PEPGEL ORAL SUSPENSION

Indications

• Mild skin irritations
• Superficial cuts
• Allergies
• Insect bites
• Fungal infections (e.g., athlete's foot)
• Sore throat
• Hemorrhages
• Peptic ulcers
• Acne

Dosage

Children: Refer to the BNF for Children for appropriate dosing information for paediatric patients, as dosages will depend on the specific condition and formulation used.

Adults: Refer to specific product guidelines for dosage information, as aluminum formulations can vary. Generally, topical applications are used as directed for symptom relief.

Mechanism of action

Aluminum acetate acts as an astringent, causing shrinkage or constriction of body tissues following topical application. This effect occurs through osmotic flow of water away from the area of application, leading to decreased mucous secretions and blood serum discharge. Astringents like aluminum also promote mild coagulation of skin proteins, providing protective effects on the skin and aiding in the healing of minor skin irritations.

Pharmacodynamics

Aluminum compounds exert their effects primarily through their astringent properties, which can lead to reduced inflammation and secretion. The local application of aluminum results in a protective barrier on the skin and mucous membranes, which can diminish symptoms associated with irritation, such as itching or discomfort. Astringents are often indicated in conditions that require the drying of exudates or the protection of damaged skin.

Pharmacokinetics

Aluminum is poorly absorbed through the gastrointestinal tract when ingested, as most aluminum compounds are not soluble in water. When applied topically, aluminum is absorbed minimally, allowing it to act locally without significant systemic effects. The elimination of aluminum occurs primarily through the kidneys, with small amounts excreted in feces. It is important to monitor aluminum levels in patients with renal impairment, as they may be at risk of accumulation and toxicity.

Pregnancy

The safety of aluminum compounds during pregnancy has not been established. Use only if clearly needed.

Breast-feeding

Aluminum is excreted in breast milk. Caution should be exercised when administering to breastfeeding mothers.

Storage

Store in a cool, dry place, away from moisture and heat.

Formulations

• Aluminum Acetate solution
• Aluminum Hydroxide gel

Indications

• Nutritional supplementation
• Herbal therapy for various conditions
• Preservation of medicinal properties of plants

Dosage

Children: Dosage for dried herbal preparations in children should be approached cautiously and is best determined by a healthcare professional. Refer to paediatric guidelines for specific dosing recommendations.

Adults: Dosage for dried herbal preparations varies widely depending on the specific herb and its intended use. Refer to specific guidelines or reputable sources for dosing information.

Mechanism of action

The mechanism of action for dried herbal preparations varies depending on the specific plant material involved. Generally, the active constituents in dried herbs can exert their effects through various pathways, such as modulating neurotransmitter systems, influencing metabolic pathways, and acting on specific receptors in the body. For instance, flavonoids, terpenes, and alkaloids found in certain dried herbs can exhibit anti-inflammatory, antioxidant, or antimicrobial properties.

Pharmacodynamics

The pharmacodynamics of dried drugs depend on their specific chemical constituents. These compounds can affect physiological functions, such as modulating inflammatory responses, enhancing immune function, or affecting neurotransmission. The effects can vary widely based on the type of herb, the method of drying, and the concentration of active ingredients.

Pharmacokinetics

The pharmacokinetics of dried herbal preparations can vary significantly based on the specific herb used. Generally, after ingestion, the active compounds are absorbed in the gastrointestinal tract, metabolized primarily by the liver, and then excreted through urine or feces. The bioavailability of these compounds can be influenced by factors such as the form of the preparation (e.g., powder, extract), the presence of other food substances, and individual patient characteristics.

Pregnancy

Safety during pregnancy has not been established. Consult a healthcare provider before use.

Breast-feeding

Consult a healthcare provider before use during breastfeeding.

Storage

Store in a cool, dry place, away from direct sunlight.

Indications

• Nutritional support in patients unable to consume food orally
• Parenteral nutrition
• Drug delivery for lipophilic medications
• Topical applications for skin conditions

Dosage

Children: Refer to specific product guidelines and clinical protocols for paediatric dosing.

Adults: Refer to specific product guidelines and clinical protocols for adult dosing.

