide. His parents mention that he complained of stomach ache, and had repeated episodes of vomiting and diarrhea. Upon clinical examination, you first notice that Federico's breath has a characteristic garlic-like odor.
Lastly, you see Richard and Lucy, a 60 year old couple that arrived at the ER, both complaining of a dull headache and nausea. They seem confused, but they mention that their symptoms started more or less at the same time, while they were both relaxing next to the fireplace. Upon clinical examination, you realize that their skin looks cherry red, so you decide to run a blood test, which reveals high carboxyhemoglobin levels.
Based on their history and presentation, all cases seem to have some form of environmental and chemical toxicity. Toxicity refers to the extent of poisoning or damage to the body due to exposure to a toxic substance. For your exams, the most high yield toxic substances include acetylcholinesterase inhibitors; methanol and ethylene glycol; heavy metals, including arsenic, iron, lead, and mercury; cyanide and carbon monoxide; as well as methemoglobin, which is an endogenous substance that can become toxic at high levels.
Let’s start with acetylcholinesterase inhibitor poisoning. Okay, normally, acetylcholinesterases are enzymes that break down the neurotransmitter acetylcholine, so that it can’t activate the cholinergic receptors in the peripheral and central nervous system. And there are two types of cholinergic receptors, called muscarinic and nicotinic receptors. Now, acetylcholinesterase inhibitors are substances that can irreversibly inhibit the acetylcholinesterases at the neuromuscular junction. As a result, acetylcholine builds up in the neuromuscular junction, leading to overstimulation of its receptors.
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