DEEP FREEZE COLD SPRAY

Indications

• Dehydration
• Fluid replacement
• Support for metabolic reactions
• Regulation of body temperature

Dosage

Children: Fluid requirements for children depend on age, weight, and activity level. It is crucial to monitor hydration status and adjust intake accordingly, referring to specific guidelines in the BNF for Children.

Adults: Dosage varies based on individual needs, activity level, and environmental conditions. General guidelines suggest approximately 2 to 3 liters per day for adults, considering factors like exercise and climate.

Mechanism of action

Water acts as a solvent in biological systems, enabling the dissolution and transport of nutrients and waste products. It also plays a vital role in metabolic reactions, including hydrolysis and dehydration synthesis, which are essential for cellular function.

Pharmacodynamics

Water maintains cellular integrity and supports physiological functions, including osmotic balance, acid-base equilibrium, and thermoregulation. Its role in enzymatic reactions and as a medium for biochemical processes is crucial for organismal health.

Pharmacokinetics

Water is absorbed efficiently in the gastrointestinal tract and distributed throughout the body via the bloodstream. It is excreted primarily through urine, sweat, and respiration. The body regulates water balance through mechanisms involving the kidneys, hormones, and thirst responses.

Pregnancy

Considered safe for use.

Breast-feeding

Considered safe for use.

Storage

Store in a cool, dry place away from sunlight.

Formulations

• Liquid
• Pure Water

Indications

• Asthma
• Rheumatoid arthritis
• Systemic lupus erythematosus
• Psoriasis
• Allergic rhinitis
• Adrenal insufficiency

Dosage

Children: Refer to the BNF for Children for appropriate dosing based on the child's age, weight, and specific condition.

Adults: Refer to specific prescribing guidelines for adult dosages based on the condition being treated. Tapering may be required in long-term use.

Mechanism of action

Cortmer works by binding to glucocorticoid receptors in the cytoplasm of target cells. This complex translocates to the nucleus, where it influences gene expression related to inflammatory mediators. It inhibits the production of pro-inflammatory cytokines and chemokines, thereby reducing inflammation and modulating the immune response.

Pharmacodynamics

The pharmacodynamic effects of Cortmer include potent anti-inflammatory effects, reduction in immune system activity, and metabolic effects such as gluconeogenesis and protein metabolism modulation. These effects can lead to improved symptoms in conditions characterized by excessive inflammation or immune activation.

Pharmacokinetics

Cortmer is well-absorbed when administered orally, with peak plasma concentrations typically reached within a few hours. It is extensively metabolized in the liver, primarily through the cytochrome P450 enzyme system, and has a half-life that varies based on formulation and route of administration. Excretion occurs mainly through urine, with metabolites being eliminated as well.

Contra-indications

• Hypersensitivity to cortmer or any of its components
• Active infections unless treated with appropriate antibiotics
• Systemic fungal infections

Adverse effects

• Increased risk of infections
• Hyperglycemia
• Hypertension
• Osteoporosis
• Adrenal suppression
• Gastrointestinal disturbances
• Mood changes, including anxiety and depression

Interactions

• May enhance the effects of non-steroidal anti-inflammatory drugs (NSAIDs), increasing the risk of gastrointestinal bleeding
• Can interact with anticoagulants, requiring careful monitoring of coagulation parameters
• May reduce the effectiveness of vaccines, particularly live vaccines

Precautions

• Use with caution in patients with diabetes mellitus due to potential for hyperglycemia
• Monitor for signs of adrenal insufficiency, particularly if doses are tapered
• Use cautiously in patients with a history of peptic ulcer disease or gastrointestinal bleeding

Pregnancy

Corticosteroids like cortmer should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Long-term use may affect fetal growth.

Breast-feeding

Cortmer is excreted in breast milk, and caution should be exercised when administered to nursing mothers, especially with high doses or prolonged use.

Storage

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

Formulations

• Tablets
• Injectable solutions
• Topical creams or ointments

Indications

• Allergic rhinitis
• Urticaria
• Allergic conjunctivitis
• Anaphylaxis (as adjunctive therapy)
• Motion sickness (off-label use)

Dosage

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

Adults: Refer to specific dosing guidelines in the BNF.

Mechanism of action

Denafred exerts its antihistaminic effects by selectively antagonizing peripheral H1 receptors, thereby inhibiting the physiological effects of histamine, including vasodilation, increased vascular permeability, and sensory nerve stimulation. This action helps to reduce symptoms such as itching, sneezing, and runny nose.

Pharmacodynamics

As an H1 receptor antagonist, denafred leads to a decrease in the symptoms of allergic reactions. It can also have mild sedative effects due to its ability to cross the blood-brain barrier, although this varies by formulation and individual response. The onset of action typically occurs within one hour, with a duration of effect lasting several hours.

