The most important antidotes and their use. Chemical antidotes. List of used literature
Active methods of emergency detoxification of the body in case of acute poisoning include specific antidote therapy. Its purpose is to bind the poison circulating in the body with appropriate substances (antidotes). In addition, in order to significantly limit the effect of the poison on the corresponding receptors, drugs are used that exhibit antagonistic, i.e. a competitive effect on these receptors for a toxic agent (pharmacological antagonists). Antidotes for poisoning and pharmacological antagonists are used only when it is precisely established which substance caused the acute poisoning.
The existing opinion about the availability of antidotes for any toxic substance is not confirmed by reality. Relatively selective effective antidotes exist for only a few classes of toxic substances. The main antidotes and antagonists are presented in the table.
Basic antidotes for poisoning
The main antidotes and pharmacological antagonists used for acute poisoning by chemical agents - table
| 1 | 2 | 3 |
| Alox | FOS (thiophos, chlorophos, karbofos, armin, etc..) | Subcutaneously 2-3 ml of a 0.1% solution of atropine sulfate in combination with Alox (intramuscular 1 mg/kg) repeatedly. In case of severe intoxication - intravenous atropine sulfate 3 ml repeatedly until signs of “atropinization” appear, + Alox 0.075 g intramuscularly every 13 hours |
| Amyl nitrite | Cyanide acid and its salts (cyanides) | Inhalation contents of 2-3 ampoules |
| Anticholinesterase drugs (physostigmine salicylate, ozerin, etc..) | Atropine, amitriptyline, tubocurarine | Subcutaneously, 1 ml of 0.1% solution of physostigmine salicylate or 1 ml of 0.05% solution of proserine. Contraindications: poisoning with tricyclic antidepressants |
| Antidote, pharmacological antagonist | Name of toxic agent | Doses and methods of use of antidotes and pharmacological antagonists |
| 1 | 2 | 3 |
| Atropine sulfate | Pilocarpine and other cholinergic receptor mimetics, anticholinesterase agents, FOS (chlorophos, karbofos, thiophos, metaphos, dichlorvos) | Subcutaneously, 2-3 ml of 0.1% solution again. In the second stage of poisoning with organophosphorus insecticides - intravenously, 3 ml of a 0.1% solution (with glucose solution) again, to eliminate bronchorrhea and the appearance of dry mucous membranes in the III stage - intravenously drip in 30-50 ml of a 0.1% solution per day until disappearance of bronchorrhea |
| Acetylcysteine | Paracetamol | Orally 140 mg/kg ( loading dose), then 70 mg/kg every 4 hours (up to 17 doses or until plasma paracetamol levels reach zero). |
| Bemegr | Barbiturates, anesthetics (for mild intoxication) | Intravenous slowly 2-5 ml of 0.5% solution 1-3 times a day or drip over 12-15 minutes to 5070 ml of 0.5% solution. If cramps of the limbs occur, the administration is stopped. |
| Vikasol | Anticoagulants are not direct action(neodicoumarin, phenylin, etc.). | Intravenous slowly 5 ml of 1% solution (under the control of prothrombin time). |
| Activated carbon | All toxic substances, except cyanides, iron compounds, lithium | Inside, 3-5 tablespoons or more, in the form of an aqueous slurry. |
| Activated carbon "SKN" | Orally 10 g 3 times a day in between meals. Children under 7 years old - 5 g, from 7 to 14 years old - 7.5 g per dose | |
| Deferoxamine | Iron supplements | To bind iron that is not absorbed in the stomach - 5-10 g of deferoxamine dissolved in water, repeated orally (30-40 g), to remove absorbed iron - intramuscularly 10-20 ml of 10% solution every 3-10 hours . 100 mg deferoxamine binds 8.5 mg iron |
| Antidote, pharmacological antagonist | Name of toxic agent | Doses and methods of use of antidotes and pharmacological antagonists |
| 1 | 2 | 3 |
| Dietixim | When the first manifestations of intoxication appear, 3-5 ml of a 10% solution is administered intramuscularly; moderate severity- 5 ml of a 10% solution 2-3 times a day until a persistent increase in cholinesterase activity in the blood. In severe cases, the dose increases. Treatment is carried out in combination with atropine | |
| Dimercaprol | Compounds of arsenic, mercury, gold, lead (in the presence of encephalopathy) | Intramuscularly, first 5 mg/kg, then 2.5 mg/kg 1-2 times a day for 10 days. It is advisable to combine with thetacine-calcium and penicillamine |
| Dipiroxime | FOS (Chlorophos, karbofos, metaphos, dichlorvos, etc..) | In the initial stage of poisoning - intramuscularly 1 ml of a 15% solution, if necessary, again, in case of severe intoxication - intravenously 1 ml of a 15% solution after 1-2 hours (up to 3-4ml), and in severe cases - up to 7-10 ml 15% solution. Should be combined with atropine sulfate |
| Enterosorbent "SKN" | Alkaloids, glycosides, heavy metal salts | Orally 10 g 3-4 times a day between meals |
| Carbolong | Alkaloids, glycosides, heavy metal salts | Orally 5-10 g 3 times a day between meals |
| Oxygen | Carbon monoxide, cyanide acid, chromium, phosgene, etc. | Inhalation, using special masks, catheters, pressure chambers, etc. |
| Naloxone | Narcotic analgesics | Intramuscularly or intravenously, 0.4-0.8 mg (contents of 1-2 ampoules) repeatedly until breathing normalizes |
| Naltrexone | Narcotic analgesics | Orally 0.25 g daily |
| Sodium bicarbonate | Acids, ethyl alcohol, tricyclic antidepressants, quinidine, etc. | Intravenous drip up to 1500 ml of 4% solution per day |
| Antidote, pharmacological antagonist | Name of toxic agent | Doses and methods of use of antidotes and pharmacological antagonists |
| 1 | 2 | 3 |
| Sodium thiosulfate | Compounds of mercury, arsenic, lead, iodine, cyanide acid and its compounds | For poisoning with metal salts - intravenously 5-10 ml of a 30% solution, for poisoning with cyanide acid and cyanides - intravenously 50-100 ml of a 30% solution (after administration of methylene blue or sodium nitrite) |
| Sodium chloride | Silver nitrate | Gastric lavage with 2% solution |
| Penicillamine | Salts of copper, mercury, lead, arsenic, gold | Orally 1 g per day before meals |
| Pyridoxine | Isoniazid and other isonicotinic acid hydrazide derivatives | Intravenously, 10 ml of 5% solution 2-4 times a day |
| Protamine sulfate | Heparin | Intravenous drip of 1-5 ml of 1% solution (1 ml neutralizes it with 1000 units of heparin) |