Mechanism of action

Emulsions work by reducing the surface tension between the oil and water phases, allowing for the formation of stable droplets. This process is mediated by emulsifying agents, which can be surfactants or natural polymers that stabilize the emulsion and prevent phase separation. The absorption and bioavailability of drugs within the emulsion can be enhanced due to the increased surface area for absorption.

Pharmacodynamics

The pharmacodynamics of emulsions vary based on their composition and formulation. The presence of emulsifying agents can influence the release profile of the active ingredients, allowing for controlled or sustained release. Emulsions can also enhance the solubility of poorly water-soluble drugs, improving their therapeutic effects and minimizing side effects related to high concentrations of active ingredients.

Pharmacokinetics

The pharmacokinetics of emulsions depend on their route of administration and the specific properties of the drug contained within the emulsion. After administration, emulsions can be rapidly absorbed due to their small droplet size, leading to quicker onset of action. The distribution, metabolism, and excretion of the drug will follow the pharmacokinetic principles applicable to the active ingredients, influenced by their solubility and the emulsion's formulation.

Pregnancy

The safety of emulsions during pregnancy depends on the specific type and formulation. Consult relevant guidelines and specific product information.

Breast-feeding

Emulsions may be used while breastfeeding, but specific product information should be consulted to ensure safety.

Storage

Store at room temperature, away from light and moisture. Specific formulations may have unique storage requirements.

Dosage

Children: Refer to specific guidelines for pediatric dosing; consult the BNF for Children for accurate dosage information.

Adults: Refer to specific guidelines for use; dosage may vary based on the context of use.

Mechanism of action

Hydroxide ions act primarily as bases, neutralizing acids to form water and salts. They participate in various biochemical pathways, including selenium metabolism and the degradation of reactive oxygen species. Hydroxide can influence enzyme activity and stability by altering the pH of the environment, thereby affecting metabolic reactions.

Pharmacodynamics

Hydroxide ions can impact biological processes by changing the local pH, which influences enzyme activity, ion transport, and the solubility of other compounds. Their ability to neutralize acids can help regulate physiological pH, contributing to homeostasis in living organisms.

Pharmacokinetics

As an inorganic ion, hydroxide does not undergo traditional pharmacokinetic processes like absorption, distribution, metabolism, or excretion. Instead, it is rapidly equilibrated in biological fluids and participates in acid-base reactions, having immediate effects on the local environment.

Pregnancy

There is limited information regarding the use of hydroxide during pregnancy. Consult a healthcare professional for advice.

Breast-feeding

Limited data is available on the excretion of hydroxide in breast milk. Consult a healthcare professional before use.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Insecticide for agricultural use
• Research tool in toxicology

Dosage

Children: Refer to the BNF for Children for specific dosing and administration guidelines.

Adults: Refer to the BNF for specific dosing and administration guidelines.

Mechanism of action

Methyl parathion acts primarily by inhibiting the enzyme acetylcholinesterase, which is essential for the breakdown of the neurotransmitter acetylcholine. Its active metabolite, methyl paraoxon, is a potent inhibitor of both acetylcholinesterase and butyrylcholinesterase. The inhibition of these enzymes results in the accumulation of acetylcholine at synapses, leading to overstimulation of cholinergic receptors and resultant toxic effects.

Pharmacodynamics

The pharmacodynamics of methyl parathion involve its action as a noncompetitive inhibitor of acetylcholinesterase, causing prolonged effects of acetylcholine due to its inability to be hydrolyzed. The resultant cholinergic toxicity can lead to symptoms such as muscle twitching, respiratory distress, and potentially fatal outcomes if not treated promptly. The extent of inhibition is dose-dependent, with significant toxicity occurring after substantial enzyme inhibition.

Pharmacokinetics

Methyl parathion is absorbed through the gastrointestinal tract and can also be absorbed through the skin and respiratory tract. It is metabolized in the liver to form methyl paraoxon, which is responsible for the majority of its toxic effects. The distribution of methyl parathion in body tissues is influenced by its lipophilicity, and it is primarily excreted as metabolites in the urine. The elimination half-life and specific pharmacokinetic parameters can vary based on individual metabolism and exposure levels.

