Paralytic

Curative treatment involves counteracting the paralytic effect of the Ba " ion on the muscle by intravenous infusion of a potassium salt. 

Beri-beri or clinically manifest thiamin deficiency exists in several subforms infantile beri-beri and adult beri-beri. Infantile beri-beri occurs in exclusively breastfed infants of thiamin-deficient mothers. Adults can develop different forms of the disease, depending on their constitution, environmental conditions, the relative contribution of other nutrients to the diet as well as the duration and severity of deficiency. First of all, there is a so called dry or atrophic (paralytic or nervous) form, including peripheral degenerative polyneuropathy, muscle weakness and paralysis. Second, a wet or exudative (cardiac) form exists. In this form, typical symptoms are lung and peripheral oedema as well as ascites. Finally, there is a cerebral form, that can occur as Wernicke encephalopathy or Korsakoff psychosis. Tli is latter form mostly affects chronic alcoholics with severe thiamin deficiency. 

Paralytic ileus 4. Increased AEA levels participate in inhibition of small intestine motility 4. CB antagonists... 

The onset of symptoms of barbiturate toxicity may not occur until several hours after the drug is administered. Symptoms of acute toxicity include CNSand respiratory depression, constriction or paralytic dilation of the pupils tachycardia, hypotension, lowered body temperature, oliguria, circulatory collapse, and coma. The nurse should report any symptoms of toxicity to the primary health care provider immediately. 

Some patients with parkinsonism communicate poorly and do not tell the primary health care provider or nurse that problems are occurring. The nurse observes the patient with parkinsonism for outward changes that may indicate one or more adverse reactions. For example a sudden change in the facial expression or changes in posture may indicate abdominal pain or discomfort, which may be caused by urinary retention, paralytic ileus, or constipation. Sudden changes in behavior may indicate hallucinations, depression, or other psychotic episodes. 

Helicobader pylori hydrochloric acid hypersecretory paralytic ileus photophobia proton pump inhibitor... 

Anorexia, nausea, vomiting, mental depression, confusion, delayed or impaired thought processes, drowsiness, abdominal distention, decreased bowel sounds, paralytic ileus, muscle weakness or fatigue, flaccid paralysis, absent or diminished deep tendon reflexes, weak irregular pulse, paresthesias, leg cramps, ECG changes Hyperkalemia... 

This is another group of diseases characterized by abnormalities in muscle fiber excitability. They are all periodic in the sense that periods of normal behavior are interspersed with periods of abnormally depressed excitability. During these latter phases, which may last for anything from a few hours to several days, there is a characteristic muscular weakness. The conditions are usually subdivided on the basis of serum levels during paralytic episodes, and are thus described as hyperkalemic, normokalemic, or hypokalemic. 

This is not a distinct clinical entity. The most frequent form of the condition is primarily associated with severe cardiac dysfunction often in combination with dysmorphy. It is confusing, however, because a paralytic attack is accompanied by extrasystoles and tachycardia. Serum may be high, low or normal. A familial form of the disorder is exacerbated by cold and high but is relieved by Na loading. It is, however, not associated with any specific changes in serum K. ... 

A fall in serum is commonly associated with hypokalemic periodic paralysis. Primary hypokalemic paralysis is usually first expressed in children and young adults. Paralytic attacks may fluctuate with remarkable frequency, and there is a common diurnal variation in severity, with weakness especially bad in the morning and evening. The condition has an autosomal dominant pattern of inheritance caused by an abnormality in or close to locus lql3. The gene product is unknown. 

Death from overdose of barbiturates may occur and is more likely when more than 10 times the hypnotic dose is ingested. The barbiturates with high lipid solubility and short half-lives are the most toxic. Thus the lethal dose of phenobarbital is 6—10 g, whereas that of secobarbital, pentobarbital, or amo-barbital is 2-3 g. Symptoms of barbiturate poisoning include CNS depression, coma, depressed reflex activity, a positive Babinski reflex, contracted pupils (with hypoxia there may be paralytic dilation), altered respiration, hypothermia, depressed cardiac function, hypotension, shock, pulmonary complications, and renal failure. 

The use of high performance liquid chromatography (HPLC) for the study of paralytic shellfish poisoning (PSP) has facilitated a greater understanding of the biochemistry and chemistry of the toxins involved. HPLC enables the determination of the type and quantity of the PSP toxins present in biological samples. An overview of the HPLC method is presented that outlines the conditions for both separation and detection of the PSP toxins. Examples of the use of the HPLC method in toxin research are reviewed, including its use in the determination of the enzymatic conversion of the toxins and studies on the movement of the toxins up the marine food chain. 

