20/Jun/2022

Rabeprazole sodium

Overview:

Rabeprazole is used to treat the symptoms of gastroesophageal reflux disease (GERD), a condition in which backward passage of acid from the stomach induces heartburn and possible damage to the esophagus. It reduces the quantity of acid produced in the stomach. In adults and children 12 years of age and older, it is also used to reduce the risk of developing Zollinger-Ellison syndrome (too much acid production) and ulcers. Also, Rabeprazole oral tablet may interfere with any drugs, vitamins, or herbal supplements you are taking. When a chemical changes the way a drug functions, this is referred to as an interaction. This can be dangerous or prevent the medicine from working properly.

Primary Characteristics:

Rabeprazole is a proton pump inhibitor (PPI) and a powerful inhibitor of stomach acidity that is used to treat gastroesophageal reflux disease and peptic ulcer disease. Rabeprazole treatment is associated with a low risk of temporary and asymptomatic serum aminotransferase increases and is a rare cause of clinically visible liver damage.

Indication:

For the treatment of acid-reflux disorders (GERD), peptic ulcer disease, H. pylori eradication, and prevention of gastrointestinal bleeds with NSAID use.

Pharmacodynamics:

Rabeprazole inhibits the formation of stomach acid. It alleviates symptoms and protects the esophagus and stomach in individuals suffering from gastroesophageal reflux disease (GERD) or ulcers. It is also beneficial in disorders characterized by excessive stomach acid production, such as Zollinger-Ellison syndrome. The medicine may also be taken in conjunction with antibiotics to eliminate microorganisms linked to certain ulcer symptoms.

Pharmacokinetics:

Rabeprazole’s pharmacokinetics are distinguished by its high and stable bioavailability, dosage proportionality, significant hepatic metabolism, and largely urine excretion of these metabolites. Furthermore, rabeprazole does not accumulate with repeated administration. It does not accumulate with repeated dosage, and its pharmacokinetic profile is unaffected by meal or antacid consumption. These findings are consistent with previous findings for some, but not all, proton pump inhibitors. Lansoprazole pharmacokinetics appear unchanged by multiple-dose dosing.

Mechanism of Action:

Rabeprazole is an antisecretory drug (substituted Benz imidazole proton-pump inhibitor) that does not affect gastric acid secretion by blocking the gastric H+/ATPase (hydrogen-potassium adenosine triphosphates) at the secretory membrane of the gastric parietal cell. Rabeprazole has been classified as a gastric proton-pump inhibitor since this enzyme is thought to be the acid (proton) pump within the parietal cell. Rabeprazole inhibits the last stage of stomach acid production. Rabeprazole is protonated, accumulates, and is converted to an active sulfonamide in gastric parietal cells. Rabeprazole is chemically activated at pH 1.2 and has a half-life of 78 seconds when examined in vitro.

Side Effects:

Many people who use this drug have no major adverse effects. Inform your doctor straight away if you get persistent diarrhea, abdominal or stomach pain/cramping, or blood/mucus in your stool. If you experience these symptoms, avoid using anti-diarrhea or opioid medications since they may worsen them. It is uncommon for this medicine to cause a severe allergic response.

Precautions:

Rabeprazole may raise the risk of bone fractures, particularly in elderly people, as well as C. difficile infection (see Side Effects section). This drug should be taken only when plainly necessary during pregnancy. It is uncertain if this medicine gets into breast milk, although related medications do. Consult your doctor before breast-feeding.

pharmavision

31/May/2022

Diclofenac Potassium

Overview:

Diclofenac is a nonsteroidal anti-inflammatory medication (NSAID). This medication works by lowering pain and inflammation-causing chemicals in the body. Diclofenac is used to treat mild to moderate pain, as well as osteoarthritis and rheumatoid arthritis symptoms. Voltaren is also prescribed to treat ankylosing spondylitis. This medication is also used to treat menstrual cramps under the trade name Cataflam. A migraine headache attack is treated with diclofenac powder (Cambia). Cambia can only cure headaches that have already started. It will not prevent headaches or decrease the frequency of episodes.