Pharmacokinetics

Denafred is generally well-absorbed from the gastrointestinal tract. It undergoes hepatic metabolism and is excreted primarily through urine. The half-life of denafred can vary based on individual patient factors, including age, liver function, and dosage. Its bioavailability can be influenced by food intake and gastrointestinal motility.

Pregnancy

There is limited data on the use of denafred during pregnancy. It is advisable to use caution and assess the risk-benefit ratio before prescribing.

Breast-feeding

It is not known if denafred is excreted in human milk. Caution is recommended when administering to breastfeeding women.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Indications

• Alcohol use disorder
• Acute alcohol intoxication
• Antiseptic for skin disinfection

Mechanism of action

Ethanol affects the brain’s neurons in several ways. It alters their membranes, ion channels, enzymes, and receptors. Ethanol binds directly to the receptors for acetylcholine, serotonin, GABA, and NMDA receptors for glutamate. The sedative effects are mediated through binding to GABA receptors and glycine receptors, while also inhibiting NMDA receptor functioning. As an anti-infective, ethanol acts as an osmolyte, disrupting the osmotic balance across cell membranes. The acute effects result from competitive inhibition of glycine binding to NMDA receptors, leading to disrupted glutamatergic neurotransmission.

Pharmacodynamics

Ethanol produces cellular injury through dehydration and precipitation of cytoplasm, contributing to its bactericidal and antifungal actions. It can lead to neuritis and nerve degeneration when injected near nerve tissues. Up to 98% of ethanol in the body is oxidized, primarily by the hepatic enzyme alcohol dehydrogenase. Its modulation of neurotransmitter receptors, particularly GABA and NMDA, leads to its sedative properties and potential for developing tolerance with chronic use.

Pharmacokinetics

Ethanol is readily absorbed from the gastrointestinal tract and distributed throughout the body. It has a volume of distribution of approximately 0.5 to 0.6 L/kg. Ethanol is metabolized predominantly in the liver by alcohol dehydrogenase to acetaldehyde, which is further oxidized to acetic acid by aldehyde dehydrogenase. The elimination half-life of ethanol varies but is generally around 4 to 5 hours. Factors such as age, sex, body weight, and genetic variability can influence ethanol metabolism.

Contra-indications

• Hypersensitivity to ethanol
• Acute alcohol intoxication
• Severe liver disease
• Pregnancy (in non-medicinal use)
• Severe pancreatitis
• Severe head injury or intracranial bleeding

Adverse effects

• Dizziness
• Nausea
• Vomiting
• Headache
• Sedation
• Cognitive impairment
• Respiratory depression
• Hypotension
• Gastrointestinal bleeding
• Alcohol withdrawal syndrome

Interactions

• CNS depressants (e.g., benzodiazepines, opioids) may enhance sedative effects
• Disulfiram may cause unpleasant reactions when taken with ethanol
• Acetaminophen may increase hepatic toxicity when used with ethanol
• Warfarin may have altered effects when used with ethanol

Precautions

• Caution in patients with a history of alcohol abuse
• Use with caution in patients with hepatic impairment
• Monitor for signs of respiratory depression
• Consider potential for addiction and withdrawal symptoms
• Use in moderation in older adults due to increased sensitivity

Pregnancy

Ethanol should be avoided during pregnancy due to the risk of fetal alcohol spectrum disorders.

Breast-feeding

Ethanol can pass into breast milk; breastfeeding should be avoided for a minimum of 2 hours after consumption.

Storage

Store in a cool, dry place away from light. Keep tightly closed and out of reach of children.

Formulations

• Oral solutions
• Topical antiseptics
• Intravenous formulations
• Medicinal tinctures

Indications

• Potential treatment for mood disorders
• Neuropathic pain management
• Investigative uses in cognitive enhancement

Dosage

Children: Refer to specific clinical guidelines or product information for dosing recommendations.

Adults: Refer to specific clinical guidelines or product information for dosing recommendations.

Mechanism of action

Ethylebdiane's mechanism of action is not fully elucidated; however, it is believed to modulate neurotransmitter release and receptor activity, possibly influencing dopaminergic and serotonergic pathways. This modulation may contribute to its pharmacological effects and therapeutic applications.

Pharmacodynamics

Ethylebdiane exhibits dose-dependent effects on physiological functions. It may alter mood, cognition, and motor control through its interaction with central nervous system receptors. The drug's pharmacodynamic profile is still being characterized in clinical studies, focusing on both efficacy and safety.

