DUOGEL 200/200/25MG/5ML SUSPENSION

Indications

• Heartburn
• Dyspepsia
• Gastroesophageal reflux disease (GERD)
• Peptic ulcer disease

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines for paediatric patients, as dosing will depend on the child's age, weight, and specific indications.

Adults: Refer to the BNF for specific dosing recommendations for adults, as doses may vary based on the formulation and clinical condition being treated.

Mechanism of action

Alumina works by neutralizing gastric acid through a chemical reaction that forms aluminum chloride and water, thereby increasing the pH level in the stomach. This action alleviates symptoms associated with hyperacidity, such as heartburn and dyspepsia, by reducing the acidity of the stomach contents and promoting a more favorable environment for gastric mucosa.

Pharmacodynamics

Alumina exhibits its pharmacological effects primarily through its antacid properties. It binds to gastric acid in the stomach, leading to a decrease in acidity and helping to relieve discomfort from acid-related conditions. The effectiveness of alumina as an antacid is influenced by its ability to form complexes with hydrochloric acid, which decreases the overall acid concentration in the gastrointestinal tract.

Pharmacokinetics

Alumina is not significantly absorbed in the gastrointestinal tract, which limits its systemic effects. The pharmacokinetic profile indicates that alumina acts locally in the stomach and intestines, where it neutralizes acid without being absorbed into the bloodstream. The elimination of aluminum from the body occurs primarily through the kidneys, and when used as directed, it typically does not lead to toxicity.

Pregnancy

Safety in pregnancy has not been established. Use only if clearly needed and the potential benefits outweigh the risks.

Breast-feeding

Safety during breastfeeding is not established. Caution is advised.

Storage

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

Formulations

• Powder
• Suspension

Indications

• Constipation
• Indigestion
• Heartburn

Dosage

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

Adults: Refer to the BNF for specific dosing information.

Mechanism of action

Milk of Magnesia acts as an osmotic laxative by drawing water into the intestines, which distends the bowel and stimulates peristalsis. Additionally, magnesium supplements can reduce platelet aggregation by inhibiting calcium influx, a key factor in platelet aggregation.

Pharmacodynamics

The osmotic effect of magnesium hydroxide increases the water content in the intestinal lumen, leading to softer stools and promoting bowel movements. This laxative effect is primarily due to its ability to retain fluid, thereby enhancing colonic motility. The reduction of platelet aggregation is mediated through modulation of calcium levels within platelets.

Pharmacokinetics

Magnesium hydroxide is not significantly absorbed in the gastrointestinal tract, and its laxative effect is local within the intestine. The onset of action typically occurs within 30 minutes to 6 hours after oral administration. Excretion of magnesium occurs primarily through the kidneys, and elevated magnesium levels can occur in patients with renal impairment.

Adverse effects

• Diarrhea
• Abdominal cramping
• Electrolyte imbalance
• Nausea

Precautions

• Use with caution in patients with renal impairment
• Avoid prolonged use to prevent dependence
• Monitor for signs of dehydration

Pregnancy

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

Breast-feeding

Magnesium hydroxide is excreted in breast milk, but is unlikely to affect the nursing infant when used in recommended doses.

Storage

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

Formulations

• Oral suspension
• Tablet

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

Mechanism of action

... Six 8 wk old female Swiss Webster mice were fed for 10 weeks 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 ... 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 /group/ brain homogenates than in the ... /control/ group (4.9 vs 3.9 nmol 2-thiobarbituric acid reactive subtances/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 /diet/ 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. /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 a 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 of magnesium into brain neurons. The hypothesis has advanced 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/ 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 exchanges between the central nervous system and peripheral circulation. The blood brain barrier owes its unique properties to the integrity of cell membranes that comprise it. Aluminum affects some of the membrane-like functions of the blood brain barrier. It increases the rate of transmembrane diffusion and selectively changes saturable transport systems without disrupting the integrity of the membranes or altering CNS hemodynamics. Such alterations in the access to the brain of nutrients, hormones, toxins, and drugs could be the basis of CNS dysfunction. Aluminum is capable of altering membrane function at the blood-brain barrier; many of its effects on the CNS as well as peripheral tissues can be explained by its actions as a membrane toxin. /Aluminum/ Chronic, oral administration of aluminum to rats increases the in vivo concentration of cyclic AMP and the phosphorylation of microtubule-associated protein-2 and the 200 kd neurofilament subunit. In the present study, the effect of t

Mechanism of action

The term "Milk of Magnesia" was first used to describe a white aqueous, mildly alkaline suspension of magnesium hydroxide formulated at about 8%w/v. Milk of magnesia is primarily used to alleviate constipation, but can also be used to relieve indigestion and heartburn. When taken internally by mouth as a laxative, the osmotic force of the magnesia suspension acts to draw fluids from the body and to retain those already within the lumen of the intestine, serving to distend the bowel, thus stimulating nerves within the colon wall, inducing peristalsis and resulting in evacuation of colonic contents. Magnesium supplements have also been shown to reduce platelet aggregation by inhibiting in the influx of calcium, a crucial component of platelet aggregation.

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.