Primary Characteristics:

Diclofenac is a phenyl acetic acid anti-inflammatory, analgesic, and antipyretic medication. It inhibits the cyclooxygenase (COX)-2 enzyme more effectively than COX-1. Other potential modes of action might include inhibiting substrate P, blocking acid-sensing ion channels, and altering interleukin-6 production. Diclofenac Potassium tablets contain benzene acetic acid. White to off-white to slightly yellowish crystalline powder that is mildly hygroscopic, soluble in methanol, soluble in alcohol, sparingly soluble in water, and faintly soluble in acetone.

Pharmacology:

Indication:

Diclofenac is used to treat pain and inflammation caused by a variety of illnesses, including inflammatory disorders such as osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis, as well as injury-related inflammation caused by surgery and physical trauma. In patients at high risk of developing NSAID-induced ulcers, it is frequently used in conjunction with misoprostol as a gastro protective medication.

Pharmacodynamics:

Diclofenac decreases inflammation and, as a result, nociceptive discomfort and heat. It also raises the risk of gastrointestinal ulcer development by decreasing the synthesis of protective mucus in the stomach.

Contradictions:

Diclofenac potassium tablets should not be administered to patients who have had asthma, urticarial, or allergic-type responses after taking aspirin or other NSAIDs. Severe, seldom fatal, anaphylactic-like responses to NSAIDs have been observed in such patients.

Mechanism of Action:

Diclofenac inhibits cyclooxygenase-1 and -2, the enzymes that produce prostaglandin (PG) G2. PGE2 is the major PG implicated in nociception modulation. PGE2 increases sensitivity to bradykinin via EP3 and further increases heat sensitivity via EP2. PGI2 and PGE2 are Gs’-coupled proteins that mediate vasodilation via the AC/PKA pathway. PGD2 is involved in the stimulation of endothelial cell cytokine release via its DP1 receptor. NSAIDs can successfully relieve inflammatory pain by decreasing sensitization, both peripheral and central.

Side Effects:

Many persons who use this drug have no major adverse effects. Nausea, vomiting, constipation, diarrhea, dizziness, or sleepiness are all possible side effects. Check your blood pressure on a regular basis and notify your doctor if it is excessive. Severe or persistent headaches, fainting, fast/pounding pulse, and indications of heart failure are all serious adverse effects.

Precaution:

Tell your doctor if you are allergic to diclofenac, aspirin, or other NSAIDs before using it (such as ibuprofen, naproxen, celecoxib) Inactive chemicals in this product may cause allergic reactions or other complications. While using this medication, older persons may be more likely to get stomach/intestinal bleeding, renal issues, a heart attack, or a stroke. This medicine may damage an unborn baby and create complications during normal labor and delivery. It is not advised to be used during pregnancy from 20 weeks till delivery.

Warnings:

NSAIDs raise the risk of major CV thrombotic events, myocardial infarction, and stroke. NSAIDs can cause new hypertension or aggravate underlying hypertension. In individuals with advanced renal disease, diclofenac potassium pills should not be used.

Vision Pharmaceuticals (PVT) Limited

Vision Pharmaceuticals are one of the best pharmaceuticals companies of the world. Different types of pharma products & drug pellets we manufacture speak volumes of the high quality, efficacy & durability. If you have any query or want to know about any product, contact us on following numbers;

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pharmavision

29/Apr/2022

Orlistat

Overview:

Orlistat is an anti-obesity medication. It acts as a lipase inhibitor, preventing fat absorption from the human diet and thereby lowering caloric intake. Orlistat’s ability to help people lose weight is undeniable yet limited. Orlistat also appears to prevent type 2 diabetes by lowering blood pressure. Obesity is becoming more common over the world. Obesity-related issues cause significant personal and financial hardship by lowering quality of life and raising healthcare costs. Diet and exercise alone are insufficient for some people to maintain weight loss, and pharmaceutical or surgical intervention is required.

