BLOKACID-O SUSPENSION

Indications

• Gastroesophageal reflux disease (GERD)
• Heartburn
• Esophagitis
• Dyspepsia

Dosage

Children: Refer to BNF for Children for specific dosing guidelines.

Adults: Refer to BNF for specific dosing guidelines.

Mechanism of action

Alginic acid works by reacting with sodium bicarbonate in the presence of gastric acid to form sodium alginate, which creates a gel-like substance that floats on top of the gastric contents. This gel acts as a physical barrier to prevent acid reflux into the esophagus, thereby alleviating symptoms associated with GERD. It may also help protect the esophageal mucosa from damage caused by acid exposure.

Pharmacodynamics

The pharmacodynamics of alginic acid are primarily associated with its ability to form a viscous gel in acidic conditions. This gel not only helps to neutralize gastric acid but also provides a protective layer against reflux. The onset of action is relatively rapid, with effects typically occurring within minutes of ingestion, making it effective for immediate relief from symptoms of heartburn and acid reflux.

Pharmacokinetics

Alginic acid is not absorbed systemically; instead, it remains in the gastrointestinal tract where it exerts its local effects. The gel formed by alginic acid is primarily eliminated through the feces. Its pharmacokinetic profile indicates a low potential for drug interactions, as it does not significantly affect the absorption of other medications when taken as directed.

Adverse effects

• Gastrointestinal disturbances (e.g., bloating, flatulence)
• Allergic reactions (rare)

Precautions

• Use with caution in patients with a history of gastrointestinal obstruction
• Monitor for allergic reactions in sensitive individuals

Pregnancy

Alginic acid is generally considered safe during pregnancy, but it is advisable to consult a healthcare professional before use.

Breast-feeding

Alginic acid is likely safe during breastfeeding, but it is recommended to consult a healthcare professional.

Storage

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

Formulations

• Oral suspension
• Chewable tablets
• Gastroesophageal reflux disease (GERD) formulations

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.

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

• Symptomatic relief of gastritis
• Management of peptic ulcers
• Treatment of hyperacidity-related symptoms

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in paediatric patients.

Adults: The dosage for adults should be determined based on the specific clinical scenario; refer to the BNF for detailed dosing recommendations.

Mechanism of action

Oxethazaine inhibits gastric acid secretion by suppressing gastrin secretion. It exerts a local anesthetic effect on the gastric mucosa by diminishing the conduction of sensory nerve impulses near the application site, which reduces the permeability of the cell membrane to sodium ions. This is facilitated by its weak base nature, allowing it to be relatively non-ionized in acidic solutions, thus penetrating cell membranes effectively.

Pharmacodynamics

Oxethazaine improves common gastrointestinal symptoms associated with hyperacidity and provides prolonged relief from pain at lower dosages. As part of the anesthetic antacids, it increases gastric pH while producing a reversible loss of sensation. Its local efficacy is significantly greater than that of traditional local anesthetics like lignocaine and cocaine. In vitro studies have shown its antispasmodic action on smooth muscle and its ability to block serotonin action, further contributing to its therapeutic effects.

Pharmacokinetics

Oxethazaine is absorbed locally at the site of application, with its effects lasting longer than typical local anesthetics due to its unique chemical properties. The metabolism and excretion pathways are not extensively documented. As a weak base, its solubility in organic solvents enhances its ability to penetrate tissues, improving its anesthetic effectiveness.

Adverse effects

• Nausea
• Vomiting
• Dizziness
• Headache
• Allergic reactions

Precautions

• Use with caution in patients with a history of hypersensitivity to local anesthetics
• Monitor for potential allergic reactions
• Avoid in patients with severe hepatic impairment

Pregnancy

Oxethazaine should only be used in pregnancy if the potential benefit justifies the potential risk to the fetus. Consult relevant guidelines.

Breast-feeding

It is not known whether oxethazaine is excreted in human milk. Caution should be exercised when administering to breastfeeding women.

Storage

Store at room temperature, protected from light and moisture. Keep out of reach of children.

Formulations

• Oral suspension
• Topical gel

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

• Gastric hyperacidity
• Heartburn
• Indigestion
• Gastritis
• Peptic ulcers

Dosage

Children: Refer to the BNF for Children for appropriate dosing information.

Adults: Refer to specific product guidelines for dosing, as it may vary based on formulation.

Mechanism of action

Trisilicate works by reacting with hydrochloric acid in the stomach to form neutral compounds, which reduces acidity. This action helps to alleviate symptoms of acid-related disorders by increasing the pH level in the stomach.

Pharmacodynamics

Trisilicate exhibits its therapeutic effects primarily through acid neutralization. By decreasing the acidity of gastric contents, it provides symptomatic relief from conditions such as gastritis, gastroesophageal reflux disease (GERD), and peptic ulcers. The onset of action is typically rapid, with effects lasting for a few hours.

Pharmacokinetics

The pharmacokinetics of trisilicate involve minimal systemic absorption since the drug primarily acts locally within the gastrointestinal tract. The compound is excreted unchanged in the feces. Its onset of action is usually within minutes after administration, with a duration of effect that can last several hours, depending on gastric emptying and the formulation used.

Pregnancy

Trisilicate is not recommended for use during pregnancy unless the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Trisilicate may be used during breastfeeding, but it is advisable to consult a healthcare professional before use.

Storage

Store in a cool, dry place, protected from light.

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

Oxetacaine inhibits gastric acid secretion by suppressing gastrin secretion. Moreover, oxetacaine exerts a local anesthetic effect on the gastric mucosa. This potent local anesthetic effect of oxetacaine may be explained by its unique chemical characteristics in which, as a weak base, it is relatively non-ionized in acidic solutions whereas its hydrochloride salt is soluble in organic solvents and it can penetrate cell membranes. Oxetacaine diminishes the conduction of sensory nerve impulses near the application site which in order reduces the permeability of the cell membrane to sodium ions. This activity is performed by the incorporation of the unionized form into the cell membrane.

Pharmacodynamics

Oxetacaine improves common gastrointestinal symptoms. Oxetacaine is part of the anesthetic antacids which increase the gastric pH while providing relief from pain for a longer period of duration at a lower dosage. This property has been reported to relieve the symptoms of hyperacidity. Oxetacaine is reported to produce a reversible loss of sensation and to provide a prompt and prolonged relief of pain. In vitro, oxetacaine was showed to produce an antispasmodic action on the smooth muscle and block the action of serotonin. The local efficacy of oxetacaine has been proven to be 2000 times more potent than lignocaine and 500 times more potent than cocaine. Its anesthetic action produces the loss of sensation which can be explained by its inhibitory activity against the nerve impulses and de decrease in permeability of the cell membrane.

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.