| Ethanol | Methyl alcohol, ethylene glycol | Intravenously 10 ml of a 30% solution in a stream or drip of a 5% solution (1 ml/kg per day) orally 100-150 ml of a 30% solution |
| Succimer | Mercury, lead, arsenic | Orally 0.5 g 3 times a day for 7 days intramuscularly 0.3 g 2 times a day for 7 days |
| Activated carbon tablets "KM" | All toxic substances except cyanide, iron compounds, malathion, DDT | Orally 1-1.5 g 2-4 times a day 1-2 hours after meals |
| Thetacine-calcium | Salts of lead, nickel, cobalt, mercury, cardiac glycosides | For acute intoxication, intravenous drip of 10-20 ml of a 10% solution in 250-500 ml of 0.9% sodium chloride solution or 5% glucose solution per day for chronic intoxication - 0.25 g orally 8 times a day or 0. 5 g 4 times a day, after 1-2 days (course of treatment 20-30 days) |
| Antidote, pharmacological antagonist | Name of toxic agent | Doses and methods of use of antidotes and pharmacological antagonists |
| 1 | 2 | 3 |
| Trimefacin | Uranium, beryllium | Intravenous or inhalation in the form of a 5% solution or 2.5% solution in calcium chloride solution |
| Ferocin | Radioisotopes of cesium and rubidium, as well as fission products of uranium | Orally 1 g in the form of an aqueous suspension (in 1/2 glass of water) 2-3 times for 10 days |
| Unithiol | Arsenic compounds, mercury salts, bismuth and other heavy metals, cardiac glycosides, anapriline, amitriptyline, etc. | Subcutaneously, intramuscularly or intravenously, 5-10 ml of a 5% solution (1 ml per 10 kg of body weight): on the 1st day - every 6-8 hours, on the 2nd day - every 8-12 hours, on subsequent days - 1-2 injections per day for 6-7 days or more |
| Cytochrome C | Sleeping pills, carbon monoxide | Intravenous drip of 20-40 ml of 0.25% solution in 250-500 ml isotonic solution sodium chloride or glucose (after a biological test - 0.1 ml of a 0.25% solution intradermally) |
Table of the main antidotes and equivalent means for the treatment of poisoning
Complexons
Complexons (chelate compounds) should be considered the most effective antidotes for metal poisoning. Due to the presence of functional groups such as OH, -SH and -NH in their structure, they can donate electrons to bond with metal cations, i.e. form coordination-covalent bonds. In this form, toxic compounds are removed from the body.
The effectiveness of a chelate compound is largely determined by the number of ligands in its base that can bind to the metal. The more of them, the more stable and less toxic the metal chelate complex. It should be remembered that complexones as antidotes have low selectivity of action. Along with toxic agents, they can bind endogenous ions necessary for the body, such as calcium and zinc.
The final result of such interaction is determined by the affinity of toxic exogenous and essential (endogenous) metals in chelate compounds. In order for a significant reduction in the level of endogenous metals to occur, their affinity for the complexones must exceed their affinity for the endogenous ligand. In turn, the relative rate of metal exchange between endogenous ligands and chelate compounds should exceed the rate of elimination of complexones complexed with metals. If complexones are cleared faster than the metal-endogenous ligand complex, its concentration may not reach the level required to effectively compete with endogenous binding sites.
This factor is especially significant in the case when the withdrawal is carried out through the formation of a ternary complex, i.e. endogenous ligand-metal exogenous complex.
Complexones include:
- deferoxamine,
- thetacine-calcium,
- dimercaprol,
- penicillamine,
- unithiol, etc.
Deferoxamine (desferal)- a complexone that actively binds iron, and to a small extent - essential microelements. Can be used to accelerate the release of aluminum from the body in case of renal failure. Competing for weakly bound iron in such iron-containing proteins as hemosiderin and ferritin, deferoxamine is not able to compete for the iron contained in biological chelate complexes: microsomal and mitochondrial cytochromes, hemoproteins, etc.
Feroxamine(iron complex with deferoxamine) is presented to demonstrate its functional groups. Here, iron is actively contained in a closed system. Dimercaprol, a succimer, traps the metal (m) into a stable heterocyclic ring by covalent bonding.
Two penicillamine molecules are capable of binding one molecule of copper or other metal.
Metabolic products of deferoxamine are excreted by the kidneys, turning the urine dark red. During treatment with deferoxamine, allergic reactions (urticaria, skin rash), collapse (with rapid injection into a vein), deafness, blurred vision, clouding of the lens. Coagulopathy, hepatic and renal failure, intestinal infarction.
Thetacine-calcium (calcium-disodium salt of ethylene-diamintetraoctic acid)- an effective complexon for many divalent and trivalent heavy metals and rare earth elements, in particular for lead, cadmium, cobalt, uranium, yttrium, cesium, etc. It penetrates cell membranes relatively poorly, therefore it binds extracellular metal ions more effectively. The highly polar ionic properties of thetacine calcium prevent its enteral absorption more or less significantly, so it is used primarily for slow intramuscular or intravenous administration.
In thetacine-calcium, calcium is replaced only by ions of those metals and rare earth elements that form a more durable complex (lead, thorium, etc.) than calcium itself. Barium and strontium, whose complex stability constant is lower than calcium, do not react with thetacine-calcium. The use of the antidote thetacin-calcium to mobilize mercury is also ineffective, apparently due to the insignificant entry of this complexone into those tissues where mercury is concentrated, as well as through its less successful competition with bound calcium.
IN large doses Thetacin calcium may cause damage to the kidneys, especially the kidney tubules.
Pentacine— calcium-trisodium salt of diethylenetriamine-pentaoctic acid is also effective as a complexone. Unlike thetacin-calcium, it does not affect the release of uranium, polonium, radium and radioactive strontium. With prolonged administration, the elimination of metals from the body decreases.
After administration of pentacin, dizziness may occur, headache, pain in the chest and limbs, kidney damage.