Pharmacokinetics

The pharmacokinetic properties of ethylebdiane, including its absorption, distribution, metabolism, and excretion, are not fully characterized in available literature. Preliminary studies suggest that it may have a moderate half-life, with variable bioavailability depending on the route of administration. Further research is needed to define its pharmacokinetic profile more accurately.

Pregnancy

There is limited data on the safety of ethylebdiane during pregnancy. It should be used only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether ethylebdiane is excreted in human milk. Caution should be exercised when administering to nursing mothers.

Storage

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

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in paediatric cases, especially in instances of overdose.

Adults: Refer to the BNF for specific dosing information based on clinical circumstances, particularly in cases of overdose.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is subsequently converted to glycolic, glyoxylic, and oxalic acids. These metabolites contribute to anion gap metabolic acidosis and are responsible for tissue injury through the formation of insoluble calcium oxalate crystals.

Pharmacodynamics

The toxicity of ethylene glycol arises from its metabolites, particularly glycolic and oxalic acids. These compounds induce metabolic acidosis, lead to renal failure through calcium oxalate crystal deposition in the kidneys, and can cause neurological impairment. The anion gap increases due to the accumulation of these acids, leading to complications such as cardiovascular instability and potential multi-organ failure.

Pharmacokinetics

Ethylene glycol is rapidly absorbed after oral ingestion. It undergoes first-pass metabolism primarily in the liver, where it is converted into its toxic metabolites. The elimination half-life of ethylene glycol varies but is generally prolonged in cases of renal impairment. Renal excretion of metabolites contributes to the duration of toxicity, necessitating prompt medical intervention in cases of overdose.

Adverse effects

• Metabolic acidosis
• Renal failure
• CNS depression
• Hypocalcemia
• Cardiovascular collapse
• Pulmonary edema

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of metabolic acidosis
• Evaluate electrolyte levels, particularly calcium

Pregnancy

There is limited data on the safety of ethylene glycol in pregnancy. It should only be used if clearly needed.

Breast-feeding

It is unknown if ethylene glycol is excreted in human milk. Caution is advised.

Storage

Store in a tightly closed container at room temperature, away from heat and moisture.

Formulations

• Liquid

Dosage

Children: Refer to specific product guidelines or consult relevant literature as dosages are not well established for therapeutic use.

Adults: Refer to specific product guidelines or consult relevant literature as dosages are not well established for therapeutic use.

Mechanism of action

Poropylene exhibits its effects mainly through its physical and chemical properties rather than specific biochemical pathways. It functions as a solvent by disrupting intermolecular forces in solutes, facilitating their dissolution and interaction with other substances.

Pharmacodynamics

The pharmacodynamics of poropylene are not well characterized due to its limited application in therapeutic settings. However, as a solvent, it may influence the solubility and bioavailability of other compounds when used in formulations.

Pharmacokinetics

The pharmacokinetics of poropylene have not been extensively studied in humans. Its absorption, distribution, metabolism, and excretion profiles are largely dependent on its route of exposure, with inhalation and dermal exposure being the most common. Generally, organic solvents are metabolized in the liver and excreted via urine, but specific data for poropylene is lacking.

Pregnancy

There is limited data on the safety of poropylene during pregnancy. Use only if clearly needed and the benefits outweigh the risks.

Breast-feeding

Caution is advised when using poropylene during breastfeeding. Monitor for potential effects on the nursing infant.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Indications

• Pain management
• Osteoarthritis
• Rheumatoid arthritis

Dosage

Children: Refer to clinical guidelines or specific product information for paediatric dosing regimens.

Adults: Refer to clinical guidelines or specific product information for adult dosing regimens.

Mechanism of action

Tetraterprygyl works primarily by inhibiting specific pathways involved in the inflammatory response. It may modulate the activity of enzymes such as cyclooxygenases (COXs) and lipoxygenases (LOXs), leading to a reduction in the production of pro-inflammatory mediators like prostaglandins and leukotrienes. This action helps alleviate symptoms associated with inflammation and pain.

Pharmacodynamics

The pharmacodynamic profile of tetraterprygyl indicates that it effectively reduces pain and inflammation through its action on peripheral and central nervous systems. The drug may exhibit dose-dependent effects, with higher doses leading to increased analgesic and anti-inflammatory outcomes. Its onset of action and duration of effect depend on the route of administration and individual patient factors.

Pharmacokinetics

Tetraterprygyl is expected to exhibit moderate oral bioavailability, with peak plasma concentrations occurring within a few hours post-administration. It is likely metabolized in the liver through phase I and phase II reactions, resulting in various metabolites that may have their own pharmacological effects. The elimination half-life is anticipated to range from several hours to a day, depending on the formulation and patient characteristics. Renal excretion plays a significant role in clearing the drug and its metabolites from the body, necessitating caution in patients with renal impairment.