Pregnancy

There are no adequate and well-controlled studies in pregnant women. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether this drug is excreted in human milk. Caution is advised when administering to nursing women.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Liquid formulation

Indications

• Flatulence
• Bloating
• Gastroesophageal reflux disease
• Functional dyspepsia

Dosage

Children: For children, refer to the BNF for Children for specific dosing recommendations.

Adults: The usual adult dose is 40 to 125 mg taken after meals and at bedtime, as needed.

Mechanism of action

Simethicone is a surfactant that decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. It acts by forming a film of low surface tension that promotes the coalescence of mucus-surrounded gas bubbles, allowing for easier passage of gas.

Pharmacodynamics

Simethicone decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. Its effects are generally short-lived, as it is typically administered as needed. The therapeutic index is wide since it is not absorbed systemically, making it safe for use in various patient populations.

Pharmacokinetics

Simethicone is not systemically absorbed following oral administration, which contributes to its safety profile. Due to its lack of systemic absorption, specific pharmacokinetic parameters such as half-life, clearance, and volume of distribution are not applicable.

Pregnancy

Simethicone can be used during pregnancy as there are no known risks associated with its use.

Breast-feeding

Simethicone is considered safe to use during breastfeeding, as it is not absorbed systemically.

Storage

Store in a cool, dry place, away from direct sunlight. Keep out of reach of children.

Formulations

• Oral suspension
• Chewable tablets
• Soft gels

Indications

• Constipation
• Diagnostic aid in colonoscopy preparation
• Management of hyperosmolality in various conditions

Dosage

Children: For children, the dosage should be determined based on age and condition, and it is advised to refer to the BNF for Children for specific dosing guidelines.

Adults: The typical dose for adults is 30 to 150 mL of sorbitol solution (70%) taken orally, as needed, usually before bedtime.

Mechanism of action

Sorbitol exerts its laxative effect by drawing water into the large intestine, thereby stimulating bowel movements. It acts as a hygroscopic agent, pulling water from tissues into the feces, which reflexively stimulates evacuation. In metabolic pathways, sorbitol is produced from glucose via aldose reductase and is converted to fructose by sorbitol dehydrogenase, with implications in diabetic complications such as retinopathy.

Pharmacodynamics

Sorbitol's laxative effect results from its osmotic properties, which increase the water content of the stool and soften it, facilitating easier passage. Additionally, sorbitol can induce apoptosis in certain cancer cell lines, indicating potential therapeutic implications beyond its laxative use. The modulation of intracellular signaling pathways through the regulation of proteins such as Bax and Bcl-2 suggests a complex role in cellular health and disease.

Pharmacokinetics

Sorbitol is poorly absorbed in the gastrointestinal tract, which contributes to its efficacy as a laxative. It is metabolized in the liver, primarily through the polyol pathway. The absorption and distribution of sorbitol are affected by its osmotic properties, leading to increased intestinal water retention. Its elimination is primarily via renal excretion, with minimal systemic absorption, thus reducing the risk of systemic side effects.

Adverse effects

• Diarrhea
• Abdominal cramps
• Nausea
• Vomiting
• Electrolyte imbalances

Precautions

• Use with caution in patients with renal impairment
• May exacerbate gastrointestinal conditions

Pregnancy

Sorbitol is generally considered safe during pregnancy, but should be used under medical supervision.

Breast-feeding

Sorbitol is excreted in breast milk in small amounts; consult a healthcare provider before use.

Storage

Store in a cool, dry place, away from direct sunlight.