Dimercaprol (2,3-dimercaptopropanol, British anti-lewisite, BAL). Available as a 10% solution in peanut oil; It is administered intramuscularly, the injections are painful. With its SH groups, dimercaprol forms strong chelate complexes with mercury, arsenic, lead and gold ions, accelerating their removal from the body and the restoration of functional proteins suppressed by the poison. The effectiveness of this antidote increases with a minimum period of use after poisoning. It is ineffective if treatment is given after 24 hours or more.
Therefore they believe that medicinal effects BAL is caused by preventing the binding of metals to components of cells, blood and tissue fluid, rather than by removing already bound poison.
Some dimercaprol derivatives turned out to be less toxic, in particular succimer (dimercaprol succinate) and 2,3-dimercapropane-1-sulfonate. They are more polar than BAL; are distributed predominantly in the extracellular fluid, therefore they damage the cellular structures of blood and tissues to a lesser extent.
Penicillamine - D-3,3-dimethylcysteine hydrochloride (cuprenil)- a water-soluble product of penicillin metabolism. Its D-isomer is relatively non-toxic. Resistant to metabolic degradation. It is used primarily for poisoning with copper compounds or to prevent their accumulation, as well as for the treatment of Wilson's disease.
As an adjuvant, penicillamine is sometimes used in the treatment of lead, gold and arsenic poisoning. Like gold preparations, this antidote inhibits the progression of bone and cartilage destruction, therefore it is used in the treatment rheumatoid arthritis. May cause allergic reactions, dyspepsia, thrombocytopenia, leukopenia, anemia, etc.
Sodium thiosulfate- sulfur-containing antidote. Unlike previous drugs, it does not form complex compounds with metals. Neutralizes halogens, cyanides, arsenic, mercury, and lead compounds.
Oxidizing agents and adsorbents are also widely used as antidotes. Weak solutions of acids, usually organic, were previously widely used to neutralize alkalis, and meadows (sodium bicarbonate, magnesium oxide) were used for acid poisoning. Now the advantage is given not to the neutralization of acids and alkalis, but to their dilution.
Potassium permanganate effective against poisoning with morphine and other alkaloids, phosphorus; tannin - alkaloids and heavy metals. Activated carbon is widely used for oral poisoning with various drugs, as well as alkaloids, heavy metal salts, bacterial toxins, etc. It does not adsorb iron, lithium, potassium, and only to a small extent - alcohol and cyanide. Completely ineffective for poisoning with acids and alkalis, boric acid, tolbutamide, etc.
Repeated doses of activated carbon every 4 hours are effective for poisoning with carbamazepine, digitoxin, theophylline, etc.
Enterosorbents
IN last years In order to eliminate exogenous (as well as endogenous) intoxication, enterosorbents began to be used. These drugs tend to sorb (retain on their surface) toxic agents located in the lumen gastrointestinal tract. Toxic substances can enter here from the outside, be released by diffusion from the blood, be present in digestive juices and bile, or be formed here. Enterosorbents, while not being fully antidotes, help reduce the level of intoxication, thereby protecting the body from damage by poison.
In addition, enterosorbents improve digestion in the stomach and intestines, as they contribute to a more rational action of digestive enzymes on food elements, especially proteins. They help neutralize toxic agents in the liver, improve oxidative processes, processes of breakdown of peroxide compounds, etc. Their high effectiveness has been proven in acute intoxication with microbial toxins, atropine, sibazon, mushrooms, and gasoline.
IN medical practice Mostly carbon and polymer sorbents are used as antidotes, in particular carbon SKN (saturated spherical carbonite) and silicon ones - Polysorb, Enterosgel.
Clinical experience shows that enterosorption is effective in food, drug, industrial poisonings. Enterosorbents are also effective for diseases accompanied by endotoxicosis, in particular the digestive, cardiovascular, respiratory and endocrine systems, allergic diseases, and toxicosis of pregnancy.
Pharmacological antagonists of many drugs
In particular, in case of poisoning with drugs that have a depressant effect on the central nervous system, central nervous system stimulants and analeptics are used:
- caffeine sodium benzoate,
- ephedrine hydrochloride,
- cordiamin,
- bemegrid,
- cititon, etc.
In case of intoxication with poisons that excite the central nervous system, drugs with a suppressive type of action are used as antagonists, in particular ether for anesthesia, often barbiturates, sibazon, etc. In case of poisoning with cholinomimetic or anticholinesterase drugs, anticholinergics are used (usually atropine sulfate, scopolamine hydrobromide), and in case of poisoning with atropine and gangliolytics - anticholinesterase drugs (especially prozerin).
- The antagonist of morphine and other narcotic painkillers is naloxone;
- carbon monoxide, hydrogen sulfide, carbon disulfide, etc. - oxygen in inhalation.
Naloxone is prescribed in an initial dose of 1-2 mg parenterally. Doses are increased for intoxication with codeine and fentanyl. The use of physostigmine salicylate is contraindicated in case of poisoning with tricyclic antidepressants.
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The use of an antidote allows you to prevent the effects of poison on the body, normalize the basic functions of the body, or slow down the functional or structural disorders that develop during poisoning.
Antidotes are of direct and indirect action.
Direct antidote
Direct action - there is a direct chemical or physical-chemical interaction between the poison and the antidote.
The main options are sorbent preparations and chemical reagents.
Sorbent preparations - the protective effect is carried out due to nonspecific fixation (sorption) of molecules on the sorbent. The result is a decrease in the concentration of poison interacting with biological structures, which leads to a weakening of the toxic effect.
Sorption occurs due to nonspecific intermolecular interactions - hydrogen and van der Waals bonds (not covalent!).
Sorption can be carried out with skin, mucous membranes, from digestive tract(enterosorption), from the blood (hemosorption, plasmasorption). If the poison has already penetrated the tissue, then the use of sorbents is not effective.
Examples of sorbents: Activated carbon, kaolin (white clay), Zn oxide, ion exchange resins.
1 gram of active carbon binds several hundred mg of strychnine.
Chemical antidotes - as a result of the reaction between the poison and the antidote, a non-toxic or low-toxic compound is formed (due to strong covalent ionic or donor-acceptor bonds). They can act anywhere - before the poison penetrates the blood, during the circulation of the poison in the blood and after fixation in the tissues.
