Histacure

Indications

• Constipation
• Bowel cleansing

Dosage

Children: Child 1–11 months: 1 g as required, Child 1–11 years: 2 g as required, Child 12–17 years: 4 g as required.

Adults: 4 g as required, usually administered rectally.

Mechanism of action

When administered rectally, glycerol exerts a hygroscopic and/or local irritant action, drawing water from the tissues into the feces and reflexively stimulating evacuation. It decreases intraocular pressure by creating an osmotic gradient between the blood and intraocular fluid, causing fluid to move from the aqueous and vitreous humors into the bloodstream. Glycerol is classified as a hyperosmotic laxative and may also have lubricating and fecal softening effects.

Pharmacodynamics

Glycerol is commonly classified as an osmotic laxative, acting through its local irritant effects and possibly having lubricating and fecal softening actions. Glycerol suppositories usually produce effects within 15 to 30 minutes, providing quick relief from constipation.

Pharmacokinetics

Glycerol is rapidly absorbed through the gastrointestinal tract. It is metabolized in the liver and other tissues, with a half-life that varies depending on the route of administration. Following rectal administration, glycerol is primarily excreted in urine. The pharmacokinetics may vary based on dosage forms and individual patient factors.

Contra-indications

• Acute abdominal conditions
• Acute inflammatory bowel disease
• Intestinal obstruction
• Severe dehydration

Adverse effects

• Abdominal cramps
• Asthenia
• Gastrointestinal disorders
• Hypermagnesaemia
• Skin reactions
• Urine discolouration

Precautions

• Avoid prolonged contact with skin, especially in incontinent patients or infants wearing nappies due to the risk of irritation and excoriation.
• Excessive use may cause diarrhea and related effects such as hypokalaemia.

Pregnancy

Manufacturers advise avoidance due to limited information available.

Breast-feeding

Manufacturers advise avoidance as there is no information available.

Storage

Store at room temperature, away from direct sunlight.

Formulations

• Glycerol 1g suppositories
• Glycerol 2g suppositories
• Glycerol 4g suppositories
• Glycerol oral suspension

Indications

• Malnutrition
• Post-operative recovery
• Chronic illnesses requiring nutritional support
• Increased caloric needs due to illness or injury
• Weight gain in undernourished patients

Dosage

Children: Refer to the specific product guidelines for paediatric dosing as it varies by formulation and patient needs.

Adults: Refer to the specific product guidelines for adult dosing as it varies by formulation and patient needs.

Mechanism of action

The mechanism of action of Complete primarily revolves around the provision of essential nutrients that support metabolic processes. Proteins are broken down into amino acids, which are used for tissue repair and synthesis. Carbohydrates serve as a primary energy source, while fats provide essential fatty acids. The vitamins and minerals included help in various biochemical pathways, including enzyme function and antioxidant defense.

Pharmacodynamics

Complete works by supplying macronutrients and micronutrients required for various physiological functions. The carbohydrates are metabolized to glucose, providing immediate energy. Proteins enhance muscle protein synthesis, aiding in recovery and growth. The fats contribute to energy reserves and are vital for the absorption of fat-soluble vitamins. The vitamins and minerals support metabolic reactions, maintain immune function, and contribute to overall health.

Pharmacokinetics

Complete is typically absorbed in the gastrointestinal tract. The components are metabolized in the liver and utilized by various tissues throughout the body. The rate of absorption and metabolism can vary based on the individual's digestive health, metabolic rate, and specific nutrient requirements. The elimination of by-products occurs mainly through urine and feces, depending on the nutrient type.

Contra-indications

• Hypersensitivity to the active substance or to any of the excipients
• Severe liver impairment
• Severe renal impairment

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Headache
• Dizziness
• Fatigue
• Insomnia

Interactions

• Increased risk of bleeding with anticoagulants
• May reduce the effectiveness of certain antihypertensives
• Potential interactions with drugs that are substrates of cytochrome P450 enzymes

Precautions

• Monitor liver function tests during prolonged therapy
• Use with caution in patients with a history of gastrointestinal disorders
• Caution in elderly patients or those with comorbidities

Pregnancy

Use during pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult healthcare providers for individualized assessment.

Breast-feeding

Caution is advised when using this drug while breastfeeding. Consider the importance of the drug to the mother against the potential risks to the infant.

