BENYLIN 4 FLUV (Each 20ml liquid contains Pseduophedre Hcl/ Diphennyldine HCL/ Paracetamol 45mg/ 25mg/ 1000mg

Indications

• Mild to moderate pain
• Fever
• Headaches
• Muscle aches
• Arthritis
• Backaches
• Toothaches
• Colds

Dosage

Adults: For adults, the typical dosage is 500 mg to 1 g every 4 to 6 hours, with a maximum daily limit of 4 g. In cases of intravenous administration, the dosage is 15 mg/kg every

Mechanism of action

Paracetamol is thought to exert its analgesic effects by inhibiting cyclo-oxygenase (COX) enzymes, specifically COX-1 and COX-2, which are involved in the synthesis of prostaglandins responsible for pain sensation. Unlike most NSAIDs, paracetamol does not exhibit peripheral anti-inflammatory effects. Its antipyretic action is believed to result from direct action on heat-regulating centers in the brain, leading to peripheral vasodilation and sweating.

Pharmacodynamics

Paracetamol has been shown to have both antipyretic and analgesic effects, lacking any significant anti-inflammatory activity. It does not interfere with platelet aggregation or disrupt hemostasis, making it a safer option for individuals at risk of bleeding. Allergic reactions to paracetamol are rare. The drug does not affect uric acid secretion or acid-base balance when used at recommended doses.

Pharmacokinetics

Paracetamol is rapidly absorbed from the gastrointestinal tract, with peak plasma concentrations typically occurring within 30 to 60 minutes after oral administration. It is primarily metabolized in the liver via conjugation with glucuronide and sulfate, with a minor pathway involving cytochrome P450 enzymes. The elimination half-life ranges from 1 to 4 hours, with renal excretion of metabolites as the primary route of elimination.

Adverse effects

• Nausea and vomiting
• Liver injury
• Renal damage
• Hypersensitivity reactions
• Flushing
• Hypotension
• Anorectal erythema
• Angioedema
• Agranulocytosis
• Thrombocytopenia
• Leukopenia
• Severe cutaneous adverse reactions (SCARs)

Interactions

• Increased risk of methaemoglobinaemia with topical prilocaine
• Increased risk of methaemoglobinaemia with topical anaesthetics
• Increased anticoagulant effect with coumarins
• Increased risk of hepatotoxicity with imatinib
• Decreased exposure with rifampicin
• Decreased exposure with pitolisant

Precautions

• Monitor patients with liver disease or heavy alcohol use for increased risk of hepatotoxicity
• Adjust doses in patients taking enzyme-inducing antiepileptic medications
• Use caution in patients with renal impairment
• Clinical judgement is required for dose adjustment in weight-based dosing

Pregnancy

Paracetamol is generally considered safe to use during pregnancy for pain and fever relief, but should be used at the lowest effective dose for the shortest duration necessary.

Breast-feeding

Paracetamol is excreted in breast milk in small amounts and is considered safe for use while breastfeeding.

Storage

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

Formulations

• Oral tablets (500 mg)
• Oral suspension (120 mg/5 mL, 500 mg/5 mL)
• Rectal suppositories (various strengths)
• Intravenous infusion (various strengths)

Indications

• Allergic rhinitis
• Urticaria
• Allergic conjunctivitis
• Anaphylactic reactions (as adjunct therapy)
• Motion sickness (in some cases)

Dosage

Children: Refer to BNF for Children for appropriate dosing information for pediatric patients.

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

Mechanism of action

Diphennyldine exerts its effects by competitively inhibiting the binding of histamine to the H1 receptor. This action prevents the physiological effects of histamine, such as increased vascular permeability, bronchoconstriction, and stimulation of gastric acid secretion. In addition, it may have some sedative effects due to its ability to cross the blood-brain barrier and antagonize central H1 receptors.

Pharmacodynamics

The pharmacodynamic effects of diphennyldine include relief from symptoms of allergic rhinitis (such as sneezing, itching, and runny nose) and the reduction of pruritus associated with allergic skin reactions. Its sedative properties may also be utilized in situations where calmness or sleep induction is desired.

Pharmacokinetics

Diphennyldine is absorbed well from the gastrointestinal tract following oral administration. It is metabolized in the liver and has a variable half-life, which can be influenced by individual patient factors. The drug is excreted primarily in the urine, with some metabolites also appearing in feces. The onset of action typically occurs within a few hours, with a duration of effect that can last several hours depending on the specific formulation used.

Pregnancy

There are no well-controlled studies in pregnant women. It should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether diphennyldine is excreted in human milk. Caution should be exercised when administering to a nursing woman.

Storage

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

Indications

• Nasal congestion due to common cold
• Sinusitis
• Allergic rhinitis

Dosage

Children: Refer to BNF for Children for specific pediatric dosing guidelines.

Adults: Refer to specific product guidelines for dosing. Commonly, standard adult doses range from 60 mg every 4 to 6 hours, not exceeding 240 mg per day.

Mechanism of action

Pseudoephedrine acts as an agonist at alpha-adrenergic receptors, causing vasoconstriction and reducing nasal congestion. It also has weak stimulant effects on beta-adrenergic receptors, which contributes to its efficacy in relieving nasal obstruction.

Pharmacodynamics

The pharmacodynamics of pseudoephedrine involve its ability to stimulate alpha-adrenergic receptors, leading to vasoconstriction. This action results in decreased blood flow to the nasal mucosa, reducing edema and congestion. The drug also has a mild stimulating effect on the central nervous system, which can lead to increased alertness.

