Central nervous system delayed

The substance is irritating to the eyes, the skin and the respiratory tract. The substance may cause effects on the central nervous system, resulting in impaired functions. Exposure may result in death. The effects may be delayed. Medical observation is indicated. 

The antidotal action of the barbiturates is probably limited to the effects of chlordan on the nervous system. They most likely have no beneficial antagonistic action against the delayed parenchymatous degenerative changes produced by chlordan (4). Therefore, they are primarily only of possible value in acute poisoning in which severe stimulation of the central nervous system may be the primary cause of death. 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

Headache, tachypnea, dizziness, confusion, and chest pain. The casualty may also experience palpitations, dyspnea on exertion, drowsiness, lethargy, hallucination, agitation, nausea, vomiting, diarrhea, and coma. If metal carbonyls have been released, there may be complaints of irritation of the eyes, mucous membrane, and respiratory system. Inflammation of lung tissue (pneumonitis) caused by metal carbonyls can may be delayed 12-36 hours. They may also cause injury to the liver, kidneys, and lungs as well as degenerative changes in the central nervous system. 

Carbon dioxide gas is an asphyxiant, a potent respiratory stimulant, and both a stimulant and depressant of the central nervous system. Fatalities have occurred after people have entered enclosures where air has been largely displaced by CO2. Therefore, fixed, automatic CO2 systems require a time delay pre-evacuation alarm period (often 30 seconds), warning signs, and an alarm signal incorporated into the system design to allow sufficient time for personnel evacuation prior to CO2 release. Verification of the oxygen level must be made prior to reentry. 

Cumulative toxic effects occurred in various animal species receiving repeated small doses of decaborane by oral, intraperitoneal, or cutaneous routes. The rate of recovery was markedly delayed in some animal species surviving repeated doses compared with those that had received a single, large dose. In dogs repeatedly given oral doses of 3mg/kg, the effects on the central nervous system were not pronounced but there was damage to the liver and kidneys. 

SYMPTOMS - Painful vomiting and diarrhea, after a delay of up to an hour or so, eventual collapse of the central nervous system. Ingestion of a large quantity of arsenic, which is rapidly absorbed, and especially if alcohol is also consumed, produces paralytic poisoning the most dangerous form of arsenic intoxication. This causes depression of the CNS and quick death. Caution should be used as large doses may cause vomiting before it can be absorbed. 

Amyotrophic lateral sclerosis (ALS) is a progressive, usually fatal, neurodegenerative disease caused by the degeneration of motor neurons in the central nervous system. No cure has yet been found for ALS. The U.S. Food and Drug Administration (FDA) has approved riluzole as the first drug treatment for the disease. It delays the onset of ventilator-dependence or tracheostomy in selected patients. A Cochrane review states a 9% gain in the probability of surviving one year (see Miller et ah, 2007). 

The risk of tachycardia, hypertension, and cardiotoxicity is increased with coadministration of dronabinol (an antiemetic) and dextroamphetamine. In addition, administration of dextroamphetamine with MAOIs may increase the risk of hypertensive crisis. Al-kalinizing agents can speed absorption (e.g., antacids) or delay urinary excretion (e.g., acetazolamide, thiazide diuretics) of dextroamphetamine, thus potentiating its effects. Gastric or urinary acidifying agents (e.g., ascorbic acid, ammonium chloride) can decrease the effects of dextroamphetamine. Propoxyphene overdose can potentiate amphetamine central nervous system stimulation, potentially resulting in fatal convulsions. 

Drug interactions Proleukin may affect central nervous system function. Therefore interactions could occur following concomitant administration of psychotropic drugs. Concurrent administration of drugs possessing nephrotoxic, myelotoxic, cardiotoxic, or hepatotoxic effects with Proleukin may increase toxicity in these organ systems. Reduced kidney and liver function secondary to Proleukin treatment may delay elimination of concomitant medications and increase the risk of adverse events from those drugs. Beta-blockers and other antihypertensives may potentiate the hypotension seen with Proleukin. 

The gastrointestinal tract is the only system outside the central nervous system (CNS) with significant concentrations of opioid receptors. This reflects their common embryonic origins. Opioids increase intestinal tone and decrease propulsive peristalsis, resulting in delayed gastric emptying and constipation or ileus. Opioids increase common bile duct pressure and decrease bile production and flow, primarily because of spasm of the sphincter of Oddi. The tone of the bile duct itself is also increased. 

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