Senseal K

Uses

Potassium nitrate is a medication used to cauterize small wounds, remove granulation tissue, warts, and verrucae, and treat tooth sensitivity.

For the relief of tooth sensitivity, and is also used as a pesticide, insecticide, as a food additive, and a rodenticide .

Sodium fluoride is an antiseptic & anticavity mouthwash which-

• Restores enamel to strengthen teeth
• Protects teeth from cavity
• Helps to prevent tooth decay
• Controls tartar that can discolor teeth
• whitens teeth safety

Senseal K is also used to associated treatment for these conditions: Tooth SensitivityCaries; Enamel, Cavity, Dental Cavity, Dental Decay, Dental Health, Partial Denture Wearers Wear of the Natural Enamel, Tooth Sensitivity, Trace Element Deficiency, Wear of the Natural Enamel caused by teeth grinding, Parenteral Nutrition

How Senseal K works

Potassium (K+) is the principal cation modulating the osmotic balance of the body fluids. In animals, the maintenance of normal cell volume and pressure is dependent on Na+ and K+ pumping . Potassium transport through the hydrophobic interior of a cell membrane may be facilitated by several naturally occurring compounds that form lipid-soluble alkali metal cation complexes. Potassium has the critical role of a calcium counter-ion for numerous carboxylates, phosphates, and sulfates, and also acts to stabilize macromolecular structures .

Potassium is the primary agent for common, over the counter de-sensitizing toothpaste that prevents the transmission of nerve endings to the teeth. Potassium salts, including potassium nitrate, potassium chloride or potassium citrate work by diffusion across the dentinal tubules, causing depolarization of the nerve cells. In turn, these cells become unresponsive to excitatory stimuli. The effect of the potassium nitrate accumulates over time, and it may take several weeks for patients to notice improvement of pain symptoms .

Potassium nitrates control pests using a unique mechanism of action. Rather than directly poisoning rodents, nitrates support the combustion of charcoal in gas cartridges, promoting the production of toxic gases, which, are lethal to the target pest. The environmental protection agency in the USA (EPA) is only minimally concerned about the risk of direct human exposure to sodium or potassium nitrates, rather than pesticide accidents--typically involving skin burns or inhalation of toxic gases .

The prevention of dental caries by topical fluoride is achieved by various mechanisms. Sodium fluoride kills bacteria that cause caries, such a Streptococcus mutans and lactobacilli by interfering with their metabolic activities that result in the formation of lactic acid. Fluoride ions cause the inhibition of glycolytic and other enzymes involved in bacterial metabolism. It changes the permeability of cell membranes, lowering the pH in the cytoplasm of the cell, leading to a decrease in acidity, which is normally implicated in tooth decay.

When administered at low topical doses, fluoride in both saliva and plaque and saliva prevent the demineralization of healthy tooth enamel while remineralizing teeth that have previously been demineralized. Sodium fluoride is absorbed by the surface of hydroxyapatite crystals on the teeth, which are necessary for mineralization. This renders the teeth more resistant to demineralization by changing the apatite crystal solubility. Sodium fluoride inhibits the demineralization of teeth in a pH-related manner. When used in high doses, in formulations such as the fluoride varnishes or gels, sodium fluoride forms a layer on the surface of tooth enamel. When the pH of the mouth is reduced due to acid production by bacteria such as S.mutans, fluoride is released, interfering with bacterial metabolism, and then acts to remineralize the teeth.

Dosage

Senseal K dosage

Rinse (gargle) with fall strength Sodium fluoride for 30 seconds with 20 ml (with the help of supplied cup) two times daily (morning and evening). Do not swallow. Don’t eat or drink within 30 minutes after rinsing with Sodium fluoride restoring.

Side Effects

Hypersensitivity reactions, rash, nausea, vomiting. Products containing stannous fluoride may cause teeth staining.

Toxicity

Acute oral toxicity (LD50): 1901 mg/kg in rabbits and 3750 mg/kg in rats .

The primary acute toxic effect of nitrates is the development of methemoglobinemia, a condition in which greater than 10% of the hemoglobin in the body is transformed into methemoglobin. When this conversion exceeds 70% the condition may result in death .

The potassium ion by itself possesses very little toxicity; the toxicity of the salts is associated with the anion. Potassium nitrate is rapidly absorbed from the upper gastrointestinal tract and is excreted mostly as the unchanged drug . This excludes a small percentage of the ingested dose that is reduced by the microbial action of the gut to nitrite. Nitrites convert the hemoglobin in red blood cells into methemoglobin . In male rats given potassium nitrate, intestinal absorption was affected .

Adverse increased potassium intake included changes in blood lipids, triglyceride, decreased high-density lipoprotein [HDL] cholesterol), changes in renal function, and increases in catecholamine levels. The decrease in blood volume caused by increased potassium activates the sympathetic nervous system, resulting in the release of adrenaline and noradrenaline. Decreases in blood volume may also contribute to the observed changes in blood lipid concentrations .

Death and severe effects of nitrate ingestion are generally associated with doses of the drugs above 10g NO3-. Doses ranging from 2-9 g NO3- have been reported to cause methemoglobinemia. These values correspond to 33 - 150 mg NO3-/kg Potassium nitrate was shown to cause low to moderate acute toxicity. Repeated dose toxicity was investigated in rats given oral doses in the range 10-100 mg/kg per day for 4 months; bronchopneumonia, local hemorrhages, and other circulatory disorders were observed in treated animals. Cattle were given oral doses of 345-450 mg/kg daily (expressed as nitrate) for several months; blood phosphate and magnesium were decreased and blood calcium, urinary magnesium, urea and milk urea were increased .

The oral LD50 of sodium fluoride is 44 mg/kg in mice and 31 mg/kg in rats. The oral LD50 of sodium fluoride in rabbits is 200 mg/kg.

