Victoria Brand Umuthi Wenyoni

Indications

• Skin disinfection
• Preparation of skin before injections
• Cleansing minor wounds

Dosage

Children: Apply to the skin as required; consult product literature for specific guidance.

Adults: Apply to the skin as required for disinfection.

Mechanism of action

Alcohol exerts its antiseptic effect by denaturing proteins, disrupting cell membranes, and dehydrating microbial cells, leading to cell lysis and death.

Pharmacodynamics

Alcohol has broad-spectrum antimicrobial activity, effective against bacteria, fungi, and viruses. Its efficacy is influenced by concentration, with higher concentrations generally being more effective.

Pharmacokinetics

Alcohol is rapidly absorbed through the skin and mucous membranes. It is metabolized primarily in the liver, with a half-life that varies based on the individual's metabolic rate and the amount consumed.

Contra-indications

• Concomitant use with lithium
• Regular use in neonates
• Patients with severe burns when diathermy has been preceded by application of alcoholic skin disinfectants

Adverse effects

• Eye erythema
• Punctate keratitis
• Cytotoxicity
• Eye discolouration

Interactions

• Increases risk of visual disturbances with antiepileptics
• Increases concentration with methylphenidate
• Increases risk of facial flushing and skin irritation with topical pimecrolimus
• Increases concentration with retinoids
• Increases concentration with acitretin
• Increases risk of facial flushing and skin irritation with topical tacrolimus
• Decreases antidiuretic effect with vasopressin

Precautions

• Avoid regular application to inflamed or broken skin or mucosa
• Avoid broken skin
• Flammable

Pregnancy

Sufficient iodine may be absorbed to affect the fetal thyroid in the second and third trimester.

Breast-feeding

Avoid regular or excessive use.

Storage

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

Formulations

• Betadine 2.5% dry powder spray
• Industrial methylated spirit
• Povidone-Iodine 25 mg per 1 gram

Indications

• Food preservative
• Treatment of urea cycle disorders
• Metabolic disorders involving benzoyl-CoA

Dosage

Children: Refer to the BNF for Children for specific dosing guidelines based on condition.

Adults: Refer to the BNF for specific dosing guidelines based on condition.

Mechanism of action

Benzoate acts mainly by inhibiting the growth of bacteria and fungi through its ability to lower the pH, creating an environment that is less favorable for microbial growth. It is also involved in metabolic pathways where it helps in the conjugation of toxic substances, facilitating their excretion from the body.

Pharmacodynamics

Benzoate is known for its antimicrobial properties, which are particularly effective against a wide range of fungi and bacteria. Its efficacy as a preservative is due to its ability to penetrate microbial cell membranes and disrupt their metabolic processes. Additionally, it has been observed to modulate various metabolic pathways, particularly those associated with aromatic compound degradation.

Pharmacokinetics

After ingestion, benzoate is rapidly absorbed in the gastrointestinal tract. It is metabolized primarily in the liver, where it undergoes conjugation with glycine to form hippurate, which is then excreted in the urine. The half-life of benzoate varies depending on individual metabolic rates but is generally short due to its efficient conversion and excretion.

Pregnancy

There is limited data on the use of benzoate in pregnancy. Consultation with healthcare professionals is advised before use.

Breast-feeding

Limited data is available on the excretion of benzoate in breast milk. Caution is recommended when administering to nursing mothers.

Storage

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

Mechanism of action

Carbonate ions participate in buffering reactions that help maintain pH homeostasis in biological systems. They can react with acids to form bicarbonate and carbon dioxide, thus neutralizing excess acidity in the body. This mechanism is crucial in processes such as respiration and metabolism.

Pharmacodynamics

As a buffer, carbonate helps to stabilize pH levels in different biological environments, preventing excessive acidity or alkalinity that could impair cellular functions. It is involved in the transport of carbon dioxide in the blood and plays a role in maintaining the acid-base equilibrium necessary for physiological processes.