Examples of chemical antidotes:
To neutralize acids that enter the body, salts and oxides are used, giving aqueous solutions alkaline reaction - K2CO3, NaHCO3, MgO.
in case of poisoning with soluble silver salts (for example AgNO3), NaCl is used, which forms insoluble AgCl with silver salts.
in case of poisoning with poisons containing arsenic, MgO and ferrous sulfate are used, which chemically bind it
in case of poisoning potassium permanganate KMnO4, which is a strong oxidizing agent, uses a reducing agent - hydrogen peroxide H2O2
for poisoning with alkalis use weak organic acids(lemon, vinegar)
poisoning with hydrofluoric acid salts (fluorides), calcium sulfate CaSO4 is used, the reaction produces slightly soluble CaF2
in case of poisoning with cyanides (salts of hydrocyanic acid HCN), glucose and sodium thiosulfate are used, which bind HCN. Below is the reaction with glucose.
Intoxication with thiol poisons (compounds of mercury, arsenic, cadmium, antimony and other heavy metals) is very dangerous. Such poisons are called thiol based on their mechanism of action - binding to thiol (-SH) groups of proteins:
The binding of the metal to the thiol groups of proteins leads to the destruction of the protein structure, which causes the cessation of its functions. The result is a disruption of the functioning of all enzyme systems of the body.
To neutralize thiol poisons, dithiol antidotes (SH-group donors) are used. The mechanism of their action is presented in the diagram.
The resulting poison-antidote complex is removed from the body without causing harm to it.
Another class of direct-acting antidotes is antidotes - complexons (complexing agents).
They form strong complex compounds with toxic cations Hg, Co, Cd, Pb. Such complex compounds are excreted from the body without causing harm to it. Among complexones, the most common salts are ethylenediaminetetraacetic acid (EDTA), primarily sodium ethylenediaminetetraacetate.
Indirect antidote
Indirect antidotes are substances that do not themselves react with poisons, but eliminate or prevent disorders in the body that occur during intoxication (poisoning).
1) Protection of receptors from toxic effects.
Poisoning with muscarine (fly agaric poison) and organophosphorus compounds occurs through the mechanism of blocking the enzyme cholinesterase. This enzyme is responsible for the destruction of acetylcholine, a substance involved in the transmission of nerve impulses from the nerve to the muscle fibers. If the enzyme is blocked, an excess of acetylcholine is created.
Acetylcholine binds to receptors, which signals muscle contraction. With an excess of acetylcholine, random muscle contractions occur - spasms, which often lead to death.
The antidote is atropine. Atropine is used in medicine to relax muscles. Anthropine binds to the receptor, i.e. protects it from the action of acetylcholine. In the presence of acetylcholine, the muscles do not contract and cramps do not occur.
2) Restoration or replacement of a biological structure damaged by poison.
In case of fluoride and HF poisoning, and in case of poisoning with oxalic acid H2C2O4, Ca2+ ions bind in the body. The antidote is CaCl2.
3) Antioxidants.
Poisoning with carbon tetrachloride CCl4 leads to the formation of free radicals in the body. Excess free radicals are very dangerous, they cause damage to lipids and disruption of the structure of cell membranes. Antidotes are substances that bind free radicals (antioxidants), such as vitamin E.
4) Competition with poison for binding to the enzyme.
Methanol poisoning:
When poisoning with methanol, very toxic compounds are formed in the body - formaldehyde and formic acid. They are more toxic than methanol itself. This is an example of lethal fusion.
Lethal synthesis is the transformation in the body during metabolism of less toxic compounds into more toxic ones.
Ethyl alcohol C2H5OH binds better to the enzyme alcohol dehydrogenase. This inhibits the conversion of methanol to formaldehyde and formic acid. CH3OH is excreted unchanged. Therefore, taking ethyl alcohol immediately after methanol poisoning significantly reduces the severity of poisoning.
1. Carbon monoxide (II) - carbon monoxide (CO)
1.1 Anthropogenic sources of input
Household sources (incomplete combustion of gas in stoves and fuel in stoves);
Fires (danger of CO poisoning; 50% of deaths in fires are CO poisoning);
Chemical industry (production of ammonia, soda, methanol synthesis, production
synthetic fibers, coke);
Metallurgical industry (steel production);
- motor transport(more than half of anthropogenic CO).
a. Mechanism toxic effect.
CO combines with hemoglobin, forming carboxyhemoglobin, the ability of the blood to transport oxygen (O2) is disrupted, and there is a lack of oxygen in the body.
b. Acute poisoning.
When inhaling concentrations up to 1000 mg/m3 - heaviness and a feeling of squeezing of the head, strong pain in the forehead and temples, dizziness, tinnitus, redness and burning of the skin of the face, trembling, feelings of weakness and fear, thirst, increased heart rate, feeling of lack of air, nausea, vomiting. Subsequently, while consciousness is maintained, there is numbness, weakness and indifference, a feeling of pleasant languor, then drowsiness and numbness, vagueness of consciousness increase, and the person loses consciousness. Next - shortness of breath and death from respiratory arrest.
At a concentration of 5,000 mg/m 3 - in 20-30 minutes - weak pulse, slowing and stopping of breathing, death.
At a concentration of 14,000 mg/m 3 - in 1-3 minutes - loss of consciousness, vomiting, death.
c. Chronic poisoning.
Headaches, dizziness, weakness, nausea, emaciation, lack of appetite; with prolonged contact - violation cardiovascular systems s, shortness of breath, pain in the heart area.
d. Standards.
MPC (mg/m 3):
MPCr.z. (during the working day) 20.0
60 minutes 50.0
15 minutes 200.0
MPCm.r. 5.0
4th hazard class.
2. Hydrogen cyanide -HCN- hydrocyanic acid
2.1 Anthropogenic sources of input
Chemical and metallurgical industry; combustion of polymers.
Hydrocyanic acid and its salts are present in wastewater from ore processing plants, mines, mines, electroplating shops, and metallurgical plants.
2.2 Toxicity of hydrocyanic acid salts
The toxicity of HCN salts is due to the formation of HCN during their hydrolysis. Hydrogen cyanide causes rapid deterioration due to blocking respiratory enzymes in cells (blocking cytochrome oxidase in mitochondria). Cells cannot consume oxygen and therefore die.
2.3 Acute poisoning
1 mg/m3 - odor.
At high concentrations (more than 10,000 mg/m3) - almost instantaneous loss of consciousness, respiratory and cardiac paralysis.
At lower concentrations, several stages of poisoning occur:
1) initial stage: scratching in the throat, burning-bitter taste in the mouth, salivation, numbness of the mouth, muscle weakness, dizziness, acute headache, nausea, vomiting.
2) Second stage: gradually intensifies general weakness, pain and tightness in the heart area, slow pulse, severe shortness of breath, nausea, vomiting (shortness of breath stage).