Primary Characteristics:

This chemical belongs to the leucine and derivatives class of organic chemicals. These are compounds containing leucine or a derivative thereof obtained by reacting leucine with an amino or carboxyl group, or by replacing any hydrogen in glycine with a heteroatom.

Pharmacology:

Orlistat inhibits the absorption of dietary fats by blocking lipase enzymes, which assists with weight loss and maintenance.

Pharmacokinetics:

Absorption: Orlistat is absorbed mostly through its local impact in the gut, with very little systemic exposure.
Distribution: The vast bulk of the medication (greater than 99 percent) is bound to plasma proteins (lipoproteins and albumin are the major binding proteins).
Metabolism: Orlistat metabolism takes place largely within the gut wall.
Elimination: 95-97 percent of the drug is not absorbed and is eliminated in the stool.

Contraindications:

Contraindications to orlistat include the following conditions:

Hypersensitivity to orlistat or its constituents
Chronic malabsorption
Cholestasis
Anorexia and bulimia
Pregnancy
Severe renal impairment

Mechanism of Action:

Orlistat works by blocking lipases, which are enzymes in the intestine that break down lipids. Triglycerides from the diet are not hydrolyzed into absorbable free fatty acids when lipase activity is inhibited, and instead are excreted unchanged. Orlistat prevents approximately 30% of dietary fat from being absorbed when taken at the standard prescription dose of 120 mg three times daily, before meals. Higher doses have the same effect as lower doses. The parasite Trypanosoma brucei may also be affected by orlistat. Orlistat prevents approximately 30% of dietary fat from being absorbed when taken in the standard prescription dose of 120 mg three times daily, before meals. Higher doses have the same effect as lower doses.

Side Effects:

Changes in gastrointestinal function are frequently caused by unabsorbed fat. Fatty/oily stool, intestinal gas with discharge, excessive bowel motions, or poor bowel control are all possible symptoms. This medicine seldom causes a severe allergic reaction. If any of these rare but serious adverse effects occur, stop taking this medication and contact your doctor straight once.

If you experience symptoms of liver illness (such as persistent nausea/vomiting, severe stomach/abdominal pain, dark urine, yellowing eyes/skin), or kidney stones (such as back discomfort, pain while urinating, pink/bloody urine), you should stop using this drug. Although a severe allergic reaction to this medication is uncommon, it should be treated seriously. Contact your doctor or pharmacist if you experience any other negative effects. This isn’t an exhaustive list of potential adverse effects.

Precautions:

Inactive chemicals in Orlistat can induce allergic responses and other complications. This drug should not be taken when pregnant. If you have diabetes, losing weight may help you control your blood sugar levels. A pregnant woman’s weight loss has no possible benefits and may harm her unborn child.

Warnings:

Orlistat is merely one component of a comprehensive treatment plan that includes food, exercise, and weight management. Keep a close eye on your nutrition, medicine, and exercise routines. Avoid eating a high-fat diet. When you take orlistat with a high-fat meal, you run the chance of having unpleasant stomach or intestine side effects. Your daily fat, protein, and carbohydrate intake should be evenly distributed across all of your meals.

Vision Pharmaceuticals (PVT) Limited

+92 (051) 449 3587, +92 (51) 449 3589, +92 (321) 517 1779

pharmavision

09/Aug/2021

Duloxetine Hydrochloric Acid

Overview

Duloxetine hydrochloride is a selective serotonin and norepinephrine reuptake inhibitor (SSNRI) for oral administration. Its chemical designation is (+)-(S)-N-methyl-?-(1-naphthyloxy)-2-thiophenepropylamine hydrochloride. The empirical formula is C18H19NOS•HCl. Duloxetine hydrochloride is a white to slightly brownish white solid, which is slightly soluble in water.

