D5 500

Indications

• Fluid and electrolyte imbalances
• Hypoglycemia
• Nutritional supplementation
• Diabetic emergencies

Dosage

Children: Refer to the BNF for Children for appropriate paediatric dosing guidelines.

Adults: The dosage varies based on the clinical condition and specific formulation used. For intravenous administration, consult product literature for precise dosing.

Mechanism of action

Glucose supplies energy to tissues by undergoing glycolysis, which begins with its phosphorylation by hexokinase to form glucose 6-phosphate. This activates glucose for breakdown, ultimately generating ATP and NADH. The aerobic metabolism of glucose can yield up to 36 ATP molecules. Glucose also serves as a precursor for other biomolecules and regulates various physiological processes including gene transcription and hormone secretion.

Pharmacodynamics

Glucose is an obligatory energy source for cellular activities and plays a significant role in metabolic signaling. It is oxidized to yield energy through glycolysis, the citric acid cycle, and oxidative phosphorylation. Glucose can be converted into fat for energy storage and is stored as glycogen in the liver and muscles. Its administration increases blood glucose levels and stimulates insulin secretion, particularly through oral routes that activate gut incretin hormones.

Pharmacokinetics

Glucose is rapidly absorbed from the gastrointestinal tract or directly into the bloodstream when administered intravenously. It is distributed widely throughout the body and metabolized primarily in tissues requiring energy. The body maintains glucose homeostasis through regulatory mechanisms involving insulin and glucagon. Excess glucose can be stored as glycogen or converted to triglycerides for long-term energy storage.

Adverse effects

• Hyperglycemia
• Increased osmolarity
• Fluid overload
• Electrolyte imbalances

Interactions

• Insulin - may require dose adjustments

Precautions

• Use with caution in patients with diabetes mellitus
• Monitor blood glucose levels in patients receiving parenteral glucose
• Adjust dosage in renal impairment

Pregnancy

Glucose is generally considered safe in pregnancy; however, monitoring is advised, especially in diabetic patients.

Breast-feeding

Glucose is considered safe during breastfeeding, as it is a natural sugar found in breast milk.

Storage

Store at room temperature, away from light. Avoid freezing.

Formulations

• Glucose 5% solution for infusion
• Glucose 10% solution for infusion
• Glucose 0.9% solution for injection
• Glucose sodium chloride combination solutions

Indications

• Dehydration
• Electrolyte imbalances
• Infections requiring immediate antibiotic therapy
• Pain management in acute settings
• Nutritional support in patients unable to eat
• Chemotherapy administration
• Anesthesia induction and maintenance

Dosage

Children: Refer to the specific drug's prescribing information in the BNF for Children for appropriate dosing guidelines.

Adults: Refer to the specific drug's prescribing information in the BNF for appropriate dosing guidelines.

Mechanism of action

The mechanism of action for intravenous drugs depends on the specific medication administered. Generally, intravenous administration allows for rapid drug distribution throughout the body, achieving high plasma concentrations quickly. This is particularly beneficial for medications that require immediate therapeutic effects.

Pharmacodynamics

Pharmacodynamics varies based on the specific drug administered intravenously. In general, drugs delivered via IV can achieve peak plasma concentrations faster than those taken orally, leading to quicker onset of action. This route is often utilized for drugs that are poorly absorbed in the gastrointestinal tract or for those that require precise titration to achieve the desired therapeutic effect.

Pharmacokinetics

Pharmacokinetics for intravenous drugs typically includes immediate bioavailability since the drug is delivered directly into circulation. Distribution is rapid, and elimination depends on the drug's specific metabolic pathways. Volume of distribution, clearance rates, and half-life can significantly vary based on the drug's properties and patient factors such as age, body weight, and organ function.

Interactions

• ataluren + intravenous aminoglycosides: Severe (increases risk of nephrotoxicity)
• intravenous dantrolene + calcium channel blockers: Severe (increases risk of acute hyperkalaemia and cardiovascular collapse)
• intravenous dantrolene + diltiazem: Severe (increases risk of acute hyperkalaemia and cardiovascular collapse)
• intravenous dantrolene + verapamil: Severe (increases risk of acute hyperkalaemia and cardiovascular collapse)
• intravenous chloramphenicol + antiepileptics: Moderate (increases concentration)
• intravenous chloramphenicol + fosphenytoin: Moderate (increases concentration)
• intravenous chloramphenicol + phenytoin: Moderate (increases concentration)
• miconazole + intravenous benzodiazepines: Moderate (increases exposure)
• intravenous magnesium + calcium channel blockers: Unknown (increases risk of hypotension)
• intravenous magnesium + amlodipine: Unknown (increases risk of hypotension)

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.