Storage

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

Formulations

• Tablets
• Oral suspension
• Injectable solution

Indications

• Allergic rhinitis
• Allergic conjunctivitis
• Urticaria (hives)
• Anaphylactic reactions (as adjunctive therapy)
• Motion sickness
• Insomnia
• Pre-medication for sedation in surgical procedures

Dosage

Adults: For allergic symptoms, the usual dose is 25 to 50 mg taken by mouth every 4 to 6 hours as needed, not exceeding 300 mg per

Mechanism of action

Diphenhydramine predominantly functions as an inverse agonist at H1 receptors, thereby reversing histamine's effects on capillaries and reducing allergic symptoms. It also acts as a competitive antagonist of muscarinic acetylcholine receptors, contributing to its antimuscarinic activity. Additionally, it blocks intracellular sodium channels, which may enhance its therapeutic profile, particularly in certain neurological conditions.

Pharmacodynamics

Diphenhydramine exhibits anti-histaminic, anti-emetic, anti-vertigo, and sedative properties. Its anti-histamine effects occur by blocking histamine's spasmogenic and congestive actions at H1 receptor sites, which prevents responses mediated by histamine. The drug's anti-emetic action is attributed to its inhibition of the medullary chemoreceptor trigger zone, while its anti-vertigo effects arise from its antimuscarinic impact on the vestibular apparatus and vomiting centers in the brain.

Pharmacokinetics

Diphenhydramine is well absorbed following oral administration, with peak plasma concentrations occurring within 1 to 4 hours. It is extensively metabolized in the liver, primarily by cytochrome P450 enzymes, and has a half-life of approximately 4 to 8 hours. The drug is eliminated mainly through urine as metabolites, with a small fraction excreted unchanged.

Contra-indications

• Hypersensitivity to diphenhydramine or any of its components
• Severe asthma or other respiratory conditions where suppression of respiratory function may be dangerous
• Narrow-angle glaucoma
• Prostate enlargement
• Urinary retention

Adverse effects

• Drowsiness
• Dizziness
• Dry mouth
• Constipation
• Blurred vision
• Urinary retention
• Confusion (especially in the elderly)
• Paradoxical excitation in children

Interactions

• Other central nervous system depressants (e.g., alcohol, benzodiazepines) may enhance sedative effects
• Anticholinergic drugs may potentiate antimuscarinic effects
• MAO inhibitors may prolong and intensify anticholinergic effects
• Caution with medications that affect the QT interval, as diphenhydramine may contribute to cardiac arrhythmias

Precautions

• Use with caution in the elderly due to increased sensitivity to adverse effects
• Caution in patients with cardiovascular disease, hyperthyroidism, or hypertension
• May impair the ability to drive or operate machinery
• Not recommended for use in neonates or premature infants

Pregnancy

Diphenhydramine should be used during pregnancy only if clearly needed, as safety in human pregnancy has not been established.

Breast-feeding

Diphenhydramine is excreted in breast 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.

Formulations

• Tablets
• Liquid formulation
• Injectable solution

Indications

• Disinfectant
• Preservative
• Sterilization of medical instruments
• Formalin for histology and pathology specimens

Dosage

Children: Refer to local guidelines and recommendations, as doses may vary based on the specific clinical situation and formulation used.

Adults: Refer to local guidelines and recommendations, as doses may vary based on the specific clinical situation and formulation used.

Mechanism of action

Formaldehyde acts primarily as a cross-linking agent, covalently binding to proteins and nucleic acids. This mechanism is responsible for its effectiveness as a preservative and disinfectant, as it disrupts cellular metabolism and integrity in microorganisms, leading to cell death.

Pharmacodynamics

The pharmacodynamics of formaldehyde involves its ability to inactivate proteins and DNA through cross-linking, which interferes with cellular functions. This action results in its antimicrobial and preservative effects, although it also contributes to toxicity. The compound can elicit inflammatory responses in tissues and has been associated with respiratory irritations and carcinogenic effects upon prolonged exposure.

Pharmacokinetics

Formaldehyde is rapidly absorbed via inhalation and dermal routes, and it is metabolized mainly by the enzyme formaldehyde dehydrogenase to formic acid, which is then converted to carbon dioxide and water. The elimination half-life in the body is relatively short due to its rapid metabolism. Formaldehyde is distributed widely in body tissues, but due to its reactivity, it does not accumulate significantly.