Tetrodotoxin poisoning has been recogniz for more than two thousand years. Japanese historical records show that the consumption of certain species of pufferOsh (Tetraodon spp.) resulted in paralytic intoxication (8), This problem continues in modern times in various i ian countries, especially Japan, where pufferfish are still regarded as a delicacy. Clinical symptoms of TTX intoxication include numbness, paralysis, and in some instances death. In fact, the "zombie state described in the Voodoo religion has been attributed to TTX in potions derived from pufferOsh (9). 

Acute poisoning of humans by freshwater cyanobacteria as occurs with paralytic shellfish poisoning, while reported, has never been confirmed. Humans are probably just as susceptible as pets, livestock, or wildlife but people naturally avoid contact with heavy waterblooms of cyanobacteria. In addition, there are no known vectors, like shellfish, to concentrate toxins from cyanobacteria into the human food chain. Susceptibility of humans to cyanobacteria toxins is supported mostly by indirect evidence. In many of these cases, however, if a more thorough epidemiological study had been possible these cases probably would have shown direct evidence for toxicity. 

The cx)ne snails are predatory, venomous molluscs which use a common general strategy to capture prey (i, 5-7). All 300-500 species of Conus have a specialized venom apparatus, diagrammed in Figure 1 (8). A venom paralytic to the prey is produced in a venom duct and injected through a disposable, harpoon-like tooth (Figure 2). Paralysis of the prey can be remarkably rapid in the case of certain piscivorous cone species, the fish prey is immobilized in less than one second. 

Figure 1. Diagram of the venom duct of Conus. The venom is produced in the venom duct, apparently expelled from the duct into the proboscis by contraction of the venom bulb. Simultaneously, a harpoon-like tooth is transferred from the radula sac to the proboscis. When injection takes place, the venom is pushed through the hollow tooth and flows into the prey through a hole at the tip of the tooth. Typically, fish-hunting cones will strike at a fish only once and grasp the tooth after injection has occurred, effectively harpooning their prey while injecting the paralytic venom. In contrast, snail-hunting cones will usually sting their prey several times before total paralysis occurs. (Reprinted with permission from the Second Revised Edition of Ref. 8. Copyright 1988 Darwin Press, Inc.)...

When a cone snail envenomates its prey, the latter is invariably paralyzed. In all cases, the paralytic toxins in the venom ("conotoxins") appear to be small peptides, most commonly with 3 disulfide bonds (although conotoxins with 2 or 4 S-S bonds... 

The biological targets of paralytic conotoxins are presumably ion channels and receptors in the fish neuromuscular system. Amphibian, avian, and mammalian systems may also be affected by a -, a-, and x-conotoxins. However, specific conotoxins vary in their phylogenetic spectrum and detailed physiological effects in vivo. 

Like the other paralytic toxins from Conus venom, a-conotoxins are small and very tightly folded, structural features which may be advantageous for rapid paralysis of prey (1). a-Conotoxins are typically 13 to 15 amino acids long with two disulfide bridges (see Table III). In addition to the five a-conotoxins shown, two new a-conotoxins (SIA and SIB) from C. striatus have recently been isolated, sequenced, and chemically synthesized. SIA is very unusual because it is 19 amino acid residues long and it contains 6 cysteine residues, three of which are contiguous near the amino terminus (C. Ramilo et al., unpublished results). 

The a -, /z-, and a-conotoxins are the best characterized of the peptides isolated from Conus venoms so far. However, a large number of other peptides are found in these venoms. These comprise both paralytic toxins to immobilize the prey of the cone snail, and other biologically active peptides which are not themselves directly paralytic. Only the briefest overview of these peptide components will be presented here. 

In the fish-hunting cone snail venoms, a- and w-conotoxins are ubiquitously distributed. As noted above, z-conotoxins have only been found in one species. Conus geographus. In addition to these three well-characterized classes, however, a fourth class of paralytic conotoxins has been found. In contrast to the a-, z-, and... 

Another potentially paralytic conotoxin was recently described this was a peptide purified from Conus geographus venom, which like / -conotoxin appeared to target to voltage-sensitive Na channels. However, the structure of "conotoxin GS" [nomenclature of Yanagawa et al. (J7)] was less homologous to / -conotoxins than to the w-conotoxins, which are Ca channel blockers. The same peptide was purified and characterized using a different assay, the induction of highly aberrant behavior upon ic injection of mice (L. J. Cruz, unpublished data). 

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