3) Stage of convulsions: feeling of melancholy, increasing shortness of breath, loss of consciousness, severe convulsions.
4) Stage of paralysis: complete loss of sensitivity and reflexes, involuntary urination and defecation, respiratory arrest, death.
2.4 Chronic poisoning
Headache, weakness, fast fatiguability, increased general malaise, impaired coordination of movements, sweating, increased irritability, nausea, pain in the epigastric region, pain in the heart.
2.5 MPC for HCN and its salts (in terms of hydrogen cyanide)
MPCr.z. 0.3 mg/m3
MPCs.s. 0.01 mg/m3
MPCv. (in water sources) 0.1 mg/l
1st class of danger.
3. Nitrogen oxides (NOAndNO2)
3.1 Anthropogenic sources of input
Combustion of fossil fuels;
Transport;
Production of nitric and sulfuric acids;
Bacterial decomposition of silage.
3.2 Toxic effects
NO is a blood poison that prevents the transfer of oxygen by hemoglobin.
NO2 - pronounced irritating and cauterizing effect on the respiratory tract, leading to the development of pulmonary edema; thiol poison, blocks SH groups of proteins.
3.3 Acute poisoning
NO - general weakness, dizziness, numbness of the legs. With more severe poisoning- nausea, vomiting, increased weakness and dizziness, decreased blood pressure. In case of severe poisoning - blue lips, weak pulse, slight chills. After a few hours - the condition improves, after 1-3 days - severe weakness, severe headache, numbness of arms and legs, drowsiness, dizziness.
At 8 mg/m3 - odor and slight irritation.
At 14 mg/m3 - irritation of eyes and nose.
Inhalation for 5 minutes 510-760 mg/m 3 - pneumonia.
950 mg/m3 - pulmonary edema for 5 minutes.
Acute poisoning is characterized by two phases:
First - swelling, then - bronchitis and its consequences.
3.4 Chronic poisoning
NO: dysfunction of the respiratory and circulatory organs;
NO2: inflammation of the mucous membrane of the gums, chronic bronchitis.
3.5 Standards
MPCm.r. 0.4 mg/m 3 MPCmr. 0.085 mg/m3
MPCs.s. 0.06 mg/m3 MPC.s. 0.04 mg/m3
3rd hazard class2nd hazard class
4. Sulfur oxide (IV) - sulphur dioxideSO2
4.1 Anthropogenic sources of input
Combustion of coal and petroleum products:
80% - in industry and everyday life;
19% - metallurgy;
1% - transport.
Min S - natural gas, max S - coal, oil (depending on the grade).
In metallurgy - in the smelting of copper, zinc, lead, nickel; from sulfide ores (pyrites)
4.2 Mechanism of action
It has a multilateral general toxic effect. Disturbs carbohydrate and protein metabolism, inhibits enzymes. Has an irritating effect. Disturbs the function of the liver, gastrointestinal tract, cardiovascular system, kidneys.
4.3 Acute poisoning
In mild cases (concentration ~ 0.001% by volume) - irritation of the upper respiratory tract and eyes. Watery eyes, sneezing, sore throat, cough, hoarseness. For moderate damage: general weakness, dry cough, pain in the nose and throat, nausea, pain in the epigastric region, nosebleeds. In severe cases - acute suffocation, painful cough, pulmonary edema, death.
4.4 Chronic poisoning
Violation of the respiratory, cardiovascular systems and gastrointestinal tract. One of the forms of damage is bronchitis: cough, chest pain, shortness of breath, weakness, fatigue, sweating. Liver damage - toxic hepatitis - heaviness and pain in the right hypochondrium, nausea, bitterness in the mouth. Stomach damage - pain on an empty stomach or after eating, heartburn, nausea, loss of appetite, stomach and duodenal ulcers.
4.5 Standards
MPCr.z. 10 mg/m3
MPCm.r. 0.5 mg/m3
MPCs.s. 0.05 mg/m3
Hazard class 2.
5 . Arsenic (As)
5.1.Anthropogenic sources of pollution
Metallurgy (arsenic is an impurity in many ores): production of Pb, Zn, Ni, Cu, Sn, Mo, W;
Production of sulfuric acid and superphosphate;
Combustion of coal, oil, peat;
Production of arsenic and As-containing pesticides;
Tanneries.
Emissions into the air with smoke and wastewater.
5.2 Toxic effects
Thiol poison has a wide spectrum of action:
Metabolic disease;
Increased permeability of vessel walls, destruction of red blood cells (hemolysis);
Destruction of tissues at the point of direct contact with arsenic;
Carcinogenic effect;
Embryotoxic and teratogenic effect.
5.3 Acute poisoning
In mild cases - general malaise, headache, nausea; then - pain in the right hypochondrium and lower back, nausea, vomiting.
Severe poisoning:
When taken orally - metallic taste, burning and dry mouth, pain when swallowing several hours after poisoning.
When entering through the respiratory system - irritation of the upper respiratory tract and eyes - tears, sneezing, coughing, hemoptysis, chest pain, swelling of the face and eyelids.
Then - severe weakness, dizziness, headache, nausea, vomiting, abdominal pain, numbness of fingers and toes. Then - uncontrollable vomiting with blood, convulsions, nosebleeds, hemorrhages in the various parts bodies.
After 8-15 days - sharp pains in the limbs, severe weakness, drowsiness, severe headaches, convulsions, paralysis, death from respiratory paralysis.
5.4 Chronic poisoning
Increased fatigue, weight loss, nausea, dizziness, pain in the limbs, stomach, intestines, chest, throat, cough, swelling of the face and eyelids. Hair and nail loss, hemorrhage, darkening of the skin. Irritability, vomiting, unstable stool, lack of appetite.
5.5 Standards
Arsenic and its inorganic compounds (in terms of arsenic):
MPCs.s. 0.003 mg/m3
MPCv. (water) 0.05 mg/l
Hazard class 2.
6 . Mercury (Hg)
6.1 Anthropogenic sources of input
Obtaining mercury and mercury-containing substances;
Combustion of fossil fuels;
Non-ferrous metallurgy;
Coking of coal;
Production of chlorine and soda;
Burning garbage.
Intake: in the form of vapors, water solubility of salts and organic compounds.
6.2. Toxic effect
Thiol poison has a wide spectrum of action.
The manifestation of the toxic effect depends on the form in which mercury enters the body.
