Glucolin dynomite

Indications

• Vitamin C deficiency
• Scurvy
• Adjunct therapy in iron overload conditions

Dosage

Children: Child 1 month–3 years: 125–250 mg daily in 1–2 divided doses; Child 4–11 years: 250–500 mg daily in 1–2 divided doses; Child 12–17 years: 0.5–1 g daily in 1–2 divided doses.

Adults: 500 mg daily, taken in 1-2 divided doses, depending on the clinical condition and dietary needs.

Mechanism of action

Ascorbic acid functions primarily as a reducing agent, facilitating enzymatic reactions in the body, including the hydroxylation of proline and lysine in collagen synthesis. It also plays a role in the absorption of iron from the gastrointestinal tract and enhances the immune response.

Pharmacodynamics

Ascorbic acid is crucial for the maintenance of connective tissue and is involved in the metabolism of several amino acids. Its antioxidant properties help to mitigate oxidative stress and may play a role in reducing the risk of chronic diseases.

Pharmacokinetics

Ascorbic acid is absorbed in the intestines and is widely distributed throughout the body. The renal clearance of ascorbic acid is dose-dependent, with higher doses leading to increased excretion. The half-life varies but is generally around 15 to 30 minutes in healthy individuals, with tissue saturation levels influencing its retention.

Contra-indications

• Hypercalcaemia
• Hyperoxaluria
• Patients with cardiac dysfunction

Adverse effects

• Abdominal pain
• Headache
• Nausea
• Vomiting
• Diarrhoea
• Constipation
• Weight loss
• Polyuria
• Sweating
• Thirst
• Vertigo

Interactions

• Increases risk of cardiovascular adverse effects with iron chelators
• Increases risk of cardiovascular adverse effects with deferiprone
• Increases risk of cardiovascular adverse effects with desferrioxamine

Precautions

• Use with caution in patients with iron overload
• Monitor for symptoms of overdose

Pregnancy

High doses teratogenic in animals but therapeutic doses unlikely to be harmful.

Storage

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

Formulations

• Ascorbic acid 50 mg tablets
• Ascorbic acid 100 mg tablets
• Ascorbic acid 200 mg tablets
• Ascorbic acid 250 mg tablets
• Ascorbic acid 500 mg capsules

Indications

• Hypoglycemia
• Caloric supplementation in patients unable to eat
• Fluid replacement therapy
• Parenteral nutrition

Dosage

Children: Paediatric doses must be determined based on clinical condition and specific needs. Refer to the BNF for Children for appropriate dosing information.

Adults: The dosage of dextrose in adults varies based on clinical condition and route of administration. For hypoglycemia, intravenous dextrose 50% (D50W) is commonly administered. Refer to the BNF for specific dosing guidelines.

Mechanism of action

Dextrose supplies energy to tissues by generating ATP and NADH through glycolysis, where glucose is phosphorylated by hexokinase to form glucose 6-phosphate. This activates glucose for breakdown, ultimately converting glucose into energy molecules. Dextrose also plays a role in gene transcription, enzyme activity, and hormone secretion, regulating glucose homeostasis and cellular metabolic integrity.

Pharmacodynamics

Blood glucose acts as a crucial energy source for cellular activities and functions as a signaling molecule. It is oxidized into carbon dioxide and water, producing energy through glycolysis, the citric cycle, and oxidative phosphorylation. Dextrose can be converted into fat for energy storage and is stored as glycogen in the liver and muscles. Its administration, particularly orally, enhances insulin secretion due to stimulation of incretin hormones.

Pharmacokinetics

Dextrose is rapidly absorbed in the gastrointestinal tract, leading to a quick elevation of blood glucose levels. It is distributed throughout the body and can be utilized by various tissues for energy. The metabolism of dextrose primarily occurs in the liver, where it can be stored as glycogen or converted into fat. Renal excretion may occur when blood glucose levels are excessively high.

Adverse effects

• Hyperglycemia
• Fluid overload
• Hypokalemia
• Thrombophlebitis at injection site

Interactions

• Corticosteroids may increase blood glucose levels
• Beta-blockers may mask symptoms of hypoglycemia
• Diuretics may cause electrolyte imbalances

Precautions

• Use with caution in patients with diabetes mellitus
• Monitor blood glucose levels regularly
• Use cautiously in patients with renal impairment or heart failure

Pregnancy

Dextrose is generally considered safe for use during pregnancy when clinically indicated, but should be used with caution.

Breast-feeding

Dextrose can be used during breastfeeding as it is a natural sugar found in breast milk.

Storage

Store at room temperature, away from direct sunlight, and protect from freezing.

Formulations

• Dextrose 5% solution for infusion
• Dextrose 10% solution for infusion
• Dextrose 50% solution for injection
• Oral dextrose tablets

Mechanism of action

Glucose supplies most of the energy to all tissues by generating energy molecules ATP and NADH during a series of metabolism reactions called glycolysis. Glycolysis can be divided into two main phases where the preparatory phase is initiated by the phosphorylation of glucose by hexokinase to form glucose 6-phosphate. The addition of the high-energy phosphate group activates glucose for the subsequent breakdown in later steps of glycolysis and is the rate-limiting step. Products end up as substrates for following reactions, to ultimately convert C6 glucose molecule into two C3 sugar molecules. These products enter the energy-releasing phase where the total of 4ATP and 2NADH molecules are generated per one glucose molecule. The total aerobic metabolism of glucose can produce up to 36 ATP molecules. These energy-producing reactions of glucose are limited to D-glucose as L-glucose cannot be phosphorylated by hexokinase. Glucose can act as precursors to generate other biomolecules such as vitamin C. It plays a role as a signaling molecule to control glucose and energy homeostasis. Glucose can regulate gene transcription, enzyme activity, hormone secretion, and the activity of glucoregulatory neurons. The types, number, and kinetics of glucose transporters expressed depends on the tissues and fine-tunes glucose uptake, metabolism, and signal generation to preserve cellular and whole body metabolic integrity. Vascular calcification is a hallmark of type 2 diabetes. Glucose stimulates calcification in culture of vascular smooth muscle cells (VSMCs) but the underlying mechanisms remain obscure. We observed that high glucose levels stimulated mouse and human VSMC trans-differentiation into chondrocytes, with increased levels of Sox9, type II collagen, glycosaminoglycan and Runx2 expression, and increased alkaline phosphatase activity and mineralization. These effects were associated with increased expression of IL-1beta, which stimulated alkaline phosphatase and calcification, suggesting that glucose induces chondrocyte differentiation of VSMCs, possibly through IL-1beta activation.

Pharmacodynamics

Blood glucose is an obligatory energy source for humans involved in various cellular activities, and it also acts as a signaling molecule for diverse glucose-sensing molecules and proteins. Glucose undergoes oxidation into carbon dioxide, water, and yields energy molecules in the process of glycolysis and subsequent citric cycle and oxidative phosphorylation. Glucose is readily converted into fat in the body which can be used as a source of energy as required. Under a similar conversion into storage of energy, glucose is stored in the liver and muscles as glycogen. Glucose stores are mobilized in a regulated manner, depending on the tissues' metabolic demands. Oral glucose tablets or injections serve to increase the supply of glucose and oral glucose administration is more effective in stimulating insulin secretion because it stimulates the incretin hormones from the gut, which promotes insulin secretion.