Primary Characteristics

Duloxetine Hydrochloride is of Synthetic origin. . The Molecular Weight of Duloxetine Hydrochloride is 333.90. It is weakly alkaline drug.

Indications

Indicated for:

1) Management of Major Depressive Disorder.

2) Management of Generalized Anxiety Disorder.

3) Management of diabetic peripheral neuropathy.

4) Management of fibromyalgia.

5) Management of chronic musculoskeletal pain.

6) Management of osteoarthritis of the knee in adults.

7) Management of chronic lower back pain in adults.

8) Management of stress urinary incontinence in adult women.

Off-label uses include:

1) Management of chemotherapy-induced peripheral neuropathy.

2) Management of stress urinary incontinence in adult men after prostatectomy until recovery is complete.

Pharmacodynamics

Duloxetine, through increasing serotonin and norepinephrine concentrations in Onuf’s nucleus, enhances glutamatergic activation of the pudendal motor nerve which innervates the external urethral sphinter. This enhanced signaling allows for stronger contraction. Increased contraction of this sphincter increases the pressure needed to produce an incontinence episode in stress urinary incontinence. Duloxetine has been shown to improve Patient Global Impression of Improvement and Incontinence Quality of Life scores. It has also been shown to reduce the median incontinence episode frequency at doses of 40 and 80 mg.

Action at the dorsal horn of the spinal cord allows duloxetine to strengthen the the serotonergic and adrenergic pathways involved in descending inhibition of pain. This results in an increased threshold of activation necessary to transmit painful stimuli to the brain and effective relief of pain, particularly in neuropathic pain. Pain relief has been noted in a variety of painful conditions including diabetic peripheral neuropathy, fibromyalgia, and osteoarthritis using a range of pain assessment surveys. While duloxetine has been shown to be effective in both animal models of mood disorders and in clinical trials for the treatment of these disorders in humans, the broad scope of its pharmacodynamic effects on mood regulation in the brain has yet to be explained.

Mechanism of action

Duloxetine is a potent inhibitor of neuronal serotonin and norepinephrine reuptake and a less potent inhibitor of dopamine reuptake. Duloxetine has no significant affinity for dopaminergic, adrenergic, cholinergic, histaminergic, opioid, glutamate, and GABA receptors.

Action on the external urinary sphincter is mediated via duloxetine’s CNS effects. Increased serotonin and norepinephrine concentrations in Onuf’s nucleus leads to increased activation of 5-HT2, 5-HT3, and ?1 adrenergic receptors. 5-HT2 and ?1 are both Gq coupled and their activation increases the activity of the inositol trisphosphate/phospholipase C (IP3/PLC) pathway. This pathway leads to release of intracellular calcium stores, increasing intracellular calcium concentrations, and facilitating neuronal excitability. 5-HT3 functions as a ligand-gated sodium channel which allows sodium to flow into the neuron when activated. Increased flow of sodium into the neuron contributes to depolarization and activation of voltage gated channels involved in action potential generation. The combined action of these three receptors contributes to increased excitability of the pudendal motor nerve in response to glutamate

Duloxetine side effects

The severe or irreversible adverse effects of Duloxetine Hydrochloride, which give rise to further complications include Hyponatremia, Hyponatremia.

The symptomatic adverse reactions produced by Duloxetine Hydrochloride are more or less tolerable and if they become severe, they can be treated symptomatically, these include Weakness, Thirst, Fatigue, Nausea, Vomiting, Diarrhea, Constipation, Insomnia, Sweating, Blurred vision, Pruritus, Lethargy, Dyspepsia, Weight gain, Somnolence, Tremor, Sexual dysfunction, Syncope, Decrease in libido, dyspepsia.

pharmavision

05/Aug/2021

Lansoprazole

Overview

Lansoprazole is an acid proton pump inhibitor. Lansoprazole is a benzimidazole sulfoxide derivative and produces long lasting inhibition of gastric acid secretion. Lansoprazole is a chiral compound with one chiral center, synthsized as a racemic mixture and both enantiomers are active. Chemically Lansoprazole is identified as 2-[[[3-methyl-4-(2, 2, 2-trifluoroethoxy)-2-pyridinyl] methyl] sulfinyl ]-1H-benzimidazole. Lansoprazole is effective in the treatment of duodenal or gastric ulcer, gastroesophageal reflux disease and in the treatment of zollinger-ellison syndrome. Lansoprazole is administered orally.

