Parenteral ingestion

LSD may be self-administered orally, nasally, or by parenteral ingestion however, the oral route is the most common. Doses of 50 to 300 pg are ingested, with a minimum effective dose of 20 to 25 pg. Absorption is rapid and complete regardless of the route of administration. However, food in the stomach slows absorption when ingested. Effects are observed within 5 to 10 min, with psychosis evident after 15 to 20 min. Peak effects have been reported 30 to 90 min after dosing effects decline after 4 to 6 h.4 The duration of effects may be 8 to 12 h. 

Abuse of phencyclidine hydrochloride (PCP) is a national problem that has reached epidemic proportions in urban areas of the United States. The drug is inexpensive, readily obtainable, and is usually used in combination with other drugs such as marijuana, heroin, cocaine, and alcohol (Golden et al. 1982). The routes of PCP use include inhalation, ingestion and parenteral administration. 

Hypophosphatemia is associated with chronic alcoholism, parenteral nutrition with inadequate phosphate supplementation, chronic ingestion of antacids, diabetic ketoacidosis, and prolonged hyperventilation. 

All botulin neurotoxins act in a similar way. They only differ in the amino-acid sequence of some protein parts (Prabakaran et al., 2001). Botulism symptoms are provoked both by oral ingestion and parenteral injection. Botulin toxin is not inactivated by enzymes present in the gastrointestinal tracts. Foodborne BoNT penetrates the intestinal barrier, presumably due to transcytosis. It is then transported to neuromuscular junctions within the bloodstream and blocks the secretion of the neurotransmitter acetylcholine. This results in muscle limpness and palsy caused by selective hydrolysis of soluble A-ethylmalemide-sensitive factor activating (SNARE) proteins which participate in fusion of synaptic vesicles with presynaptic plasma membrane. SNARE proteins include vesicle-associated membrane protein (VAMP), synaptobrevin, syntaxin, and synaptosomal associated protein of 25 kDa (SNAP-25). Their degradation is responsible for neuromuscular palsy due to blocks in acetylcholine transmission from synaptic terminals. In humans, palsy caused by BoNT/A lasts four to six months. 

Accidental overdoses were especially common. Of 576 cases of atropine intoxication, almost half were due to oral ingestion of plant material, particularly by children below the age of five. Opthalmological, liquid medicinal, parenteral and percutaneous overdoses made up the remainder. Significant differences in the source of the drug occurred among age groups, however. Individuals above the age of 61, for example, were inclined to encounter overdosage from eye drops or medicinal plasters. 

IV or IM IV or IM injection can be substituted for the oral dosage form when oral ingestion is precluded for long periods of time. The initial parenteral dosage should be approximately one-half of the previously established oral dosage. A daily maintenance dose of 50 to 100 meg parenterally should suffice to maintain the euthyroid state once established. Close observation of the patient, with individual adjustment of the dosage as needed, is recommended. 

Pharmacokinetics Hydralazine is rapidly absorbed after oral use. Half-life is 3 to 7 hours. Protein binding is 87%, and bioavailability is 30% to 50%. Plasma levels vary widely among individuals. Peak plasma concentrations occur 1 to 2 hours after ingestion duration of action is 6 to 12 hours. Hypotensive effects are seen 10 to 20 minutes after parenteral use and last 2 to 4 hours. Slow acetylators generally have higher plasma levels of hydralazine and require lower doses to maintain control of blood pressure. Hydralazine undergoes extensive hepatic metabolism it is excreted in the urine as active drug (12% to 14%) and metabolites. 

Drugs enter our bodies in various ways. Examples of the modes of entry include dermal, oral ingestion, parenteral such as intravenous and intramuscular route, and inhalational routes. 

Chloramphenicol is rapidly and completely absorbed from the gastrointestinal tract and is not affected by food ingestion or metal ions. Parenteral administration is generally reserved for situations in which oral therapy is contraindicated, as in the treatment of meningitis and septicemia or when vomiting prohibits oral administration. The biological half-life of chloramphenicol is 1.5 to... 

Certain mushrooms, especially those of the genus Inocybe, contain muscarinic alkaloids. Ingestion of these mushrooms causes typical signs of muscarinic excess within 15-30 minutes. These effects can be very uncomfortable but are rarely fatal. Treatment is with atropine, 1-2 mg parenterally. (Amanita muscaria, the first source of muscarine, contains very low concentrations of the alkaloid.)... 

Many drugs can now be delivered rectally instead of by parenteral injection (intravenous route) or oral administration. Generally, the rectal delivery route is particularly suitable for pediatric and elderly patients who experience difficulty ingesting medication or who are unconscious. However, rectal bioavailabilities tend to be lower than the corresponding values of oral administration. The nature of the drug formulation has been shown to be an essential determinant of the rectal absorption profiles. The development of novel absorption enhancers with potential efficacy without mucosal irritation (low toxicity) is very important. The delivery of peptide and protein drugs by the rectal route is currently being explored and seems to be feasible. 

Acute intravasation of barium sulfate into the circulatory system of an adult female patient following a barium enema procedure caused the compound to be deposited in blood vessels throughout the body, including the lungs, and resulted in respiratoryfailure (Cove and Snyder 1974). Acute parenteral administration of barium compounds to animals has been shown to result in paralysis of the respiratory muscles (Roza and Berman 1971). Similar respiratory paralysis is frequently encountered in cases of acute exposure in humans and animals by ingestion or inhalation. Intratracheal administration of barium sulfate into rat lungs produced a mild inflammatory reaction (Huston et al. 1952). Barium sulfate could not be removed by either polymorphonuclear leukocytes or monocytes. A tissue reaction followed however, no fibrosis was observed. Since this mode of entry is similar to inhalation, these results may be significant for cases of inhalation exposure. 

Brain enlargement and cerebral edema were observed upon autopsy of a boy who died after ingesting potassium dichromate (Kaufman et al. 1970). However, more chronic lower exposures to chromium(III) did not result in any somatopsychic changes in patients on total parenteral nutrition (TPN) solutions (Lovrincevic et al. 1996). In this study, the TPN patients were examined for somatopsychic responses. 

Because Al toxicity is a serious iatrogen complication, any preventive measures to avoid exposure to Al is incumbent. Unfortunately, with the current treatment practices, there continues to be a risk that patients receive excessive amounts of Al orally or parenterally. If Al compounds cannot be avoided in patients with renal failure, routine Al tests performed every 3-4 months in serum will identify persons at greatest risk (s-Al levels >100 to 150 pg/L) for chronic Al intoxication. Ideally, any patient with s-Al higher than 40 to 50 pg/L should discontinue Al gels and use other substitutes. These patients should also be warned not to ingest these compounds with liquids containing citrate, for example, fruit juices. 

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