Pregnancy

Safety in pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether tetraterprygyl is excreted in human milk. Caution is advised when administering to nursing mothers.

Storage

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

Mechanism of action

Ethanol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate. The sedative effects of ethanol are mediated through binding to GABA receptors and glycine receptors (alpha 1 and alpha 2 subunits). It also inhibits NMDA receptor functioning. In its role as an anti-infective, ethanol acts as an osmolyte or dehydrating agent that disrupts the osmotic balance across cell membranes. ... Ethanol is known to affect a large number of membrane proteins that participate in signaling pathways such as neurotransmitter receptors, enzymes, and ion channels, and there is extensive evidence that ethanol interacts with a variety of neurotransmitters. The major actions of ethanol involve enhancing the inhibitory effects of gamma-aminobutyric acid (GABA) at GABAa receptors and blockade of the N-methyl-D-aspartate (NMDA) subtype of glutamate, an excitatory amine acid (EAA) receptor. Animal studies indicate that the acute effects of ethanol result from competitive inhibition of glycine binding to NMDA receptor and disruption of glutamatergic neurotransmission by inhibiting the response of the NMDA receptor. Persistent glycine antagonism and attenuation of glutamatergic neurotransmission by chronic ethanol exposure results in tolerance to ethanol by enhancing EAA neurotransmission and NMDA receptor upregulation. The latter appears to involve selective increases in NMDA R2B subunit concentrations and other molecular changes in specific brain loci. The abrupt withdrawal of ethanol thus produces a hyperexcitable state that leads to the ethanol withdrawal syndrome and excitotoxic neuronal death. GABA-mediated inhibition, which normally acts to limit excitation, is eliminated during ethanol withdrawal syndrome and further intensifies this excitation. In addition, NMDA receptors function to inhibit the release of dopamine in the nucleus accumbens and mesolimbic structures, which modulate the reinforcing action of addictive xenobiotics such as ethanol. By inhibiting NMDA receptor activity, ethanol could increase dopamine release from the nucleus accumbens and ventral tegmental area and could thus create dependence. Chronic ethanol administration also results in tolerance, dependence, and an ethanol withdrawal syndrome, mediated, in part, by desensitization and or downregulation of GABAa receptors. The development of alcoholic ketoacidosis (AKA) requires that a combination of physical and physiologic events occur. The normal response to starvation and depletion of hepatic glycogen stores is for amino acids to be converted to pyruvate. Pyruvate can serve as a substrate for gluconeogenesis, be converted to acetyl-CoA, which can enter the Krebs cycle or can be utilized in various biosynthetic pathways (eg, fatty acid, ketone bodies, cholesterol, and acetylcholine) ... Ethanol metabolism generates NADH, resulting in an excess of reducing potential. This high redox state favors the conversion of pyruvate to lactate, diverting pyruvate from being a substrate for gluconeogenesis. To compensate for the lack of normal metabolic substrates, the body mobilizes fat from adipose tissue and increased fatty acid metabolism as an alternative source of energy. This response is mediated by a decrease in insulin and an increased secretion of glucagon, catecholamines, growth hormone, and cortisol. Fatty acid metabolism results in the formation of acetyl-CoA and it combines with the excess acetate that is generated from ethanol metabolism to form acetoacetate. Most of the acetoacetate is reduced to beta-hydroxybutyrate due to the excess reducing potential or high redox state of the cell. Volume depletion interferes with the renal elimination of acetoacetate and beta-hydroxybutyrate, and contributes to the acidosis. An elevated lactate concentration may result from shunting from pyruvate or

Pharmacodynamics

Alcohol produces injury to cells by dehydration and precipitation of the cytoplasm or protoplasm. This accounts for its bacteriocidal and antifungal action. When alcohol is injected in close proximity to nerve tissues, it produces neuritis and nerve degeneration (neurolysis). Ninety to 98% of ethanol that enters the body is completely oxidized. Ethanol is also used as a cosolvent to dissolve many insoluble drugs and to serve as a mild sedative in some medicinal formulations. Ethanol also binds to GABA, glycine, NMDA receptors and modulates their effects. Ethanol is also metabolised by the hepatic enzyme alcohol dehydrogenase.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is then metabolized to glycolic, glyoxylic, and oxalic acids. These acids, along with excess lactic acid are responsible for the anion gap metabolic acidosis. Oxalic acid readily precipitates with calcium to form insoluble calcium oxalate crystals. Tissue injury is caused by widespread deposition of oxalate crystals and the toxic effects of glycolic and glyoxylic acids.