Primary Characteristics

It is of Synthetic origin and belongs to Sulphinyl Benzimidazole. It belongs to H/K Atpase proton pump inhibitor pharmacological group on the basis of mechanism of action and also classified in Antacids pharmacological group. The Molecular Weight of Lansoprazole is 369.00.

Its pKa is 8.85.

Indications

Lansoprazole is primarily indicated in conditions like Acid-related dyspepsia, Benign gastric ulcer, Duodenal ulcer, Duodenal ulcer associated with h. Pylori, Esophagitis, Gastric ulcer, Gastro-esophageal reflux disease, Heart burn, Helicobacter pylori positive duodenal ulcer, NSAID-associated gastric and duodenal ulcers, NSAID-associated gastric and duodenal ulcers (prophylaxis), NSAID-associated gastric or duodenal ulcers, Peptic ulcer, Resistant ulcers, Zollinger-ellison syndrome, and can also be given in adjunctive therapy as an alternative drug of choice in GI bleeding.

Pharmacokinetics

Oral absorption of Lansoprazole is found to be 40% ±40. Volume of distribution is found to be 24 ± 8 liter and plasma proteins binding is 97-99%. and metabolism is reported Hepatic(extensively). Renal Excretion accounts for 30% and plasma half life is 1-2 hr.

Pharmacodynamics

Lansoprazole decreases gastric acid secretion by targeting H+,K+-ATPase, which is the enzyme that catalyzes the final step in the acid secretion pathway in parietal cells. Conveniently, lansoprazole administered any time of day is able to inhibit both daytime and nocturnal acid secretion. The result is that lansoprazole is effective at healing duodenal ulcers, reduces ulcer-related pain, and offers relief from symptoms of heartburn Lansoprazole also reduces pepsin secretion, making it a useful treatment option for hypersecretory conditions such as Zollinger-Ellison syndrome.

Mechanism of action

As a PPI, lansoprazole is a prodrug and requires protonation via an acidic environment to become activated. Once protonated, lansoprazole is able to react with cysteine residues, specifically Cys813 and Cys321, on parietal H+,K+-ATPase resulting in stable disulfides. PPI’s in general are able to provide prolonged inhibition of acid secretion due to their ability to bind covalently to their targets.

Side Effects

The severe or irreversible adverse effects of Lansoprazole, which give rise to further complications include Atrophic gastritis, Epidermal necrolysis.

The symptomatic adverse reactions produced by Lansoprazole are more or less tolerable and if they become severe, they can be treated symptomatically, these include Headache, Nausea, Diarrhea, Constipation, Rashes, Pruritus.

Interference in Pathology

Elevations of SGPT and SGOT
Abnormal LFTs
Increased Alkaline Phosphatase Levels
Elevation in ALT or AST
Increased in serum creatinin

pharmavision

02/Aug/2021

Itraconazole

Overview

Itraconazole is a broad-spectrum antifungal agent for oral treatment of vulvovaginal candidiasis, pityriasis versicolor and dermatophytes. Itraconazole is a substituted triazole derivative. Itraconazole active works against many Candida species, endemic mycoses and dermatophytes. Itraconazole is the most potent of available azoles, but effectiveness can be limited by reduced bio availability. The requirement for intravenous administration and the toxicity of the older antifungal agents created a need for antifungal agents with a better therapeutic profile. The relatively non-toxic oral azole medications represent the first major advance in this direction. Since their introduction in the 1980s, these medications have played an increasingly important role in the systemic therapy of fungal diseases.

