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The authors reported that "the hazards of amygdalin therapy were evidenced in several patients by symptoms of cyanide toxicity or by blood cyanide levels approaching the lethal range." The study concluded "Patients exposed to this agent should be instructed about the danger of cyanide poisoning, and their blood cyanide levels should be ...
Cyanide poisoning is poisoning that results from exposure to any of a number of forms of cyanide. [4] Early symptoms include headache, dizziness, fast heart rate, shortness of breath, and vomiting. [2] This phase may then be followed by seizures, slow heart rate, low blood pressure, loss of consciousness, and cardiac arrest. [2]
Symptoms include nausea, fever, headaches, insomnia, increased thirst, lethargy, nervousness, various aches and pains in joints and muscles, and a drop in blood pressure. [ 9 ] [ 10 ] [ 11 ] In 2016, the European Food Safety Authority reported that eating three small bitter apricot kernels or half of a large bitter kernel would exceed safe ...
Ingestion may also lead to nausea, mental disturbances, methemoglobinemia, chocolate-colored blood, dizziness, epigastric pain, difficulty in hearing, thready pulse and liver damage. Other symptoms reported via ingestion include hemolytic anemia, porphyria and severe gastrointestinal bleeding. Bone marrow depression also occurs.
The patient survived and was discharged after 9 days of treatment with follow up tests showing no signs of liver damage but based on this case it was estimated that an oral dose of 0.32 mg amatoxin per kg of body mass could be lethal with an approximate lethal dose of alpha-amanitin being 0.2 mg/kg when taken orally.
The symptoms of an opiate toxidrome include the classic triad of coma, pinpoint pupils and respiratory depression [3] as well as altered mental states, shock, pulmonary edema and unresponsiveness. Complications include bradycardia , hypotension and hypothermia .
The progressive symptoms of anatoxin-a exposure are loss of coordination, twitching, convulsions and rapid death by respiratory paralysis. The nerve tissues which communicate with muscles contain a receptor called the nicotinic acetylcholine receptor. Stimulation of these receptors causes a muscular contraction.
Standard treatment for nerve agent poisoning is a combination of an anticholinergic to manage the symptoms, and an oxime as an antidote. [12] Anticholinergics treat the symptoms by reducing the effects of acetylcholine, while oximes displaces phosphate molecules from the active site of the cholinesterase enzymes, allowing the breakdown of ...