Pharmacokinetics

Pseudoephedrine is well absorbed from the gastrointestinal tract, with peak plasma concentrations typically occurring within 1 to 2 hours after oral administration. It is metabolized in the liver and has a half-life of approximately 5 to 8 hours. The drug is primarily excreted unchanged in the urine, and its elimination can be influenced by urinary pH.

Contra-indications

• Severe hypertension
• Severe coronary artery disease
• Concurrent use with monoamine oxidase inhibitors (MAOIs)
• Hypersensitivity to pseudoephedrine or any component of the formulation

Adverse effects

• Insomnia
• Nervousness
• Dizziness
• Headache
• Dry mouth
• Nausea
• Hypertension
• Tachycardia

Interactions

• Increased risk of hypertension when used with other sympathomimetics
• May reduce effectiveness of antihypertensive medications
• Caution with other medications that can increase blood pressure

Precautions

• Use with caution in patients with cardiovascular disease
• Caution in patients with diabetes mellitus
• Caution in patients with hyperthyroidism
• May cause urinary retention in men with prostatic hypertrophy
• Monitor for CNS effects in elderly patients

Pregnancy

Pseudoephedrine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. It is advisable to consult healthcare professionals before use.

Breast-feeding

Pseudoephedrine is excreted in breast milk. Caution should be exercised when administering to nursing mothers, as it may affect milk production and infant behavior.

Storage

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

Formulations

• Oral tablets
• Oral liquid
• Extended-release formulations

Mechanism of action

According to its FDA labeling, acetaminophen's exact mechanism of action has not been fully established - despite this, it is often categorized alongside NSAIDs (non-steroidal anti-inflammatory drugs) due to its ability to inhibit the cyclo-oxygenase (COX) pathways. It is thought to exert central actions which ultimately lead to the alleviation of pain symptoms. One theory is that acetaminophen increases the pain threshold by inhibiting two isoforms of cyclo-oxygenase, COX-1 and COX-2, which are involved in prostaglandin (PG) synthesis. Prostaglandins are responsible for eliciting pain sensations. Acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, therefore, has no peripheral anti-inflammatory effects. Though acetylsalicylic acid (aspirin) is an irreversible inhibitor of COX and directly blocks the active site of this enzyme, studies have shown that acetaminophen (paracetamol) blocks COX indirectly. Studies also suggest that acetaminophen selectively blocks a variant type of the COX enzyme that is unique from the known variants COX-1 and COX-2. This enzyme has been referred to as _COX-3_. The antipyretic actions of acetaminophen are likely attributed to direct action on heat-regulating centers in the brain, resulting in peripheral vasodilation, sweating, and loss of body heat. The exact mechanism of action of this drug is not fully understood at this time, but future research may contribute to deeper knowledge. Although further investigation is warranted, the active metabolite of acetaminophen (AM404) was shown to interact with several molecular targets, including the Ca_v3.2 calcium channel, the cannabinoid CB1 receptors, TRPV1 receptors, and Na_v1.8 and Na_v1.7 channels. Acetaminophen produces analgesia and antipyresis by a mechanism similar to that of salicylates. Unlike salicylates, however, acetaminophen does not have uricosuric activity. There is some evidence that acetaminophen has weak anti-inflammatory activity in some nonrheumatoid conditions (e.g., in patients who have had oral surgery). ... Acetaminophen lowers body temperature in patients with fever but rarely lowers normal body temperature. The drug acts on the hypothalamus to produce antipyresis; heat dissipation is increased as a result of vasodilation and increased peripheral blood flow. The effects of acetaminophen on cyclooxygenase activity have not been fully determined. Acetaminophen is a weak, reversible, isoform-nonspecific cyclooxygenase inhibitor at dosages of 1 g daily. The inhibitory effect of acetaminophen on cyclooxygenase-1 is limited, and the drug does not inhibit platelet function. Therapeutic doses of acetaminophen appear to have little effect on cardiovascular and respiratory systems; however, toxic doses may cause circulatory failure and rapid, shallow breathing. Acetaminophen (N-acetyl-p-aminophenol (APAP)) is the most common antipyretic/analgesic medicine worldwide. If APAP is overdosed, its metabolite, N-acetyl-p-benzo-quinoneimine (NAPQI), causes liver damage. However, epidemiological evidence has associated previous use of therapeutic APAP doses with the risk of chronic obstructive pulmonary disease (COPD) and asthma. The transient receptor potential ankyrin-1 (TRPA1) channel is expressed by peptidergic primary sensory neurons. Because NAPQI, like other TRPA1 activators, is an electrophilic molecule, /the researchers/ hypothesized that APAP, via NAPQI, stimulates TRPA1, thus causing airway neurogenic inflammation. NAPQI selectively excites human recombinant and native (neuroblastoma cells) TRPA1. TRPA1 activation by NAPQI releases proinflammatory neuropeptides (substance P and calcitonin gene-related peptide) from sensory nerve terminals in rodent airways, thereby causing neurogenic edema and neutrophilia. Single or repeated administration of therapeutic (15-60 mg/kg) APAP doses to mice produces detectable levels of NAPQI in the lung, and increases neutrophil numbers, myeloperoxidase

Pharmacodynamics

Animal and clinical studies have determined that acetaminophen has both antipyretic and analgesic effects. This drug has been shown to lack anti-inflammatory effects. As opposed to the _salicylate_ drug class, acetaminophen does not disrupt tubular secretion of uric acid and does not affect acid-base balance if taken at the recommended doses. Acetaminophen does not disrupt hemostasis and does not have inhibitory activities against platelet aggregation. Allergic reactions are rare occurrences following acetaminophen use.