Pregnancy

Safety in pregnancy has not been established.

Breast-feeding

It is unknown whether this drug is excreted in human milk.

Storage

Store at room temperature, away from moisture and heat.

Dosage

Children: Refer to specific product guidelines for dosing information, as monoethanolamine is primarily used in industrial applications and as a chemical intermediate rather than a therapeutic agent.

Adults: Refer to specific product guidelines for dosing information, as monoethanolamine is primarily used in industrial applications and as a chemical intermediate rather than a therapeutic agent.

Mechanism of action

Monoethanolamine acts by participating in the biosynthesis of phospholipids. It is involved in the formation of phosphatidylethanolamine and other phospholipids that are crucial for maintaining cell membrane integrity and function. This compound's role in lipid metabolism indicates its significance in cellular signaling and membrane fluidity.

Pharmacodynamics

Monoethanolamine's pharmacodynamic properties are linked to its function as a precursor in the synthesis of phospholipids. These phospholipids play critical roles in cell membrane structure, signaling pathways, and cellular communication. The modulation of phospholipid composition can influence cellular responses to various stimuli, highlighting the compound's importance in cell biology.

Pharmacokinetics

The pharmacokinetics of monoethanolamine are not well-documented in the available literature. However, as a small molecule, it is likely to be absorbed readily and distributed throughout the body. Its metabolic pathways involve conversion into various phospholipids, and it may be excreted as part of these metabolites. Additional studies would be needed to detail its absorption, distribution, metabolism, and excretion (ADME) characteristics.

Pregnancy

There is insufficient data on the use of monoethanolamine in pregnancy. Caution is advised.

Breast-feeding

There is limited information on the effects of monoethanolamine during breastfeeding. Caution is recommended if used.

Storage

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

Mechanism of action

When administered rectally, glycerin exerts a hygroscopic and/or local irritant action, drawing water from the tissues into the feces and reflexively stimulating evacuation. Glycerin decreases intraocular pressure by creating an osmotic gradient between the blood and intraocular fluid, causing fluid to move out of the aqueous and vitreous humors into the bloodstream. Glycerin (glycerol) and sorbitol are hyperosmotic laxatives. When administered rectally, glycerin and sorbitol exert a hygroscopic and/or local irritant action, drawing water from the tissues into the feces and reflexly stimulating evacuation. The extent to which the simple physical distention of the rectum and the hygroscopic and/or local irritant actions are responsible for the laxative effects of some of these drugs is not known. Only extremely high oral doses of sorbitol (25 g daily) or glycerin exert laxative action. /Glycerin/ decreases intraocular pressure by creating an osmotic gradient between the blood and intraocular fluid, causing fluid to move out of the aqueous and vitreous humors into the bloodstream. The physicochemical effects of a series of alkanols, alkanediols and glycerol on erythrocyte shape and hemolysis at 4 and 20 degrees C were examined. We calculated the dielectric constant of the incubation medium, Ds, and the dielectric constant of the erythrocyte membrane Dm in the presence of organic solutes. The ratio Ds/Dm = -38.48 at 20 degrees C defines the normal biconcave shape in a medium without hemolytic agents. A decrease in Ds/Dm favors externalization or internalization with consequent hemolysis. Alkanols and alkanediols convert biconcave erythrocytes into echinocytes, which is accompanied by an increase in the projected surface area. Glycerol converts biconcave erythrocytes into stomatocytes, which was accompanied by a marginal decrease in the projected surface area. Progressive externalization in alkanols and alkanediols or internalization in glycerol resulted in a decrease in the projected surface area and the formation of smooth spheres. The degree of shape change induced was related to the degree of hemolysis and the ratio Ds/Dm. A decrease in temperature reduced both the degree of shape change and hemolysis. .../Thus/ physicochemical toxicity may be a result of a temperature dependent hydrophobic interaction between the organic solutes and the membrane and is best interpreted by the ability of the solutes to change Ds and Dm.

Pharmacodynamics

Glycerin is commonly classified as an osmotic laxative but may act additionally or alternatively through its local irritant effects; it may also have lubricating and fecal softening actions. Glycerin suppositories usually work within 15 to 30 minutes.