Pharmacokinetics

Carbonate ions are readily absorbed in the gastrointestinal tract when ingested and can be found in various body fluids. They are involved in the bicarbonate buffering system, where they are converted to bicarbonate (HCO3-) and carbon dioxide (CO2) through reactions with acids. The kidneys regulate the levels of bicarbonate and carbonate in the body, excreting or reabsorbing them as needed to maintain homeostasis.

Pregnancy

There is no specific information available regarding the use of carbonate compounds during pregnancy. Consult a healthcare provider for advice.

Breast-feeding

There is no specific information available regarding the use of carbonate compounds while breastfeeding. Consult a healthcare provider for advice.

Storage

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

Indications

• Vision correction
• Phototherapy for skin conditions (e.g., psoriasis, eczema)
• Treatment of seasonal affective disorder (SAD)
• Circadian rhythm disorders
• Wound healing

Dosage

Children: Light therapy for paediatric patients should be approached with caution and always under professional guidance. Specific dosages will depend on the individual treatment protocol and condition being addressed.

Adults: Dosage of light therapy varies based on the condition being treated and should be tailored to individual needs, typically ranging from 15 minutes to 2 hours of exposure per day depending on the specific treatment protocol.

Mechanism of action

Light affects biological systems primarily through phototransduction, which involves the conversion of light into electrical signals within photoreceptor cells in the retina. This process initiates a cascade of biochemical reactions that ultimately lead to visual perception. In addition, specific wavelengths of light can interact with various biological molecules, triggering cellular responses such as the production of vitamin D through skin exposure to UVB radiation.

Pharmacodynamics

The pharmacodynamic effects of light are highly dependent on its wavelength and intensity. Short-wavelength blue light (around 480 nm) is known to influence circadian rhythms by affecting melatonin secretion. In therapeutic settings, light can modulate biological responses, such as promoting wound healing, reducing inflammation, and alleviating symptoms of seasonal affective disorder (SAD) through bright light therapy.

Pharmacokinetics

Light does not undergo traditional pharmacokinetic processes such as absorption, distribution, metabolism, or excretion. Instead, its effects are immediate and localized, depending on the intensity and duration of exposure. The penetration depth of light varies with wavelength; for example, UV light can penetrate the skin and affect deeper tissues, while visible light primarily affects the surface layers.

Pregnancy

There is limited data on the effects of light exposure during pregnancy. However, excessive exposure to bright light can be harmful to both the mother and the developing fetus.

Breast-feeding

Light exposure is generally considered safe while breastfeeding, but excessive exposure should be avoided to prevent potential harm to the infant.

Storage

Light should be properly controlled and managed in environments where it is used, ensuring that exposure levels are safe and effective.

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

• Preservative in cosmetics
• Preservative in pharmaceutical formulations
• Antimicrobial agent in food products

Dosage

Children: Refer to specific product guidelines for dosing information, as methylparaben is primarily used as a preservative rather than a therapeutic agent.

Adults: Refer to specific product guidelines for dosing information, as methylparaben is primarily used as a preservative rather than a therapeutic agent.

Mechanism of action

The mechanism of cytotoxic action of parabens, including methylparaben, may be linked to mitochondrial failure. This is dependent on the induction of membrane permeability transition, which is accompanied by mitochondrial depolarization and depletion of cellular ATP through the uncoupling of oxidative phosphorylation.

Pharmacodynamics

Methylparaben exhibits antimicrobial activity against a range of bacteria and fungi. Its effectiveness as a preservative is attributed to its ability to disrupt microbial cell membranes and inhibit essential metabolic processes, ensuring the stability and safety of various formulations.

Pharmacokinetics

Methylparaben is absorbed following topical application and is metabolized by hydrolysis to p-hydroxybenzoic acid, which is then excreted in urine. The pharmacokinetics may vary based on the route of administration and formulation. Studies suggest a relatively low systemic absorption when used in topical applications.

Pregnancy

There is limited data on the use of methylparaben in pregnancy. It should be used only if clearly needed and the benefits outweigh any potential risks.

Breast-feeding

Methylparaben is excreted in breast milk. Caution is advised when using products containing methylparaben while breastfeeding.

Storage

Store in a cool, dry place away from direct sunlight. Keep container tightly closed.

