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Alkali ingestion

The most frequent injury following alkali ingestion is esophageal burns. Diffuse circumferential esophageal burns are more common in patients ingesting liquid forms of concentrated alkaline corrosives granular forms tend to produce more oral burns and... [Pg.1226]

B. Acid or alkali ingestions, unless other drugs have also been ingested (charcoal makes endoscopic evaluation more difficult). [Pg.427]

Zinn MB. Quinidine intoxication from alkali ingestion. Tex Med (1970) 66, 64-6. [Pg.277]

In metabolic alkaloses, e.g. excessive alkali ingestion or potassium depletion. [Pg.48]

Ingestible materials get into the mouth through hand-to-mouth contact, and through coughing when inhaled particulate material is removed from the lungs to the throat and then swallowed. Since there are acids, alkalies and enzymes in the gastrointestinal tract, the toxic nature of a compound may be enhanced or diminished. [Pg.5]

SI sol in cold w freely sol in hot w, ale, benz, eth, CS2 and alkali hydroxides. Highly toxic by ingestion and inhalation. Forms salts, of which the Pb salt explds mildly when heated rapidly (Ref 1, [209])... [Pg.707]

Edwards, P.R. and N.W.J. Pumphery. 1982. Ingestion and retention of mercury by sheep grazing near a chlor-alkali plant. Jour. Sci. Food Agric. 33 237-243. [Pg.428]

Several of bariums compounds are explosive as well as toxic if ingested or inhaled. Care should be used when working with barium and other alkali metals in the laboratory or in industry. [Pg.81]

Lead is probably one of the most widely distributed poisons in the world. Not only is the metal poisonous, but most lead compounds are also extremely toxic when inhaled or ingested. A few, such as lead alkalis, are toxic when absorbed through skin contact. [Pg.206]

In livestock, selenium has been found to be the cause of blind staggers and alkali disease. Blind staggers occurs as a result of acute ingestion of seleniferous plants and is characterized by impaired vision, depressed appetite, a tendency to wander in circles, paralysis, and death from respiratory failure. A more chronic syndrome described in horses and livestock is alkali disease, which also is associated with consumption of grains or plants containing selenium. The disease is characterized by lack of vitality, loss of appetite, emaciation, deformed hoofs, loss of hair, erosion of the joints of long bones, anemia, cirrhosis, and cardiac atrophy ... [Pg.624]

Induce emesis with syrup of ipecac if victim is conscious and has not ingested acids, alkali, hydrocarbons, or petroleum distillates... [Pg.67]

Perform gastric lavage if victim is unconscious or in some instances when conscious Administer activated charcoal to bind poison Administer milk or water if alkali, acid, hydrocarbon, or petroleum distillates have been ingested Administer antidote, if one exists, that is specific for the poison... [Pg.67]

The physician is concerned with at least three factors when prescribing antacids (1) Acid rebound (associated with calcium carbonate) (2) milk-alkali syndrome (caused by ingestion of large quantities of alkali) and (3) phosphorus depletion (by aluminum salts). The mechanism of add rebound, especially in the long-term use of caldum carbonate, is poorly understood. It has been established that there is an excessive re-addification of the antrum (pylonc gland area) a number of hours after ingestion of calcium caibonate. [Pg.104]

Factors which decrease availability of the vitamin include (1) biliary obstruction (2) liver damage—cirrhosis, toxins (3) poor food preparation (vitamin is strong-add, alkali, light, and reduction labile) (4) impaired lipid absorption in gut (5) presence of antagonists (6) ingestion of mineral oil (7) sterilization of gut with antibiotics and sulfa drugs and (8) excessive excretion in feces. Availability may be increased by way of storage in the liver and absorption aids, such as bile salts. [Pg.1707]

If the patient has ingested a corrosive poison, such as a strong acid or alkali (e.g., drain cleaners), emesis increases the likelihood of gastric perforation and further necrosis of the esophagus. [Pg.431]

Note Moderately polar, weakly hydrogen bonding solvent, heavy liquid gradually decomposes to acquire a yellow color, air and light will accelerate this decomposition nonflammable commercial product is often stabilized by the addition of 3 to 4% (mass/mass) alcohols highly toxic by ingestion, inhalation, and skin absorption soluble in alcohols, organohalogen compounds, hydrocarbons, benzene, and many oils incompatible with many alkali and alkaline earth metals. Synonyms tribromomethane. [Pg.333]

Metabolic Transit of Lysinoalanine. Urinary and Fecal Excretion of Protein-Bound Lysinoalanine (113). Three different alkali-treated proteins (lactalbumin, fish protein isolate, and soya protein isolate) containing, respectively, 1.79, 0.38, and 0.14 g of lysinoalanine/16 g nitrogen were given to rats and the urines and feces were collected. Lysinoalanine was measured before and after acid hydrolysis. The fecal excretion varied from 33 to 51% of the total ingested lysinoalanine and the urinary excretion varied from 10 to 25%. The higher level of lysinoalanine found after acid hydrolysis indicates that a certain quantity is excreted in the urines as combined lysinoalanine (see Table VII). The total recovery was inferior to the ingested quantity (50 to 71%) indicating that the molecule is transformed or retained in the body of the rat. [Pg.114]