The peculiarity of mercury vapor is its neutrotoxicity, its effect on higher nervous activity.
6.3. Acute poisoning
Mercury vapor:
Symptoms appear 8-24 hours after poisoning.
General weakness, headache, pain when swallowing, fever, bleeding, inflammation in the mouth, abdominal pain, stomach damage (nausea, vomiting, loose stools), kidney damage.
6.4 Chronic poisoning
Mainly - the effect on the central nervous system.
Decreased performance, fatigue, increased excitability. Weakened memory, anxiety, self-doubt, irritability, headaches.
Further - weakness, drowsiness, apathy, emotional instability, trembling of the hands, tongue, eyelids (in severe cases of the whole body). Increased mental excitability, fearfulness, general depression, stubbornness and irritability, weakened memory, neuralgia.
6.5. Standards
Metallic mercury (vapor):
MPCr.z. 0.01 mg/m3
MPCs.s. 0.0003 mg/m3
1st class of danger.
7 . Lead (Pb)
7.1 Anthropogenic sources of input
Lead and lead-zinc plants (non-ferrous metallurgy);
Car exhaust gases (tetraethyl lead is added to increase the octane number);
Wastewater from the following industries: metalworking, engineering,
petrochemical, match, photographic materials;
Burning coal and household waste.
7.2 Toxic effects
Thiol poison, but less toxic than mercury and arsenic.
Affects the central nervous system, peripheral nervous system, bone marrow, blood, blood vessels, genetic apparatus, cells.
7.3 Acute poisoning
Acute (lead salt poisoning): cramping abdominal pain, constipation, general weakness, dizziness, pain in the limbs and lower back.
7.4 Chronic poisoning
Externally: lead (black) border along the edge of the gums, earthy-gray skin color.
Change nervous system.: headache, dizziness, fatigue, irritability, sleep disturbance, memory impairment, epileptic seizures.
Movement disorders: paralysis individual muscles, trembling of hands, eyelids and tongue; pain in the limbs, changes in the blood system - lead anemia, metabolic and endocrine disorders, disorders of the gastrointestinal tract, cardiovascular system.
7.5 Standards
Pb metal. MPCr.z. 0.01 mg/m 3, Pb salts MPC.s. 0.0003 mg/m3,
MPCs.s. 0.003 mg/m3.
Hazard class 2.
8 . Chrome (Cr)
8.1 Anthropogenic sources of input
Emissions from enterprises where chromium is mined, received, processed and used (including electroplating and tanning industries).
8.2 Toxic effects
Toxicity depends on valency:
Cr(VI) > Cr(III) > Cr(II)
Affects the kidneys, liver, pancreas, has a carcinogenic effect. Irritating effect, Cr (VI) is an allergen.
8.3 Acute poisoning
Aerosol compounds of Cr (VI), chromates, bichromates - runny nose, sneezing, nosebleeds, irritation of the upper respiratory tract; in severe cases - acute renal failure.
8.4 Chronic poisoning
Damage to the upper respiratory tract and the development of bronchitis and bronchial asthma; liver damage (functional dysfunction, development of cirrhosis), allergic diseases skin - dermatitis, ulcers, “chromic eczema”.
Chromates - main reason production contact dermatitis on the hands, forearms, face, eyelids.
With prolonged contact with chromium compounds, the likelihood of cancer increases.
8.5 Standards
Cr+6 in terms of CrO3 (chromates, bichromates):
MPCm.r. 0.0015 mg/m3
MPCs.s. 0.0015 mg/m3
1st class of danger.
9 . Copper (Cu)
9.1 Anthropogenic sources of input
Non-ferrous metallurgy enterprises;
Galvanic production;
Burning coal and oil.
9.2 Toxic effects
Thiol poison
9.3 Acute poisoning
If ingested - nausea, vomiting blood, abdominal pain, diarrhea, impaired coordination of movements, death from renal failure.
When inhaling the aerosol - coughing attacks, abdominal pain, nose bleed. Temperature increase.
9.4 Chronic poisoning
Disorders of the nervous system, kidney liver, destruction of the nasal septum.
9.5 Standards
CuSO4 MPC.z. 0.5 mg/m3
MPCm.r. 0.003 mg/m3
MPCs.s. 0.001 mg/m3
Hazard class 2.
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ABSTRACT
on the topic of:
__________________________________________________________
Completed by: student of group 23
A.A. Firman
Checked:
Novosibirsk, 2010
1. The concept of an antidote
2. Delayed-acting toxic substances
3. Antidote therapy when affected by slow-acting substances
Antidote concept
Antidote or antidote (from ancient Greek ἀντίδοτον, lit. - given against) - medicine, stopping or weakening the effect of poison on the body.
Antidotes (antidotes)- substances capable of reducing the toxicity of a poison by physical or chemical action on it or by competing with it when acting on enzymes and receptors.
The choice of antidote is determined by the type and nature of the action of the substances that caused the poisoning; the effectiveness of use depends on how accurately the substance that caused the poisoning is identified, as well as on how quickly assistance is provided.
Depending on the mechanism of action, several groups of antidotes are distinguished:
· Sorbents are antidotes whose action is based on physical processes (activated carbon, Vaseline oil, polyphepane).
· Antidotes that neutralize poison by chemical interaction with it (potassium permanganate, sodium hypochloride), which leads to the formation of less toxic substances.
Antidotes are designed to influence the kinetics of a toxic substance entering the body, its absorption or elimination, reduce the effect of poison on receptors, prevent dangerous metabolism, and eliminate threatening disorders of the functions of organs and systems caused by poisoning. IN clinical practice antidotes and other medications used for poisoning are used in parallel with general resuscitation and detoxification methods of treatment. And in cases where resuscitation measures cannot be carried out, the victim’s life can only be saved by administering an antidote.
Currently, antidotes have been developed only for a limited group of toxicants. In accordance with the type of antagonism to the toxicant, they can be classified into several groups (Table 1).
