Atropine absorption

Inhalation and dermal absorption Atropine (2 mg) IV repeat q 5 min, titrate until effective, average dose 6 to >f5 mg -use IM in the held before IV access (establish airway for oxygenation). Pralidoxime chloride (2-PAMC1) 600-f800 mg IM or 1.0 g IV over 20-30 min (maximum 2 g IM or IV per hour). 

Fenvalerate toxicity is antagonized by atropine sulfate or methocarbamol, which may be effective in treating severe cases of poisoning (Hiromori et al. 1986). Conversely, some compounds exacerbate the toxicity of fenvalerate and interfere with a desired use. Domestic cats (Felis domes-ticus) treated with Fendeet (an aerosol mixture of fenvalerate and A-A-diethyl-m-toluamide) to control fleas and ticks sometimes show signs of toxicosis, such as tremors, hypersalivation, ataxia, vomiting, depression, and seizures. Signs usually appeared within hours of topical application, and females and juveniles seem to be the most sensitive groups. The demonstrated ability of N-N-diethyl-m-toluamide to enhance the dermal absorption of fenvalerate is the probable cause of toxicosis (Dorman et al. 1990). 

Nerve agent intoxication requires rapid decontamination to prevent further absorption by the patient and to prevent exposure to others, ventilation when necessary, administration of antidotes, as well as supportive therapy. Skin decontamination is not necessary with exposure to vapor alone, but clothing should be removed to get rid of any trapped vapor. With nerve agents, there can be high airway resistance due to bronchoconstric-tion and secretions, and initial ventilation is often difficult. The restriction will decrease with atropine administration. Copious secretions which maybe thickened by atropine also impede ventilatory actions and will require frequent suctioning. For inhalation exposure to nerve agents, ventilation support is essential. 

Despite the gastrointestinal absorption characteristics discussed above, it is common for absorption from the alimentary tract to be facilitated by dilution of the toxicant. Borowitz et al. (1971) have suggested that the concentration effects they observed in atropine sulfate, aminopyrine, sodium salicylate, and sodium pentopar-bital were due to a combination of rapid stomach emptying and the large surface area for absorption of the drugs. 

Belladonna acts in the same way as atropine it is available as a tincture and in certain polycomponent preparations used for their biliary and intestinal antispasmodic action. Belladonna alkaloids show rapid absorption from the gastrointestinal tract. 

Hyoscyamine is a tertiary amine. It is the levo-isomer to atropine. Tetertiary amines have the potential to cross the bloodbrain barrier and their oral absorption is also considerably better. Other synthetic tertiary amines used for their antispasmodic properties are dicyclomine and phencyclimine. 

Pharmaceutical interactions and modified absorption will not be described here, as they are relatively unimportant in anaesthetic practice, where few drugs are given by the oral route. However, it should be noted that the absorption of drugs from the jejunum may be delayed by drugs, such as opioids or atropine, which reduce gastric motility. 

The method of drug administration or exposure to a poison may impart selectivity to a xenbiotic. For example, atropine can be applied directly to the eye for the dilation of the pupils. Note that eventual absorption into the blood stream from this site will cause systemic effects. Another example would be the topical (skin) application of a local anesthetic such as benzocaine. Monoclonal antibodies, which are specific for chemical functional groups, are tissue and cell-specific natural agents to which drugs can be chemically bonded. 

Opiates produce constipation by affecting receptors in the intestines. Opium extracts were used in this capacity to treat diarrhea. Today there are other related compounds on the market which accomplish the peripheral task without affecting the CNS because of their poor absorption from the Gl tract when taken orally. Imodium A-D , an OTC, contains loperamide. It is also available as a generic OTC. The prescription mixture of diphenoxylate and atropine is called Lomotil . 

The absorption of sulfonamides by diseased animals may be quite different from that observed in healthy individuals of the same species. Experimental rumen stasis, produced by atropine, markedly reduced the absorption of sulfamethazine following its oral administration to sheep. 

The magnetic non-equivalence of the 13C nuclei of the tropane ring in protonated scopolamine [260] and in protonated atropine [261] indicates the tropic acid group to be near C(6) and C(7) in [260] but to be in a position affecting all the carbon nuclei on one side of the tropane ring in [261], (170) The absorption of the equatorial and axial A-methyl 13C nuclei in [261] and [260] respectively may be compared to the corresponding absorptions in methylatropine [262],... 

B. Coadministration of atropine speeds the absorption of a second drug. 

MEXILETINE ANTIMUSCARINICS -ATROPINE Delayed absorption of mexiletine Anticholinergic effects delay gastric emptying and absorption May slow the onset of action of the first dose of mexiletine, but this is not of clinical significance for regular dosing (atropine does not l the total dose absorbed)... 

ANTIMUSCARINICS ANALGESICS - PARACETAMOL Atropine, benzatropine, orphenadrine, procydidine and trihexyphenidyl may slow the onset of action of intermittent-dose paracetamol Anticholinergic effects delay gastric emptying and absorption Warn patients that the action of paracetamol may be delayed. This will not be the case when paracetamol is taken regularly... 

Disposition in the Body. Rapidly absorbed after oral administration but it is usually administered together with a small quantity of atropine and this may delay absorption, especially with high doses. It is extensively metabolised by hydrolysis, hydroxylation, and conjugation with glucuronic acid. The major metabolites are diphenoxylic acid (difenoxin), which is active, and hydroxy-diphenoxylic acid in both free and conjugated forms. About 14% and 50% of a dose, respectively, is excreted in the urine and faeces in 96 hours less than 0.1% of a dose is excreted in the urine as unchanged drug in 24 hours. 

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