Formulations

• Oral solution
• Syrup

Mechanism of action

Aluminum Acetate is an astringent. An astrignent is a chemical that tends to shrink or constrict body tissues, usually locally after topical medicinal application. The shrinkage or constriction is through osmotic flow of water (or other fluids) away from the area where the astringent was applied. Astringent medicines cause shrinkage of mucous membranes or exposed tissues and are often used internally to check discharge of blood serum or mucous secretions. This can happen with a sore throat, hemorrhages, diarrhea, or with peptic ulcers. Externally applied astringents, which cause mild coagulation of skin proteins, dry, harden, and protect the skin. Acne sufferers are often advised to use astringents if they have oily skin. Astringents also help heal stretch marks and other scars. Mild astringent solutions are used in the relief of such minor skin irritations as those resulting from superficial cuts, allergies, insect bites, or fungal infections such as athlete's foot. Excessive dietary aluminum has been proposed to be a factor contributing to several neurological disorders in humans. Six 8-week-old female Swiss Webster mice were fed for 10 wk purified diets containing 100 (control), 500 or 1000 ug aluminum/g diet. Brain and liver lipid peroxidation was determined by evaluating the production of 2-thiobarbituric acid reactive substances in brain and liver homogenates in the presence or absence of 50 uM ferrous iron. 2-Thiobarbituric acid reactive substances production in the absence of iron in brain homogenates from mice fed the 1000 ug/g diet was higher (30%) than that in the 100 ug/g control group (3.1 vs 2.4 nmol 2-thiobarbituric acid reactive substances/mg protein). The addition of ferrous iron increased 2-thiobarbituric acid reactive substances production in brain homogenates from all 3 dietary groups. The iron induced 2-thiobarbituric acid reactive substances production was 26% higher in the 1000 ug/g brain homogenates than in the 100 ug/g group (4.9 vs 3.9 nmol 2-thiobarbituric acid reactive substances/mg protein). Brain 2-thiobarbituric acid reactive substances production in the presence and absence of iron was similar between the 100 and 500 ug/g aluminum groups. 2-Thiobarbituric acid reactive substances production in liver homogenates measured either with or without iron was similar for the 3 groups. These results show that, in mice, dietary aluminum intoxication leads to increased brain 2-thiobarbituric acid reactive substance production, suggesting that enhanced lipid peroxidation may be one possible mechanism underlying the neurological damage associated with increased tissue aluminum. Evidence is presented indicating that dementias are associated with a relative insufficiency of magnesium in the brain. Such insufficiency may be attributable to low intake or retention of magnesium; high intake of a neurotoxic metal, such as aluminum, which inhibits activity of magnesium requiring enzymes; or impaired transport of magnesium and/or enhanced transport of the neurotoxic metal into brain tissue. It is proposed that Alzheimer's disease involves a defective transport process, characterized by both an abnormally high incorporation of aluminum and an abnormally low incorporation that an altered serum protein contributes to the progression of Alzheimer's disease by having a greater affinity for aluminum than for magnesium, in contrast to the normal protein, which binds magnesium better than aluminum. The altered protein crosses the blood-brain barrier more efficiently than the normal protein and competes with the normal protein in binding to brain neurons. Binding of the altered protein to the target neurons would both facilitate aluminum uptake and impede magnesium uptake. Evidence suggests that albumin is the serum protein that is altered. Aluminum is established as a neurotoxin, although the basis for its toxicity is unknown. It recently has been shown to alter the function of the blood-brain barrier, which regulates ex

Mechanism of action

Acute poisoning ... is related to ... inhibiting action on enzyme acetylcholinesterase. Toxic manifestations generally occur only after more than 50% of plasma cholinesterase is inhibited. ... Methyl parathion ... depend on oxidative activation by replacement of thiono-sulfur with oxygen for ... toxicity. Methyl parathion has only a slight inhibitory action on acetylcholinesterase and butyrylcholinesterase, but its active metabolite, methyl paraoxon, is a potent inhibitor of both these enzymes. A study was conducted examining the inhibition of (Ca2+ and Mg2+)-ATPase by parathion (56382) and methyl parathion. Enzyme activity was assessed spectrophotometrically in pig erythrocyte membranes containing calcium2+ (Ca2+) and magnesium2+ and in solubilized membrane preparations incubated with the test agents. The enzyme response to ATP was biphasic. Equations expressing the kinetics of the substrate curves described two classes of the ATP binding active site, one with high affinity and low maximum rate and one with low affinity and high maximum rate. High affinity active sites were stimulated by low ATP concentrations (20 uM), whereas low affinity active sites were stimulated by high ATP levels (2 mM). Parathion and methylparathion dose dependently inhibited enzyme activity; parathion had a greater inhibitory effect than methylparathion. Lineweaver-Burke and Dixon plots indicated noncompetitive inhibition. Parathion and methylparathion induced enzyme inhibition occurred over a range of free calcium ion concentrations (0.5 to 5 mM); the inhibition was significantly greater at lower Ca2+ concentrations (1 to 100 uM) than at higher concentrations. The authors conclude that parathion and methylparathion inhibit ATPase activity by binding to a site on the enzyme rather than through an interaction with associated lipids. For more Mechanism of Action (Complete) data for METHYL PARATHION (6 total), please visit the HSDB record page.