Primary Characteristics

Itraconazole is also known as Oriconazole. It is of Synthetic origin and belongs to Triazole. It belongs to Antifungals pharmacological group. The Molecular Weight of Itraconazole is 705.60.

Its pKa is 3-4.

Indications

Itraconazole is primarily indicated in conditions like Advanced breast or prostate cancer, Antifungal prophylaxis, Candidiasis, Cryptcoccal meningitis, Dermatophytic infections, Histoplasmosis, Oculomycoses, Onychomycoses, Oral candidiasis, Oropharangeal candidiasis, Orophyrangeal candidiasis, Pityriasis versicolor, Sporotrichosis, Superficial candidiasis, Systemic mycoses, Tinea pedis, Tinae manuum, To reduce intestinal secretions and vomiting, To reduce intestinal secretions and vomiting (palliative care), and can also be given in adjunctive therapy as an alternative drug of choice in Cushing`s syndrome due to malignant disease, Fungal keratitis, Leishmaniasis, Vulvo-vaginal candidosis.

Pharmacokinetics

Oral absorption of Itraconazole is found to be 42.5% ±42.5. Volume of distribution is found to be 10.7 l/kg and plasma protien binding is 99.8%. Presystemic metabolism is noted to be 22.5% ±22.5 and metabolism is reported Hepatic. Renal Excretion accounts for 40% (inactive metabolite) and plasma half life is 20 hr.

Mechanism of action

Itraconazole interacts with 14-? demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Itraconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis

Side Effects

The severe or irreversible adverse effects of Itraconazole, which give rise to further complications include Hypotension, Hepatitis, Hypotension.

Itraconazole produces potentially life-threatening effects which include Dysrhythrics. which are responsible for the discontinuation of Itraconazole therapy.

The signs and symptoms that are produced after the acute overdosage of Itraconazole include Constipation, Gastritis, Depression.

The symptomatic adverse reactions produced by Itraconazole are more or less tolerable and if they become severe, they can be treated symptomatically, these include Dizziness, Vertigo, Headache, Fatigue, Nausea, Vomiting, Diarrhea, Abdominal pain, Pruritus, Hallucination, Somnolence, Hair loss, Edema, Photophobia, Vasculitis, dizziness.

Warning / Precautions

Itraconazole should be used with caution in patients with liver disease, heart rhythm disorders (arrhythmias) and of any drug allergies. It should be used with caution while engaging in activities requiring alertness because this medication causes dizziness or drowsiness. It should be used only when clearly needed during pregnancy or lactation. Safe use of itraconazole in the children under the age 16 has not been established. The drug should be used with caution in the patients with azole hypersensitivity. Patients who develop abnormal liver function tests during itraconazole therapy should be monitored and therapy discontinued if symptoms of the liver disease develop. Should not be administered to treat onchonycosis in pateints with ventricular dysfurution.

Storage Conditions

Capsules:

Store Between 15°C-30°C. Protect from Sunlight, Moisture and Heat.

Solution:

Store at room temperature, Below 25°C. Do not Freeze. Protect from Sunlight and Heat.

Interference in Pathology

Elevated liver enzymes

pharmavision

29/Jul/2021

Azithromycin

The antimicrobial agents or antibiotics develops during the last 60 years are among the most dramatic examples of the advances of science. The remarkably powerful and specific activity of antimicrobial drug is due to their selectivity for highly specific targets that are either unique to micro-organism or much more important in them than in humans. Azithromycin belongs to a macrolide antibiotic. Azithromycin is a 15-atom lactone macrolide ring compound. Azithromycin is a semisynthetic derivative of Erythromycin obtained by the addition of methylated nitrogen into the lactone ring of Erythromycin. Azithromycin is effective against gram positive bacteria. Antibiotics require constant drug level in body for therapeutic effect. This is achieved by taking the medication at regular interval of time throughout the day and night as prescribed. Azithromycin is important to take the drug for the full time period as prescribed. If you discontinue the therapy, it may result in ineffective treatment.