Table 1. Antidotes used in clinical practice
| Type of antagonism | Antidotes | Toxicant |
| 1.Chemical | EDTA, unithiol, etc. Co-EDTA and other nitrous acid Na amyl nitrite diethylaminophenol antibodies and Fab fragments | heavy metals cyanides, sulfides -//- -//- glycosides FOS paraquat toxins |
| 2.Biochemical | Oxygen reactivators ChE are reversible. inhibit. ChE pyridoxine methylene blue | SO FOS FOS hydrazine methemoglobin formers |
| 3.Physiological | atropine and others aminostigmine and others sibazone and others flumazenil naloxone | FOS, carbamates anticholinergics, TAD, antipsychotics GABA-lytics benzodiazepines opiates |
| 4.Modification of metabolism | Na thiosulfate acetylcysteine ethanol 4-methylpyrazole | cyanide acetaminophen methanol, ethylene glycol |
There are no true antidotes, that is, substances that would completely neutralize the effect of poison in the body.
The use of an antidote allows you to prevent the effects of poison on the body, normalize the basic functions of the body, or slow down the functional or structural disorders that develop during poisoning.
Antidotes are of direct and indirect action.
Direct action antidote.
Direct action - direct chemical or physical– chemical interaction between poison and antidote.
The main options are sorbent preparations and chemical reagents.
Sorbent drugs – the protective effect is carried out due to nonspecific fixation (sorption) of molecules on the sorbent. The result is a decrease in the concentration of poison interacting with biological structures, which leads to a weakening of the toxic effect.
Sorption occurs due to nonspecific intermolecular interactions - hydrogen and van - der– Waals bonds (not covalent!).
SorptionIt is possible to carry out from the skin, mucous membranes, from the digestive tract (enterosorption), from the blood (hemosorption, plasma sorption). If the poison has already penetrated the tissue, then the use of sorbents is not effective.
Examples of sorbents: activated carbon, kaolin (white clay), oxideZn, ion exchange resins.
1 gram of active carbon binds several hundred mg of strychnine.
Chemical antidotes - as a result of the reaction between the poison and the antidote, a non-toxic or low-toxic compound is formed (due to strong covalent ionic or donor-acceptor bonds). They can act anywhere - before the poison penetrates the blood, during the circulation of the poison in the blood and after fixation in the tissues.
Examples of chemical antidotes:
To neutralize acids that have entered the body, salts and oxides are used, which give an alkaline reaction in aqueous solutions - K 2 CO 3, NaHCO3, MgO.
in case of poisoning with soluble silver salts (for exampleAgNO 3) useNaCl, which forms insoluble with silver saltsAgCl.
for poisoning with poisons containing arsenic, useMgO, ferrous sulfate, which chemically bind it
in case of poisoning with potassium permanganateKMnO4, which is a strong oxidizing agent, use a reducing agent - hydrogen peroxide H2O2
in case of alkali poisoning, use weak organic acids (citric, acetic)
poisoning with hydrofluoric acid salts (fluorides) use calcium sulfateCaSO4, the reaction produces slightly solubleCaF 2
in case of poisoning with cyanides (salts of hydrocyanic acid HCN ) glucose and sodium thiosulfate are used, which bind HCN . Below is the reaction with glucose.
Intoxication with thiol poisons (compounds of mercury, arsenic, cadmium, antimony and And other heavy metals). Such poisons are called thiol based on their mechanism of action - binding to thiol (- SH ) protein groups:
The binding of the metal to the thiol groups of proteins leads to the destruction of the protein structure, which causes the cessation of its functions. The result is a disruption of the functioning of all enzyme systems of the body.
To neutralize thiol poisons, dithiol antidotes are used (donors SH -groups). The mechanism of their action is presented in the diagram.
The resulting poison-antidote complex is removed from the body without causing harm to it.
Another class of direct-acting antidotes is antidotes—complexones (complexing agents).
They form strong complex compounds with toxic cations Hg, Co, Cd, Pb. Such complex compounds are excreted from the body without causing harm to it. Among complexones, the most common salts are ethylenediaminetetraacetic acid (EDTA), primarily ethylenediaminetetraacetate sodium
Indirect antidote.
Indirect antidotes are substances that do not themselves react with poisons, but eliminate or prevent disorders in the body that occur during intoxication (poisoning).
1) Protection of receptors from toxic effects.
Poisoning with muscarine (fly agaric poison) and organophosphorus compounds occurs by the mechanism of blocking the enzyme cholinesterase. This enzyme is responsible for the destruction of acetylcholine, a substance involved in the transmission of nerve impulses from the nerve to the muscle fibers. If the enzyme is blocked, an excess of acetylcholine is created.
Acetylcholine binds to receptors, which signals muscle contraction. When there is an excess of acetylcholine, random muscle contractions occur - cramps, which often lead to death.
The antidote is atropine. Atropine is used in medicine to relax muscles. Anthropine binds to the receptor, i.e. protects it from the action of acetylcholine. In the presence of acetylcholine, the muscles do not contract and cramps do not occur.
2) Restoration or replacement of a biological structure damaged by poison.
For fluoride poisoning and HF , for poisoning with oxalic acid H2C2O 4 the binding of Ca2+ ions occurs in the body. Antidote –CaCl 2.
3) Antioxidants.
Carbon tetrachloride poisoningCCl4 leads to the formation of free radicals in the body. Excess free radicals are very dangerous, they cause damage to lipids and disruption of the structure of cell membranes. Antidotes are substances that bind free radicals (antioxidants), such as vitamin E.
4) Competition with poison for binding to the enzyme.
Methanol poisoning:
When poisoning with methanol, very toxic compounds are formed in the body - formaldehyde and formic acid. They are more toxic than methanol itself. This is an example of lethal fusion.
Lethal synthesis – transformation in the body during metabolism of less toxic compounds into more toxic ones.
Ethyl alcohol C 2 H 5 OH binds better to the enzyme alcohol dehydrogenase. This inhibits the conversion of methanol to formaldehyde and formic acid. CH3OH is output unchanged. Therefore, taking ethyl alcohol immediately after methanol poisoning significantly reduces the severity of poisoning.
An antidote is a special medicine that allows you to neutralize poison in the human body. Therapy is effective if the antidote is used at the first signs of the pathological process.
It is equally important to diagnose poisoning in time, since the use of an antidote often provokes the appearance of acute psychosis. In case of development of toxic effects medicinal product on the patient’s body, it is necessary to carry out resuscitation measures.
The antidote should be administered with caution to patients suffering from heart failure, since there is a high risk of developing vascular complications. In many patients, symptoms of acute poisoning quickly disappear with adequate antidote therapy.
Distribution of substances by groups
For acute intoxication, the following antidotes are used:
- sorbents;
- medications that neutralize toxins;
- compounds similar to poisons (amyl nitrite, methyl alcohol);
- competitors of toxic substances of exogenous nature;
- drugs that disrupt the metabolism of poison;
- immunological preparations (serums).
