Lacrimators clinical signs

Clinical signs of ocular irritation (lacrimation, hyperemia of the conjunctiva) were observed throughout a 24-week study in rabbits exposed to 3,000 ppm -hexane (Lungarella et al. 1984). These effects were the result of direct contact of -hcxanc vapor with the eye. 

Occlusion of the lacrimal puncta is called atresia when congenital and stenosis when it is acquired. Each produces true epiphora, although congenital cases tend to produce fewer clinical signs and symptoms than do acquired cases. 

The clinical signs of excess acetylcholine at nerve endings mimic hyperactivity of the parasympathetic nervous system. Signs relative to the alimentary tract include excess salivation, lacrimation, abdominal pain, vomiting, intestinal hypermotility, and diarrhea. The muscarinic effects of acetylcholine cause bronchoconstriction and an increase in bronchial secretions. The nicotinic effects of acetylcholine consist of involuntary irregular, violent muscle contractions and weakness of voluntary muscles. Death occurs as a result of respiratory failure. 

Clinical signs Lacrimation Salivation Hair coat Palpebral closure Ocular abnormalities Muscle tone/mass... 

Clinical signs are indistinguishable from organophosphate poisoning. Muscarinic signs include salivation, lacrimation, urinary incontinence, and defecation. Nicotinic signs include muscle tremors and fascicula-tions, convulsions, and respiratory failure (Mahmood and Carmichael, 1986). The muscarinic effects of ana-toxin-a(s) can be suppressed by atropine (Cook et al., 1990), but it is relatively resistant to oxime reactivation, compared with typical organophosphate insecticides, because of the formation of an enzyme-adduct (Hyde and Carmichael, 1991). 

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. 

Regardless of their subclassification, all of these compounds have the identical mechanism of action, which is inhibition of acetylcholinesterase at nerve junctions where the molecule acetylcholine is the neuotransmitter. Most acute signs of toxicity are expressed as uncontrollable activity of the nervous system, which clinically is presented as salivation, lacrimation, urination, defecation, and dyspnea. After lethal doses, death results from failure of the respiratory system. Variations in the specific nerves affected, in how the body metabolizes the individual chemical, in where the chemical enters the body, and in the route of administration employed will change the specific clinical presentation seen for an individual exposure scenario. 

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