BENA EXPECTORANT

Indications

• Hypocalcemia
• Hyperkalemia
• Cardiac arrest
• Calcium channel blocker overdose
• Magnesium toxicity

Dosage

Children: Refer to clinical guidelines for specific dosing based on the condition being treated.

Adults: Refer to clinical guidelines for specific dosing based on the condition being treated.

Mechanism of action

Calcium chloride dissociates in solution to release calcium ions (Ca2+), which play a crucial role in various cellular processes. The elevation of calcium ion concentration in the extracellular fluid facilitates muscle contraction, neurotransmitter release, and blood coagulation, among other physiological functions. It also competes with potassium ions, which can be beneficial in treating hyperkalemia.

Pharmacodynamics

Calcium chloride increases serum calcium levels, which helps to restore normal physiological functions affected by hypocalcemia. Its pharmacological effects are dose-dependent, with higher concentrations leading to more pronounced cardiovascular and neuromuscular effects. Calcium chloride can also stabilize myocardial membranes, reducing the risk of arrhythmias in hyperkalemic patients.

Pharmacokinetics

Calcium chloride is rapidly absorbed when administered intravenously, with peak plasma concentrations occurring shortly after administration. The distribution of calcium ions occurs throughout the extracellular fluid, and calcium is primarily excreted via the kidneys. The half-life of calcium in the body is variable, influenced by factors such as age, overall health, and renal function.

Contra-indications

• Hypercalcemia
• Severe renal impairment
• Cardiac arrhythmias
• Hypersensitivity to calcium or any component of the formulation

Adverse effects

• Constipation
• Nausea
• Vomiting
• Abdominal pain
• Hypercalcemia
• Bradycardia
• Hypotension
• Thirst

Interactions

• Calcium may reduce the absorption of certain antibiotics (e.g., tetracyclines, fluoroquinolones)
• Calcium may interact with bisphosphonates, affecting their efficacy
• Thiazide diuretics may enhance the hypercalcemic effect of calcium supplements
• Calcium may interfere with the effects of certain medications for heart conditions

Precautions

• Monitor serum calcium levels in patients with renal impairment
• Use with caution in patients with a history of kidney stones
• Caution in patients receiving digoxin or other cardiac glycosides
• Assess for potential hypercalcemia in patients with cancer

Pregnancy

Calcium is essential during pregnancy for fetal bone development, but excessive intake should be avoided. Consult a healthcare professional for specific guidance.

Breast-feeding

Calcium is excreted in breast milk. Adequate calcium intake is important for lactating women, but supplementation should be considered based on dietary intake.

Storage

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

Formulations

• Calcium chloride injection
• Calcium chloride oral tablets
• Calcium chloride oral solution

Indications

• Hypokalemia (potassium deficiency)
• Prevention of potassium depletion
• Acid-base balance disturbances

Dosage

Children: Dosing for children is dependent on the child's age and condition. Refer to the BNF for Children for specific dosing information.

Adults: Dosage varies based on the severity of potassium deficiency and clinical condition. Refer to clinical guidelines for specific dosing recommendations.

Mechanism of action

Chloride potassium dissociates in the body to provide potassium ions (K+) and chloride ions (Cl-). Potassium is essential for maintaining resting membrane potential, transmembrane potentials, and normal function of excitable tissues, including nerves and muscles. Chloride ions help maintain osmotic balance and are important in the production of gastric acid.

Pharmacodynamics

Potassium is vital for numerous physiological functions, including the regulation of heartbeat, muscle contractions, and nerve signaling. It also plays a role in enzymatic reactions, protein synthesis, and energy metabolism. Chloride is involved in maintaining fluid balance and acid-base homeostasis, and helps in the transport of carbon dioxide in the blood.

Pharmacokinetics

Chloride potassium is absorbed in the gastrointestinal tract and is distributed throughout the body's fluids. Its elimination is primarily renal, with potassium being excreted in urine. The half-life of potassium can vary but is typically around 1-2 hours, depending on individual renal function.