The classification of antidotes facilitates their use in cases of severe poisoning and allows the additional use of the entire arsenal of drugs for symptomatic therapy.
The antidote prevents the development of complications from poisoning with drugs, household chemicals, pesticides, plant and animal poisons. The most common intoxications are hypnotics and tranquilizers, analgesics, and disinfectants. An antidote allows you to completely neutralize a toxic substance or prevent its further absorption.
Antidotes are used to treat intoxication in strictly defined doses, introduced into the patient’s body through intramuscular and intravenous injections or respirable aerosol.
Powerful sorbents
Antidotes exhibit chemical antagonism towards poisons. To provide emergency assistance the following substances are used:
- zinc oxide;
- white clay (kaolin);
- starch paste;
- Activated carbon.
To treat intoxication after taking pilocarpine hydrochloride (aceclidine), use a 0.1% solution of potassium permanganate. Then adsorption is carried out with activated carbon. The unabsorbed part of the poison is removed from the body with the help of kaolin in case of poisoning with heavy metal salts or drugs.
The drugs Enterodes or Enterosorb are used for food poisoning and take them several times a day in the dose prescribed by the doctor. If acute intoxication with a narcotic substance has developed, the patient is prescribed activated carbon and the adsorbent Polyphepan.
Polysorb quickly removes toxins from the body. Smecta - aluminosilicate of natural origin, prevents the loss of water and electrolytes during acute poisoning. Carbolene adsorbs alkaloids, gases, and heavy metal salts. In case of acute intoxication with ethyl alcohol, the drug Carbactin has the greatest antitoxic effect. It is used as a first aid remedy for chronic alcoholism.
Therapy of acute and chronic poisoning
In case of prolonged intoxication of the body, which appears against the background of poisoning, the drug Unitol is used, which provides antiarrhythmic effect. It is effective during the period of resorptive action of the poison after an overdose of cardiac glycosides. The antidote is used to treat acute carbon monoxide poisoning. In the body of a patient suffering from alcoholism, Unitol forms a non-toxic substance with ethyl alcohol. The drug is prescribed to treat arsenic poisoning.
The drug is not used in geriatric patients suffering from allergies, hypertension Stages II-III, pregnant women. Antidotes are powerful weapons in the fight against poisons, but in some cases Unitol causes the following adverse reactions:
- nausea;
- vomiting;
- headache;
- rapid heartbeat.
In patients suffering from chronic alcoholism, the drug improves the functioning of the central nervous system and prevents the development of visual and auditory hallucinations. It should be remembered that Unitol is not used for the treatment of acute ethyl alcohol poisoning. In any case, it is used only as prescribed by a doctor.
Antidote for cyanide poisoning
Antidotes have proven to be indispensable medicinal products, preventing fatal poisoning and death. Amyl nitrite is a drug that relaxes the smooth muscles of the coronary and cerebral vessels. In acute cyanide poisoning, it reduces the oxygen demand of the heart muscle, but affects the frequency of myocardial contractions and causes an accelerated heartbeat. The antidote is successfully used in medical practice and is highly effective against poisoning with hydrocyanic acid salts.
The drug prevents the development of sexual disorders in a patient after prostate surgery. Caution must be exercised when using antivenom. The drug should not be prescribed to patients suffering from anemia or thyrotoxicosis. The use of an antidote in a patient who has suffered an acute myocardial infarction or traumatic brain injury may cause the development of adverse reactions.In no case should Amyl Nitrite be used for inhalation in a pregnant woman, and the likelihood of a decrease in blood pressure, even collapse, should be taken into account. simultaneous administration antidote with ethanol.
How to neutralize the effects of poisons and drugs
Toxic substances affect the brain and cause severe mental disorders. Convulsive poisons include:
- cicutotoxin;
- tetraethyl lead;
- curare;
- coniine;
- atropine;
- strychnine.
Antidote to the opioid drug Morphine and narcotic analgesics Omnopon, Promedol, Fentanyl is their antagonist Naloxone, which is administered intramuscularly or intravenously as needed. In case of poisoning with tranquilizers, Flumazenil solution is used for treatment, eliminating the consequences of intoxication - shortness of breath, memory loss. The drug should be prescribed with caution to elderly and old age and administered intravenously only under the supervision of a physician.An overdose of the drug LSD leads to the development of toxic shock. The antidote is the drug Aminazine, which eliminates hallucinations. In some cases, for liquidation acute symptoms poisoning use the tranquilizer Diazepam and the anticonvulsant drug Phenobarbital.
In some cases, severe adverse reactions occur after the use of antidotes:
- arrhythmia;
- increased blood pressure;
- pulmonary edema;
- respiratory depression.
Serums in the fight for life
After a cobra bite, the patient develops paralysis of the respiratory muscles. The patient is administered a specific antidote - anti-snake serum. In some cases, the antidote is combined with other solutions for infusion.
An antidote against scorpion venom is used in a hospital setting, and for a karakurt bite, an active chemical reagent is used that destroys the toxin, which is harmless to the victim’s body.
The drug Anascorp contains sucrose, sodium chloride, glycine, pepsin, cresol and is used for course therapy. Anti-caracourt serum is the most effective remedy from a spider bite. However, in a weakened patient, administration of an antidote causes the appearance of allergic reaction up to anaphylactic shock.
There is no specific antidote for the ray injection of the coral polyp of P. toxica and the skin mucus of the dart frog. Many people died from the bite of an Australian snake before the advent of an antidote - antitoxic taipan serum.
Detoxification for atropine intoxication
The drug Nivalin contains the alkaloid galantamine, which affects the membrane of the damaged cell. The medicine is administered intravenously in the first hours after poisoning with anticholinergics. The patient's condition improves after a few hours.
The patient's heart function stabilizes and decreases arterial pressure and body temperature. Antidotes for acute poisoning with anticholinergics are used after gastric lavage through a tube.
To neutralize the toxin, the drug Proserin is used. Atropine is an antidote to physostigmine, an alkaloid from the seeds of a poisonous plant native to western Africa. A 0.1% solution is used as an antidote for poisoning with Clonidine, Aconitine, and cardiac glycosides. If muscle twitching or excessive excitability occurs in a patient after accidentally using a means to kill harmful insects, atropine is used as an antidote.
A diagnosis of poisoning is not uncommon. The antidote neutralizes toxins and restores health.