Direct Tests on Stomach Contents. Odour, colour, and pH. Characteristic smells may indicate the presence of substances such as camphor, cresol, cyanide, etiianol and otiier organic solvents, ethchlorvynol, methyl salicyl-ate, paraldehyde, and phenelzine. A high pH may indicate ingestion of alkali. Undegraded tablets or capsules should be retrieved and examined separately. A green or blue colour suggests the presence of iron salts. 2.Salicylates—Trinder s test To 2ml of tiie sample add 2ml of O.IM hydrochloric acid, boil for 10 minutes, filter if necessary, neutralise the filtrate with... [Pg.5]

In such cases, the alkali enters the vapor phase by vaporization from coal minerals, dolomite (10) or limestone, as in sulfurscrubbing processes, or from air-ingested salt particles (e.g., in marine environments). Hardesty and Pohl ( ) have recently reviewed the major problem areas and data limitations relating to the properties of coal mineral matter and ash. [Pg.545]

Most psychoactive drugs come from plants, and there are hundreds of plants with psychoactive properties. People have put most of them to use in one part of the world or another at one time or another. Often drug plants taste bad, are weak, or have unwanted side effects. Traditional peoples who use these plants, such as Native Americans, have come up with clever ways of preparing and ingesting them to maximize the desired effects or make them easier to take. Traditional peoples do not tamper with the chemical composition of the plants, however. For example, South American Indians have found that drying coca leaves and mixing them with ashes or other alkalis increases their stimulant effect. They have also learned to make a powerful snuff from the resin of the virola tree (a DMT-containing plant) in order to take... [Pg.31]

ACGIH TLV TWA 2 mg(Al)/m3 DOT CLASSIFICATION 4.3 Label Dangerous When Wet, Poison SAFETY PROFILE A human poison by inhalation and ingestion. Dangerous in contact with water, steam, or alkali it slowly yields PH3, which is spontaneously flammable in air. Explosive reaction on contact with mineral acids produces phosphine. When heated to decomposition it yields toxic POx. See also ALUMINUM COMPOUNDS, PHOSPHIDES, and PHOSPHINE. [Pg.48]

DOT CLASSIFICATION 6.1 Label KEEP AWAY FROM FOOD SAFETY PROFILE A poison by ingestion. A skin sensitizer upon long or repeated contact. Moderately explosive. When heated to decomposition it emits acrid smoke and fumes and may explode. Explosive reaction with traces of alkalies, alkali earth hydroxides, halide salts, strong acids, mercury salts + strong acids. See also ACETYLENE COMPOUNDS. [Pg.247]

SAFETY PROFILE Poison by ingestion, inhalation, and intraperitoneal routes. Moderately toxic by skin contact. Experimental reproductive effects. Combustible when exposed to heat or flame. To fight fire, use CO2, dry chemical. Thermally unstable. Contact with moisture (water), acids, or alkalies may cause a violent reaction above 40°. Concentrated aqueous solutions may undergo explosive polymerization. Mixture with 1,2-phenylenediamine salts may cause explosive polymerization. When heated to decomposition or on contact with acid or acid fumes, it emits toxic fumes of CN and NOx. See also CYANIDE and AMIDES. [Pg.396]

SAFETY PROFILE A deadly human poison by ingestion. An experimental poison by ingestion, inhalation, intravenous, intraperitoneal, subcutaneous, and intramuscular routes. Moderately toxic by skin contact. Experimental teratogenic and reproductive effects. Human systemic effects body temperature increase, change in heart rate, coma. A skin irritant. Mutation data reported. Phytotoxic. A pesticide. An explosive. Forms explosive salts with alkalies and ammonia. When heated to decomposition it emits toxic fumes of NOx. See also NITRO COMPOUNDS of AROMATIC HYDROCARBONS. [Pg.556]

SAFETY PROFILE Mldly toxic by ingestion. An experimental teratogen. Experimental reproductive effects. Questionable carcinogen with experimental mmorigenic data. Mutation data reported. Potentially explosive reaction with potassium nitrate + sodium peroxide when heated in a sealed container. Mixtures with alkali release carbon monoxide when heated. When heated to decomposition it emits acrid smoke and irritating fumes. [Pg.695]


See other pages where Alkali ingestion is mentioned: [Pg.662]    [Pg.662]    [Pg.261]    [Pg.353]    [Pg.705]    [Pg.7]    [Pg.280]    [Pg.762]    [Pg.5]    [Pg.403]    [Pg.28]    [Pg.51]    [Pg.52]    [Pg.52]    [Pg.104]    [Pg.242]    [Pg.1004]    [Pg.1274]    [Pg.209]    [Pg.403]    [Pg.414]    [Pg.257]    [Pg.37]    [Pg.397]   
See also in sourсe #XX -- [ Pg.100 , Pg.101 ]




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