Contra-indications

• Hyperkalemia
• Severe renal impairment
• Adrenal insufficiency
• Untreated Addison's disease
• Acute dehydration
• Severe tissue trauma

Adverse effects

• Hyperkalemia
• Gastrointestinal disturbances (nausea, vomiting, diarrhea)
• Cardiac arrhythmias
• Muscle weakness
• Fatigue
• Metabolic acidosis

Interactions

• ACE inhibitors (may increase the risk of hyperkalemia)
• Potassium-sparing diuretics (concurrent use may lead to hyperkalemia)
• Non-steroidal anti-inflammatory drugs (may impair renal function and increase potassium levels)
• Heparin (may interfere with potassium levels)

Precautions

• Monitor potassium levels regularly in patients receiving potassium supplements
• Use with caution in patients with renal impairment
• Caution in patients with heart disease or those on digoxin (risk of arrhythmias)
• Avoid rapid intravenous administration to prevent cardiac complications

Pregnancy

Potassium chloride is generally considered safe during pregnancy, but potassium levels should be monitored to prevent hyperkalemia.

Breast-feeding

Potassium chloride is excreted in breast milk; however, therapeutic doses are usually considered safe.

Storage

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

Formulations

• Oral tablets
• Oral solution
• Intravenous infusion

Indications

• Hyponatremia
• Dehydration
• Fluid resuscitation
• Electrolyte imbalances
• Intravenous fluid therapy

Dosage

Children: Paediatric dosing is highly individualized based on weight and clinical condition. Refer to the BNF for Children for specific dosing recommendations.

Adults: Dosage varies based on clinical indication, typically administered as needed to restore electrolyte balance or hydration. Consult specific guidelines for detailed dosing regimens.

Mechanism of action

Sodium chloride dissociates into sodium and chloride ions in solution. Sodium ions play a critical role in generating action potentials in neurons and muscle cells, while chloride ions are important for maintaining osmotic balance and cellular homeostasis. The presence of sodium ions in extracellular fluid is crucial for maintaining blood pressure and volume.

Pharmacodynamics

Sodium chloride helps regulate osmotic pressure in the body, which is essential for maintaining cell turgor and proper hydration. It contributes to the excitability of neurons and muscle fibers by influencing the resting membrane potential. The body tightly regulates sodium levels, as deviations can lead to complications such as hypernatremia or hyponatremia, affecting muscle function and neurological status.

Pharmacokinetics

Sodium chloride is readily absorbed from the gastrointestinal tract when ingested. It is distributed throughout the extracellular fluid compartments, with a significant portion residing in plasma and interstitial fluid. The kidneys play a pivotal role in regulating sodium and chloride excretion, adjusting levels based on dietary intake and physiological needs. Sodium chloride has a rapid onset of action, with effects observable shortly after administration, particularly in IV formulations.

Adverse effects

• Hypernatremia
• Fluid retention
• Hypertension
• Edema
• Nausea
• Vomiting
• Abdominal cramps

Interactions

• Corticosteroids may enhance sodium retention
• Diuretics may counteract the effects of sodium chloride
• Lithium levels may be increased due to sodium chloride intake

Precautions

• Use with caution in patients with heart failure
• Monitor sodium levels in patients with renal impairment
• Assess fluid status in patients with conditions predisposing to fluid overload

Pregnancy

Sodium chloride is generally considered safe during pregnancy when used as directed.

Breast-feeding

Sodium chloride is excreted in breast milk, but is not expected to cause adverse effects in nursing infants.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Oral solution
• Injection
• Tablet

Indications

• Allergic rhinitis
• Allergic conjunctivitis
• Urticaria

Mechanism of action

Diphenhydramine primarily functions by antagonizing H1 (Histamine 1) receptors located in various tissues, including the respiratory system, gastrointestinal tract, and central nervous system. By acting as an inverse agonist at H1 receptors, it mitigates the effects of histamine, thereby reducing allergic symptoms. As a first-generation antihistamine, it also crosses the blood-brain barrier, leading to sedative effects. Furthermore, diphenhydramine exhibits antimuscarinic activity by competitively antagonizing muscarinic acetylcholine receptors, contributing to its use in treating parkinsonian symptoms.