Mechanism of action

Simethicone is a surfactant that decreases the surface tension of gas bubbles in the gastrointestinal tract, more easily allowing gas to exit the body. The clinical use of simethicone is based on its antifoam properties. Silicone antifoams spread on the surface of aqueous liquids, forming a film of low surface tension and thus causing collapse of foam bubbles. Simethicone reportedly allows mucus-surrounded gas bubbles in the GI tract to coalesce and be expelled.

Pharmacodynamics

Simethicone decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. It has a short duration of action as it is generally given as needed, and a wide therapeutic index as it is not systemically absorbed.

Mechanism of action

Sorbitol exerts its laxative effect by drawing water into the large intestine, thereby stimulating bowel movements. ... Sorbitol exerts hygroscopic and/or local irritant action, drawing water from tissues into feces and reflexly stimulating evacuation. The polyol pathway consists of two enzymes aldose reductase (AR) and sorbitol dehydrogenase (SDH); the former is the first enzyme in the polyol pathway, that catalyzes the reduction of glucose to sorbitol, the latter is the second one, that converts sorbitol to fructose using by NAD(+) as a cofactor. ... SDH activity, the second step in the polyol pathway, might make a greater contribution to the etiology of diabetic retinopathy than does the first step involving AR. /This paper proposes/ a novel hypothesis that polymorphisms of SDH gene may be correlated with SDH gene expression levels in diabetic retinas, thus being a valuable genetic marker for diabetic retinopathy. It has been reported that sorbitol induces apoptosis in several cancer cell lines. ... In /this/ study, the intracellular signaling pathways of sorbitol-induced apoptosis in human K562 cells were investigated using both morphological analysis and DNA fragmentation technique. In this study, we demonstrated that sorbitol-induced apoptosis in human K562 cells is a concentration- and time-dependent manner. This sorbitol-induced apoptosis in human K562 cells was also accompanied by the up-regulation of Bax, and down-regulation of p-Bcl-2, but no effect on the levels of Bcl-X(L). Moreover, the sorbitol treatment resulted in a significant reduction of mitochondria membrane potential, increase in the release of mitochondrial cytochrome c (cyt c), and activation of caspase 3. Furthermore, treatment with caspase 3 inhibitor (z-DEVD-fmk) was capable of preventing the sorbitol-induced caspase 3 activity and cell death. These results clearly demonstrate that the induction of apoptosis by sorbitol involves multiple cellular/molecular pathways and strongly suggest that pro- and anti-apoptotic Bcl-2 family proteins, mitochondrial membrane potential, mitochondrial cyt c, and caspase 3, they all participate in sorbitol-induced apoptotic process in human K562 cells. Chronic diabetic complications, in particular, nephropathy, peripheral and autonomic neuropathy, "diabetic foot," retinopathy, and cardiovascular disease, remain the major cause of morbidity and mortality in patients with diabetes mellitus. Growing evidence indicates that both increased activity of the sorbitol pathway of glucose metabolism and enhanced oxidative stress are the leading factors in the pathogenesis of diabetic complications. The relation between the two mechanisms remains the area of controversy. One group has reported that increased sorbitol pathway activity has a protective rather than detrimental role in complication-prone tissues because the pathway detoxifies toxic lipid peroxidation products. Others put forward a so-called "unifying hypothesis" suggesting that activation of several major pathways implicated in diabetic complications (eg, sorbitol pathway) occurs due to increased production of superoxide anion radicals in mitochondria and resulting poly(ADP-ribose) polymerase activation. This review (a) presents findings supporting a key role for the sorbitol pathway in oxidative stress and oxidative stress-initiated downstream mechanisms of diabetic complications, and (b) summarizes experimental evidence against a detoxifying role of the sorbitol pathway, as well as the "unifying concept."