STRESS-CARE COMBINATION PRODUCT POWDER

Indications

• Alcohol use disorder
• Sedation
• Antiseptic for skin and surfaces
• Solvent in pharmaceutical formulations

Dosage

Children: Refer to the BNF for Children for appropriate pediatric dosing recommendations.

Adults: Refer to the BNF for specific dosing guidelines, as dosages may vary based on the indication and formulation used.

Mechanism of action

Ethanol affects the brain's neurons by altering their membranes, ion channels, enzymes, and receptors. It binds to GABA receptors, enhancing inhibitory neurotransmission, and inhibits NMDA receptors, disrupting excitatory neurotransmission. This dual action leads to its sedative effects and contributes to its anti-infective properties by acting as a dehydrating agent that disrupts osmotic balance across cell membranes.

Pharmacodynamics

Ethanol induces cell injury through dehydration and cytoplasmic precipitation, which underlies its bactericidal and antifungal actions. It is metabolized primarily by alcohol dehydrogenase in the liver, with 90 to 98% of ingested ethanol being oxidized. Ethanol also modulates neurotransmitter receptor activity, particularly at GABA and glutamate receptors, influencing various physiological responses.

Pharmacokinetics

Ethanol is rapidly absorbed from the gastrointestinal tract, with peak blood concentrations occurring approximately 30 to 90 minutes after ingestion. It is distributed throughout body tissues, with a volume of distribution that varies among individuals. Ethanol is primarily metabolized in the liver via alcohol dehydrogenase and is excreted through urine, breath, and sweat.

Contra-indications

• Hypersensitivity to ethanol or any of the excipients
• Severe liver disease
• Acute pancreatitis
• Pregnancy

Adverse effects

• Drowsiness
• Dizziness
• Nausea
• Vomiting
• Headache
• Impaired motor skills
• Tolerance and dependence with chronic use
• Neurotoxicity at high doses

Interactions

• CNS depressants may enhance sedative effects of ethanol
• Alcohol may interfere with the metabolism of other drugs through inhibition of liver enzymes
• Use with caution in combination with other substances that affect the liver

Precautions

• Use with caution in patients with a history of substance abuse
• Monitor for signs of alcohol intolerance or allergy
• Assess liver function before use
• Avoid use before activities requiring mental alertness

Pregnancy

Ethanol is contraindicated in pregnancy due to the risk of fetal alcohol syndrome and other developmental disorders.

Breast-feeding

Ethanol can enter breast milk and may affect the infant, thus should be used with caution or avoided during breastfeeding.

Storage

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

Formulations

• Oral solutions
• Topical solutions
• Injectable solutions

Indications

• Generalized anxiety disorder
• Major depressive disorder
• Panic disorder
• Social anxiety disorder
• Post-traumatic stress disorder

Dosage

Children: Refer to specific medication guidelines as stress management in paediatric populations may involve various pharmacological agents, each with unique dosing recommendations.

Adults: Refer to specific medication guidelines as stress management may involve various pharmacological agents, each with unique dosing recommendations.

Mechanism of action

Stress activates the hypothalamic-pituitary-adrenal (HPA) axis, leading to the release of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and subsequently cortisol from the adrenal cortex. This cascade prepares the body for a 'fight or flight' response, altering metabolic processes and modulating immune function. Various medications targeting neurotransmitter systems, such as serotonin and norepinephrine, can alleviate stress symptoms by modulating these pathways.

Pharmacodynamics

Pharmacological agents used to treat stress-related symptoms often target neurotransmitter receptors, including serotonin reuptake inhibitors (SSRIs) that enhance serotonin levels, and benzodiazepines that increase the effect of the neurotransmitter gamma-aminobutyric acid (GABA), promoting relaxation and reducing anxiety. The effectiveness of these agents can vary based on individual neurobiology and the specific nature of the stress experienced.

Pharmacokinetics

The pharmacokinetics of stress-related medications can vary widely. For example, SSRIs typically have a half-life ranging from 24 to 48 hours, allowing for once-daily dosing, while benzodiazepines may have shorter half-lives, necessitating more frequent dosing. The absorption, distribution, metabolism, and excretion of these drugs are influenced by factors such as age, liver function, and concurrent medications, which can affect both the onset of action and the duration of effects.

Adverse effects

• Anxiety
• Depression
• Fatigue
• Irritability
• Sleep disturbances
• Headaches
• Gastrointestinal issues

Precautions

• Chronic stress can lead to serious health issues, including heart disease and mental health disorders.
• Individuals with pre-existing mental health conditions should be monitored closely.
• Stress management techniques should be considered as adjunctive treatments.

Pregnancy

Stress can affect pregnancy outcomes. It is important for pregnant individuals to manage stress effectively.

Breast-feeding

High levels of stress may impact breastfeeding. Support and stress management strategies are recommended.

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.