Pharmacodynamics

Diphenhydramine possesses anti-histaminic, anti-emetic, anti-vertigo, and sedative properties. Its antihistaminic action blocks the effects of histamine by competing for H1 receptor sites, preventing symptoms associated with histamine release. Its anti-emetic effects are due to inhibition at the medullary chemoreceptor trigger zone, while its anti-vertigo action arises from a central antimuscarinic effect on the vestibular apparatus and the vomiting center in the midbrain.

Pharmacokinetics

Diphenhydramine is well-absorbed following oral administration and reaches peak plasma concentrations within 1 to 2 hours. It is metabolized in the liver and has a half-life of approximately 4 to 8 hours, although this can vary based on individual factors. The drug is excreted primarily in the urine, with a significant portion eliminated as metabolites rather than unchanged drug. Due to its lipophilic nature, diphenhydramine readily crosses the blood-brain barrier, contributing to its sedative effects.

Contra-indications

• Severe asthma exacerbation
• Hypersensitivity to diphenhydramine or any of its components
• Newborns or premature infants

Adverse effects

• Drowsiness
• Dizziness
• Dry mouth
• Constipation
• Urinary retention
• Blurred vision
• Confusion

Interactions

• CNS depressants (e.g., alcohol, sedatives, tranquilizers) may enhance sedative effects
• MAO inhibitors can prolong and intensify anticholinergic effects

Precautions

• Use with caution in patients with glaucoma
• Prostatic hypertrophy
• Cardiovascular disease
• Elderly patients may be more sensitive to side effects

Pregnancy

Diphenhydramine should only be used during pregnancy if clearly needed. Consult a healthcare provider for advice.

Breast-feeding

Diphenhydramine is excreted in breast milk. Use caution when administering to nursing mothers.

Storage

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

Formulations

• Tablets
• Capsules
• Liquid formulations
• Topical preparations

Indications

• Topical antiseptic for minor wounds
• Skin disinfectant
• Surface disinfectant in healthcare settings
• Pre-surgical skin preparation

Dosage

Children: Refer to specific product guidelines for paediatric dosing, as appropriate formulations and concentrations may differ.

Adults: Refer to specific product guidelines, as dosages may vary by formulation and intended use. Generally, apply as directed for topical use.

Mechanism of action

Hclammonium exerts its antimicrobial effects by interacting with the phospholipid bilayer of microbial cell membranes. This interaction destabilizes the membrane, causing increased permeability and ultimately leading to cell lysis. Its cationic nature allows it to bind to negatively charged microbial cell surfaces, enhancing its effectiveness against a broad range of bacteria, viruses, and fungi.

Pharmacodynamics

Hclammonium demonstrates rapid bactericidal activity, with effectiveness varying among different microbial species. Its action is not only limited to bacteria but also extends to enveloped viruses and fungi. The compound's surface-active properties contribute to its ability to reduce microbial load on surfaces and skin. The efficacy may be influenced by factors such as concentration, contact time, and the presence of organic matter.

Pharmacokinetics

The pharmacokinetics of Hclammonium can vary based on the formulation and route of administration. When used topically, systemic absorption is generally minimal, limiting systemic effects and toxicity. However, when applied to damaged skin or mucous membranes, absorption may increase. The elimination of the compound primarily occurs through excretion, with the majority being eliminated unchanged in urine. Due to its low volatility and high stability, it remains effective over extended periods.

Pregnancy

Hclammonium should only be used if the potential benefit justifies the potential risk to the fetus. Consult relevant guidelines.

Breast-feeding

It is not known whether hclammonium is excreted in human milk. Caution should be exercised 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

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.