Syndromes of intoxication

An alternative nomenclature (Type I and Type II) has been proposed for subgroups of pyrethroids based not only on the syndromes of intoxication produced in mammals but also on their chemical structures, their signs of poisoning in insects, and their actions on insect nerve preparations [2, 14, 18]. The Type I/II nomenclature has been used in parallel with the T/CS nomenclature, so that Type I and Type II pyrethroids are generally considered to induce T- or CS syndrome, respectively [4]. However, the relationship between the two syndromes and types are neither necessarily confirmed in all pyrethroids nor absolute from the recent available data. 

Self-administration of psychostimulants by humans produces a syndrome of intoxication, the symptoms of which can include elevated pulse and blood pressure, pupillary dilation, euphoria, and psychomotor agitation. Ingestion of excessive amounts can result in compulsive behavior, psychotic symptoms that include auditory and visual hallucinations and paranoid delusions, chest pain, arrhythmias, dyskinesias, and seizures. 

Acute administration of opioids, particularly in non-tolerant individuals, produces a syndrome of intoxication characterized by pupillary dilation and initial euphoria, followed by apathy, psychomotor retardation, slurred speech, and impaired attention and memory. Opioid overdose can produce fatal respiratory depression and thus is a medical emergency. 

Salicylates are widely used for their analgesic and anti-inflammatory properties. They are found in a variety of prescription and over-the-counter analgesics, cold preparations, and topical keratolytic products (methyl salicylate), and even Pepto-Bismol (bismuth subsalicylate). Eiefore the introduction of child-resistant containers, aspirin overdose was one of the leading causes of accidental death in children. Two distinct syndromes of intoxication may occur, depending on whether the exposure is acute or chronic. 

III. Clinical presentation. Two distinct syndromes of intoxication may occur, depending on whether the exposure is acute or chronic. 

Treatment of cholinergic symptoms by autonomic ganglionic blockade would be undesirable in that the effect of such treatment is to abolish sympathetic as well as parasympathetic tone. Removal of sympathetic tone adds to the existing bradycardia and hypotension which form part of the syndrome of intoxication by cholinesterase inhibitors. 

Ethanol also reduces the activity of the noradrenergic system in the locus coeruleus, and alterations in norepinephrine activity may account for some aspects of intoxication and the abstinence syndrome. The 0.2 antagonist clon-idine and the P-receptor antagonist propranolol reduce some symptoms of alcohol withdrawal (Bailly et al. 1992 Carlsson and Fasth 1976 Dobrydnjov et al. 2004 Kahkonen 2003 Petty et al. 1997 Wong et al. 2003). 

Clinical Signs and Symptoms of Intoxication and Abstinence Syndrome... 

One of the major problems In the treatment of patients with vitamin D compounds (l.e., patients with hypoparathyroidism) has been the unpredictable development of hypercalcemia and the syndrome of vitamin D Intoxication. Although this problem may become less serious when some of the faster-acting metabolites and analogues of metabolites of vitamin D become available for clinical use. It Is likely that monitoring of serum levels of... 

In adult patients, the manifestations of PCP use can be grouped into nine clinical patterns of intoxication. Four of these are called major patterns because they may be associated with severe toxicity and often necessitate hospitalization. Patients with major patterns are usually unpredictable symptoms wax and wane, and the patient may abruptly change from one pattern of intoxication to another. Five other symptom complexes are designated as minor patterns since toxicity is usually mild and of short duration. Major Patterns consist of coma, catatonic syndrome, toxic psychosis, and acute brain syndrome. Minor Patterns are lethargy, bizarre behavior, violent behavior, agitation, and euphoria (McCarron et al. 1981b). 

Although most Type I pyrethroids produce the T-syndrome and most Type II pyrethroids produce the CS-syndrome, there are exceptions to this classification. Fenpropathrin, a Type II pyrethroid, and permethrin, a Type I pyrethroid, produce mixed intoxication syndromes depending on the study and animal examined. Lastly, the signs of intoxication may not be independent of the routes of administration [1]. As reported recently, the results of a functional observational battery study of 12 pyrethroids in rats following acute oral exposure did not correlate well with the signs of intoxication following intravenous dosing [19]. 

In extreme cases of intoxication, a Parkinsonism-like syndrome may result, characterized by speech disturbances, muscle spasticity, tremor, memory loss, mental depression, and marked psychic symptoms permanent disability is likely. Psychosis and suicide are established risks of overexposure to carbon disulfide. ... 

Prophylactic and therapeutic administration of Enterosgel to rats with experimental peptic ulcer and ulcerative colitis, significantly decreased the number and surface area of lesions on gastro-intestinal tract (GIT) mucosa and reduced the severity of the syndrome of endogenous intoxication that accompanied these injuries [21, 22]. The first evidence of clinical use of Enterosgel in combined therapy of peptic gastric ulcer and duodenum was reported by S.M. Tkach, who had noted that enterosorp-tion significantly reduced the number of side effects of treatment, and the rate of Helicobacter eradication increased from 83.3 to 93.3% [23]. 

A.M. Mosunov and A.V. Pozdnyakov used Enterosgel for acceleration of regression of hepato-depressive syndrome in patients with severe diffuse liver pathology, and reported shortened terms of disability of these patients from 29.4 3.8 to 18.3 2.4 days [81], A.B. Kaydulov and I.V. Vasilenko observed fast reduction of toxic and abstinent events as well as improved functional state of the Uver and decreased requirement for transfusion therapy in patients with alcoholic intoxication and in patients with abstinence syndrome of moderate severity, treated with Enterosgel [82]. 

It Is clear enough from the available data that no acute cases of intoxication by chemical pollutants have been observed within any part of the Love Canal community, wet or dry. That is, no clusters of cases of acute liver disease, or kidney disease, or pulmonary manifestations, or hemolytic anemia or agranulocytosis, and certainly no peripheral or central nervous system syndromes. 

Later, in his safety update of the NDA on October 17, 1986, Kapit spoke of several cases of a syndrome of fluoxetine-induced hyper-arousal and excessive stimulation... [that] resemble episodes of stimulant drug intoxication. It was especially likely to occur at higher doses, but it could occur at the standard 20 mgs. The state of overstimulation included anxiety, agitation, insomnia, headache, confusion, dizziness, obnubilation [mental clouding], memory dysfunction, tremor, impaired motor coordination. Hyperactivity, hypomania, and mania may sometimes occur. In overdose, the drug produces an even more flagrant stimulant syndrome culminating in seizures. Thus there is a continuum of stimulation effects. 

Chronic neurological sequelae of intoxication included two patients with a persistent cerebellar syndrome and severe cerebellar atrophy (175), one with subcortical dementia (176), and one with a diffuse sensorimotor peripheral neuropathy (177). 

Early signs of intoxication include ataxia, dysarthria, coarse tremor, weakness, and drowsiness. More advanced toxicity can involve progressively impaired consciousness, neuromuscular irritability (myoclonic jerks), seizures, cardiac dysrhythmias, and renal insufficiency. A reversible Creutzfeldt-Jakob-like syndrome has been described (162). The severity of intoxication depends on both the extent and duration of exposure to raised lithium concentrations, as well as idiosyncratic factors. 

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