Indications

• Nutritional supplementation
• Bone health support
• Growth and development in children
• Muscle repair and recovery
• Hydration

Dosage

Children: Refer to pediatric dietary guidelines; daily intake varies by age, generally 2-2.5 servings per day for children.

Adults: Refer to dietary guidelines for recommended daily intake of dairy products, typically 2-3 servings per day.

Mechanism of action

The components of milk, particularly its proteins and fats, are digested and metabolized to provide energy and essential nutrients. Lactose is broken down into glucose and galactose by the enzyme lactase. Calcium and vitamin D are crucial for bone metabolism, while proteins support muscle and tissue repair and growth.

Pharmacodynamics

The consumption of milk leads to increased levels of calcium and other minerals in the bloodstream, which are vital for maintaining bone density and structure. The proteins in milk contribute to muscle protein synthesis and repair, alongside providing a source of energy. The bioactive compounds in milk may also have protective effects against certain diseases.

Pharmacokinetics

After ingestion, milk is digested in the stomach and small intestine, where nutrients are absorbed into the bloodstream. The absorption of lactose depends on the presence of lactase. The fats are emulsified and absorbed through the lymphatic system. Calcium absorption can be enhanced by vitamin D. The metabolic effects vary based on individual tolerance and the presence of digestive enzymes.

Adverse effects

• Lactose intolerance may cause gastrointestinal discomfort, bloating, and diarrhea in sensitive individuals.
• Allergic reactions may occur in individuals with a milk allergy, potentially leading to anaphylaxis.

Precautions

• Use with caution in individuals with lactose intolerance or milk allergies.
• Consult a healthcare provider before introducing milk into the diet of infants.

Pregnancy

Milk is generally considered safe during pregnancy, providing essential nutrients such as calcium and vitamin D. However, pregnant individuals should opt for pasteurized milk to reduce the risk of infections.

Breast-feeding

Milk can be consumed during breastfeeding, but it is important to monitor for any allergic reactions in the infant, especially if there is a family history of allergies.

Storage

Store milk in a cool place, preferably refrigerated at 4°C or lower. Consume before the expiration date to ensure safety and quality.

Formulations

• Whole milk
• Skimmed milk
• Low-fat milk
• Condensed milk
• Evaporated milk
• Milk powder

Indications

• Preservative in cosmetics
• Preservative in pharmaceuticals
• Preservative in food products

Dosage

Children: Refer to the specific product guidelines, as dosages may vary based on formulation and intended use.

Adults: Refer to the specific product guidelines, as dosages may vary based on formulation and intended use.

Mechanism of action

The mechanism of propyl paraben may be linked to mitochondrial failure dependent on induction of membrane permeability transition accompanied by the mitochondrial depolarization and depletion of cellular ATP through uncoupling of oxidative phosphorylation.

Pharmacodynamics

Propylparaben acts primarily as an antimicrobial agent, inhibiting the growth of bacteria and fungi. Its effectiveness is attributed to its ability to disrupt microbial cell membranes and interfere with metabolic processes, particularly in energy production within the mitochondria.

Pharmacokinetics

Propylparaben is absorbed through the skin and gastrointestinal tract. It undergoes rapid metabolism, primarily in the liver, where it is conjugated to glucuronic acid and excreted in urine. Its half-life is relatively short, resulting in quick clearance from the body. The compound exhibits low systemic toxicity at typical exposure levels.

Pregnancy

Propylparaben is generally considered safe for use in pregnant women, but caution is advised due to limited human data.

Breast-feeding

Propylparaben is considered safe during breastfeeding, but it is advisable to consult a healthcare provider.

Storage

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

Formulations

• Topical creams
• Lotions
• Cosmetic products

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

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

...The mechanism of cytotoxic action of parabens may be linked to mitochondrial failure dependent on induction of membrane permeability transition accompanied by the mitochondrial depolarization and depletion of cellular ATP through uncoupling of oxidative phosphorylation.

Mechanism of action

...The mechanism of propyl paraben may be linked to mitochondrial failure dependent on induction of membrane permeability transition accompanied by the mitochondrial depolarization and depletion of cellular ATP through uncoupling of oxidative phosphorylation...