Primary Characteristics

It is of Semi Synthetic origin and belongs to Azalide. It belongs to Antibacterial (Protein synthesis inhibitor) pharmacological group on the basis of mechanism of action and also classified in Antibiotics pharmacological group. The Molecular Weight of Azithromycin is 785.00.

Indications

Azithromycin is primarily indicated in conditions like Cervicitits, Lower respiratory tract infections, Multiple myeloma, Otitis media, Reversal of excessive bradycardia, Rtis, otitis media, Skin and soft tissue infections, Soft tissue and skin infections, Status epilepticus (unlicensed use), Upper respiratory tract infections, Urethritis.

Pharmacokinetics

Oral absorption of Azithromycin is found to be 34% ±19. Volume of distribution is found to be 31.1 l/kg and plasma proteins binding is 51%. Renal Excretion accounts for < 10% unchanged. Also excreted in bile and plasma half life is 68%.

Contraindications

Azithromycin is contraindicated in conditions like Hepatic impairment, Hypersensitivity.

Drug Interactions

Azithromycin is known to interact with other drugs, the details of drug interactions is as follows:

Severity

Triazolam, Aluminium Hydroxide and Oxide, Cyclosporin, Terfenadine, Theophylline, Ergotamine (Tartrate), Ibrutinib

Moderate

Astemizole, Digoxin.

These interactions are sometimes beneficial and sometimes may pose threats to life. Always consult your physician for the change of dose regimen or an alternative drug of choice that may strictly be required.

Side Effects

The severe or irreversible adverse effects of Azithromycin, which give rise to further complications include Maculopapular rash, Cholestasis, Pseudomembranous colitis, Jaundice.

Azithromycin produces potentially life-threatening effects which include Anaphylaxis, Angioneurotic edema. which are responsible for the discontinuation of Azithromycin therapy.

The signs and symptoms that are produced after the acute over dosage of Azithromycin include severe nausea, Severe diarrhoea, Severe vomiting, Hearing loss.

The symptomatic adverse reactions produced by Azithromycin are more or less tolerable and if they become severe, they can be treated symptomatically, these include Flatulence, Dizziness, Vertigo, Headache, Fatigue, Nausea, Vomiting, Diarrhoea, Palpitation, Abdominal pain, Rashes, Photosensitivity, Deafness, GI disturbance.

High Risk Groups

Drug should not be given to Pregnant Mothers, patients suffering from Kidney dysfunction, patients suffering from Liver Malfunction, and Neonates.

If prescribing authority justifies the benefits of the drug against the possible damages he/she should re-evaluate them and consult the reference material and previous +

studies.

Warning / Precautions

Azithromycin should be used with caution in patients with illness or any allergy, especially allergies to drugs, liver disease, jaundice, history of colitis or stomach problems or kidney disease. This drug should be used only if clearly needed during pregnancy or lactation.

Storage Conditions

Tab, Caps, Oral Suspension

Store Below 40°C. Protect from Sunlight and Moisture.

Interference in Pathology

The use of Azithromycin may show false elevated serum aspartate.

pharmavision

26/Jul/2021

Clarithromycin

Clarithromycin is a macrolide antibiotic. Macrolides are compounds characterized by a macrocyclic lactone ring to which deoxy sugars are attached. Clarithromycin is a semisynthetic derivative of Erythromycin obtained by the addition of methyl group to hydroxyl group at carbon 6. Clarithromycin is effective against gram positive bacteria. Antibiotics require constant drug level in body for therapeutic effect. This is achieved by taking the medication at regular interval of time throughout the day and night as prescribed. Clarithromycin is important to take the drug for the full time period as prescribed. If you discontinue the therapy, it may result in ineffective treatment.

Primary Characteristics

clarithromycin is of Semi Synthetic origin and belongs to Hexopyranosyl. It belongs to Antibacterial (Proetin synthesis inhibitor) pharmacological group on the basis of mechanism of action and also classified in Antibiotics pharmacological group. The Molecular Weight of Clarithromycin is 748.00.