Mechanism of action

Diphenhydramine predominantly works via the antagonism of H1 (Histamine 1) receptors. Such H1 receptors are located on respiratory smooth muscles, vascular endothelial cells, the gastrointestinal tract (GIT), cardiac tissue, immune cells, the uterus, and the central nervous system (CNS) neurons. When the H1 receptor is stimulated in these tissues it produces a variety of actions including increased vascular permeability, promotion of vasodilation causing flushing, decreased atrioventricular (AV) node conduction time, stimulation of sensory nerves of airways producing coughing, smooth muscle contraction of bronchi and the GIT, and eosinophilic chemotaxis that promotes the allergic immune response. Ultimately, diphenhydramine functions as an inverse agonist at H1 receptors, and subsequently reverses effects of histamine on capillaries, reducing allergic reaction symptoms. Moreover, since diphenhydramine is a first-generation antihistamine, it readily crosses the blood-brain barrier and inversely agonizes the H1 CNS receptors, resulting in drowsiness, and suppressing the medullary cough center. Furthermore, H1 receptors are similar to muscarinic receptors. Consequently, diphenhydramine also acts as an antimuscarinic. It does so by behaving as a competitive antagonist of muscarinic acetylcholine receptors, resulting in its use as an antiparkinson medication. Lastly, diphenhydramine has also demonstrated activity as an intracellular sodium channel blocker, resulting in possible local anesthetic properties. Antihistamines used in the treatment of allergy act by competing with histamine for H1-receptor sites on effector cells. They thereby prevent, but do not reverse, responses mediated by histamine alone. Antihistamines antagonize, in varying degrees, most of the pharmacological effects of histamine, including urticaria and pruritus. Also, the anticholinergic actions of most antihistamines provide a drying effect on the nasal mucosa. /Antihistamines/ H1 antagonists inhibit both the vasoconstrictor effects of histamine and, to a degree, the more rapid vasodilator effects mediated by activation of H1 receptors on endothelial cells (synthesis/release of NO and other mediators). /H1 Receptor Antagonists/ H1 antagonists suppress the action of histamine on nerve endings, including the flare component of the triple response and the itching caused by intradermal injection. /H1 Receptor Antagonists/ The first-generation antihistamines are widely prescribed medications that relieve allergic reactions and urticaria by blocking the peripheral histamine H(1) receptor. Overdose of these drugs often results in serious neuronal toxic effects, including seizures, convulsions and worsening of epileptic symptoms. The KCNQ/M K(+) channel plays a crucial role in controlling neuron excitability. Here, we demonstrate that mepyramine and diphenhydramine, two structurally related first-generation antihistamines, can act as potent KCNQ/M channel blockers. Extracellular application of these drugs quickly and reversibly reduced KCNQ2/Q3 currents heterologously expressed in HEK293 cells. The current inhibition was concentration and voltage dependent. The estimated IC(50) (12.5 and 48.1 microM, respectively) is within the range of drug concentrations detected in poisoned patients (30-300 microM). Both drugs shifted the I-V curve of KCNQ2/Q3 channel to more depolarized potentials and altered channel gating properties by prolonging activation and shortening deactivation kinetics. Mepyramine also inhibited the individual homomeric KCNQ1-4 and heteromeric KCNQ3/Q5 currents. Moreover, mepyramine inhibited KCNQ2/Q3 current in an outside-out patch excised from HEK293 cells and the inhibitory effect was neither observed when it was applied intracellularly nor affected by blocking phospholipase C (PLC) activity, indicating an extracellular and direct channel blocking mechanism. Finally, in cultured rat superior cervical ganglion (SCG) neurons, mepyramine reduced the

Pharmacodynamics

Diphenhydramine has anti-histaminic (H1-receptor), anti-emetic, anti-vertigo and sedative and hypnotic properties. The anti-histamine action occurs by blocking the spasmogenic and congestive effects of histamine by competing with histamine for H1 receptor sites on effector cells, preventing but not reversing responses mediated by histamine alone. Such receptor sites may be found in the gut, uterus, large blood vessels, bronchial muscles, and elsewhere. Anti-emetic action is by inhibition at the medullary chemoreceptor trigger zone. Anti-vertigo action is by a central antimuscarinic effect on the vestibular apparatus and the integrative vomiting center and medullary chemoreceptor trigger zone of the midbrain.