Overdose information

The ingestion of toothpaste is the major cause of sodium fluoride overdose. This is followed by sodium fluoride supplements and mouth rinses. Most causes of sodium fluoride toxicity have been observed in children under the age of 6 years old. The manifestations of a sodium fluoride overdose may include gastrointestinal disturbance, abdominal pain, alterations in taste, seizures, salivation, bradycardia, tachycardia, headache, tremor, and shallow breathing. Gastrointestinal bleeding may also occur in addition to a sensation of burning in the mouth. Hypotension, bronchospasm, fixed mydriasis, and elevated potassium can also occur which, in turn, may lead to arrhythmias and cardiac arrest.

Management

If a dose greater than 5 mg fluoride per kilogram of body weight (2.3 mg fluoride per pound of body weight) has been taken, it is advisable to induce vomiting. Administer calcium in an oral, soluble form (for example, 5% calcium gluconate, a solution of calcium lactate, or milk). The patient should seek immediate medical attention. If a sodium fluoride ingestion of 15 mg fluoride/kg of body weight or more occurs (i.e. higher than 6.9 mg fluoride per pound), immediately induce vomiting, provide supportive care, and admit the patient to the hospital for observation.

Precaution

Prolonged treatment with large amounts of fluoride may result in dental fluorosis and osseous changes; do not exceed recommended dosage. Renal impairment. Pregnancy.

Interaction

Absorption of fluoride may be reduced by aluminium, calcium and magnesium salts.

Volume of Distribution

Nitrates are absorbed into the general blood circulation and are transported across the body. Radioactive tracer experiments have demonstrated that nitrates are distributed evenly among body organs, and their rate of distribution depends on blood flow .

Fluoride distributes to the saliva, bones, and teeth, and is also found in lesser quantities in the breastmilk and sweat. After the ingestion of sodium fluoridated drinking water, the fluoride ions are found to distribute to the plasma and blood cells. Plasma levels of fluoride concentrations are twice as the concentrations found in blood cells. Adults have been found to retain 36% of ingested fluoride and children have been found to retain about 50% of a dose. Most of the retained fluoride is localized to bone and teeth and 1% accumulates in soft tissues. Fluoride crosses the placenta and the blood-brain barrier. The central nervous system concentrations of sodium fluoride are estimated to reach 20% the plasma concentrations. Studies conducted in communities with high levels of fluoride in water did not show any increase in birth defects. The placenta is able to regulate the accumulation of excess fluoride, possibly protecting the fetus from high levels of fluoride. Despite this, excessively high exposure to fluoride in utero may lead to skeletal fluorosis.

Elimination Route

It is established that nitrate is quickly and almost entirely absorbed from the proximal and small intestine subsequent to ingestion in most animals, with little if any absorption from the stomach and lower intestine .

The vast majority of intestinal K+ absorption occurs in the small intestine; the contribution of the normal colon to net K+ absorption and secretion is trivial .

Sodium fluoride is 90% absorbed from the gastrointestinal tract, with 77% of absorption in the proximal intestine and about 25% in the stomach. The rate of absorption may vary according to gastric pH. Cmax is reached 20-60 minutes after ingestion. Cmax was estimated to be 848 ± 116 ng/mL after a 20mg sodium fluoride solution was ingested, with a Tmax of 0.46 ± 0.17 hours. The bioavailability of sodium fluoride tablets administered in the fasted state during one pharmacokinetic study approached 100%. Another resource reports a sodium fluoride AUC of 1.14 ± 0.12 μg × h/mL after the ingestion of fluoridated water.

Half Life

The terminal plasma elimination half-life following the ingestion of fluoridated drinking water generally ranges from 3 to 10 hours. The half-life of sodium fluoride in the bones is 20 years.

Clearance

Sodium fluoride is rapidly cleared by the kidneys and depends on various factors, including glomerular filtration rate, urine flow, and urine pH. According to one clinical study evaluating the pharmacokinetics of oral sodium fluoride tablets in healthy young adults, the renal clearance was determined to be 77.4 ± 11.2mL/min for acidic urine and 78.4 ± 6.9mL/min for alkaline urine. Another reference estimates the renal clearance of fluoride ions from sodium fluoridated water at 35–45 mL/min.

Elimination Route

Nitrates are excreted in the urine primarily as inorganic nitrates .

Sodium fluoride is rapidly excreted, mainly in the urine. About 90% of fluoride is filtered by the glomerulus and reabsorbed by the renal tubules. About 10% is excreted in the feces.

Contraindication

Not to use 1 mg tablets in children less then 3 yr of age or when drinking water fluoride content is >= 0.3 ppm.

Acute Overdose

In acute poisoning, symptoms include a salty or soapy taste, increased salivation, GI disturbances, abdominal pain, weakness, drowsiness, faintness and shallow breathing; more serious effects include hypocalcaemia, hypomagnesaemia, hyperkalaemia, tremors, convulsions, cardiac arrhythmias, shock, respiratory arrest and cardiac failure. Death may occur within 2-4 hr. Treatment includes gastric lavage with lime water or a weak solution of another calcium salt to precipitate fluoride. Maintain high urine output, slow IV inj of calcium gluconate 10% may be used for hypocalcaemia and tetany. Magnesium sulfate may be given to treat hypomagnesaemia, and aluminium hydroxide may help to reduce fluoride absorption. Haemodialysis may be considered. Chronic fluoride poisoning may cause skeletal fluorosis resulting in bone pain, stiffness, limited movment and in severe cases, crippling deformities. In children, prolonged excessive intake during tooth development before eruption may cause dental fluorosis characterised by mottled enamel.

Storage Condition

Store in tight plastic containers.

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