Nicotine intoxication symptoms

One of the most common substances known to interfere with neurotransmission is nicotine. Neurotoxic effects from nicotine have occurred in children who have ingested nicotine, people who have accidentally ingested nicotine-based insecticides, and even workers who have absorbed nicotine through the skin from handling wet tobacco leaves. The first symptoms of nicotine intoxication include accelerated heart rate, perspiration, and nausea. Later, the heart may slow to such an extent that blood pressure becomes too low. The subject may become drowsy and confused and lapse into a coma. Death occurs from respiratory muscle paralysis. 

The signs of OPC intoxication can develop either immediately or several hours later after the exposure. The intoxication symptoms can develop slowly and sustain for several days in case of more lipophilic compounds that require metabolic activation. The clinical picture of acute OPC intoxication includes muscarine-like and nicotine-like disorders, changes on side of the central nervous system and respiration. Depending upon the substance structure, metabolism rate and direction as well as the evidence of one or another disorder on side of the central nervous system can change. 

A. Oximes are used to treat poisoning caused by cholinesterase inhibitor insecticides and nerve agents, ie, organophosphates, mixtures of organophospho-ms and carbamate insecticides, or pure carbamate insecticide intoxication with nicotinic-associated symptoms. Because of its low toxicity, possible ineffectiveness if treatment is delayed until after the cholinesterase enzyme has aged, ability to reverse nicotinic as well as muscarinic effects, and ability to reduce atropine requirements, pralidoxime should be used early and empirically for suspected cholinesterase inhibitor poisoning. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

The clinical picture of carbaryl intoxication results from inactivation of cholinesterase, resulting in the accumulation of acetylcholine at synapses in the nervous system, skeletal and smooth muscle, and secretory glands. Signs and symptoms of overexposure may include (1) muscarinic manifestations such as miosis, blurred vision, lacrimation, excessive nasal discharge or salivation, sweating, abdominal cramps, nausea, vomiting, and diarrhea (2) nicotinic manifestations including fasiculation of fine muscles and tachycardia and (3) central nervous system manifestations characterized by headache, dizziness, mental confusion, convulsions, coma, and depression of the respiratory center. 

Based on available data from 627 victims treated at St Luke s Hospital, symptoms in order of occurrence were miosis 568 (90.5%), headache 316 (50.4%), visual darkness 236 (37.6%), eye pain 235 (37.5%), dyspnea 183 (29.2%), nausea 168 (26.8%), cough 118 (18.8%), throat pain 115 (18.3%), and blurred vision 112 (17.9%) (Okumura et al, 1998). Cases were defined as severe for seizures or respiratory arrest requiring mechanical ventilation, moderate for respiratory distress or fasciculations, and mild for eye symptoms only. Of 640 cases reported by St Luke s Hospital, degree of intoxication was severe in five, moderate in 107, and mild in 528 victims with nicotinic effects observed in those with moderate or severe symptoms. 

Symptoms of intoxication are as follows when an individual is exposed to low amounts of a nerve agent, the initial symptoms include runny nose, contraction of the pupils, miosis, deterioration of visual accommodation, headache, slurred speech, nausea, hallucination, pronounced chest pain, and an increase in the production of saliva (muscarinic central and peripheral symptoms). At higher doses of a nerve agent the aforementioned symptoms are more pronoimced. Coughing and breathing problems also occur. The individual then may begin to experience convulsions (nicotinic symptoms) and a subsequent disturbed ventilation, coma, and death. At even higher doses an exposed individual would almost immediately go into convulsions and die from ventilation and cardiovascular failure because of the... 

In another letter to Lancet, doctors from Kelo University Hospital confirmed the somewhat unexpected domination of nicotinic signs and symptoms over the muscarinic ones (only one patient had mild bradycardia, 50 beats per minute) and questioned usefulness of treatment of mild cases of sarin intoxication with atropine sulphate eye drops, because of atropine-induced photophobia and poor focusing [25]. 

Acute intoxication by anti-ChE agents causes muscarinic and nicotinic signs and symptoms, and, except for compounds of extremely low lipid solubility, affects the CNS. Systemic effects appear within minutes after inhalation of vapors or aerosols. The onset of symptoms is delayed after GI and percutaneous absorption. Duration of effects is determined largely by the properties of the compound lipid solubility, whether it must be activated to the oxon, stability of the organophos-phorus-AChE bond, and whether aging of phosphorylated enzyme has occurred. 

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