Indications

Clarithromycin is primarily indicated in conditions like Chronic bronchitis, Metastatic germ cell cancer, Mycobacterial infection, Otitis media, Pharyngitis, Pneumonia, Respiratory tract infections, Rtis, otitis media, Sinusitis, Skin infections, Soft tissue infections, To counteract the folate-antagonist action of methotrexate, Tonsillitis, and can also be given in adjunctive therapy as an alternative drug of choice in Duodenal ulcer, Endocarditis.

Pharmacokinetics

Oral absorption of Clarithromycin is found to be 50% ±50. Volume of distribution is found to be 250 litre and plasma protien binding is 80%. Presystemic metabolism is noted to be 20% ±20 and metabolism is reported via liver. Renal Excretion accounts for 20-30%(unchanged) 10-15%(metabolite) and plasma half life is 2.9-9.2 hr.

Pharmacodynamics

Clarithromycin is a macrolide antibiotic whose spectrum of activity includes many gram-positive (Staphylococcus aureus, S. pneumoniae, and S. pyogenes) and gram-negative aerobic bacteria (Haemophilus influenzae, H. parainfluenza, and Moraxella catarrhalis), many anaerobic bacteria, some mycobacteria, and some other organisms including Mycoplasma, Ureaplasma, Chlamydia, Toxoplasma, and Borrelia. Other aerobic bacteria that clarithromycin has activity against include C. pneumoniae and M. pneumoniae. Clarithromycin has an in-vitro activity that is similar or greater than that of erythromycin against erythromycin-susceptible organisms. Clarithromycin is usually bacteriostatic, but may be bactericidal depending on the organism and concentration of drugs.

Mechanism of action

Clarithromycin is first metabolized to 14-OH clarithromycin, which is active and works synergistically with its parent compound. Like other macrolides, it then penetrates bacteria cell wall and reversibly binds to domain V of the 23S ribosomal RNA of the 50S subunit of the bacterial ribosome, blocking translocation of aminoacyl transfer-RNA and polypeptide synthesis. Clarithromycin also inhibits the hepatic microsomal CYP3A4 isoenzyme and P-glycoprotein, an energy-dependent drug efflux pump.

Side Effects

The severe or irreversible adverse effects of Clarithromycin, which give rise to further complications include Renal failure, Interstitial nephritis, Pseudomembranous colitis.

Clarithromycin produces potentially life-threatening effects which include cerebial hemorrhage. which are responsible for the discontinuation of Clarithromycin therapy.

The signs and symptoms that are produced after the acute overdosage of Clarithromycin include Hypoxia, Hypokalemia.

The symptomatic adverse reactions produced by Clarithromycin are more or less tolerable and if they become severe, they can be treated symptomatically, these include Headache, Nausea, Vomiting, Diarrhea, Abdominal pain, Phlebitis, Glossitis, StomatitisX, Elevation of liver enzymes, Taste perversion, Increased intracranial pressure, Hypoglycemia.

Warning / Precautions

Clarithromycin should be used with caution in patients with other illnesses or any allergy, especially allergies to drugs, arrythmias ,liver disease, jaundice (yellowing of the skin or eyes), kidney disease , or a history of colitis or stomach problems. This drug should be used only if clearly needed during pregnancy or lactation.

Storage Conditions

Oral suspension (reconstituted)

Store at room temperature. Refrigeration and Freezing is not recommended. Protect from Sunlight. Use within 14 days if kept at room temperature.

Tablets:

Store in a well closed container, Below 40°C. Protect from Sunlight and Moisture.

Interference in Pathology

Elevations of SGPT and SGOT

Alkaline phosphatase levels are elevated.

Serum creatinine raised.

Interference with serum aspartate amino transferase, urinary catecholamine and 17- hydroxy corticosteroids.

pharmavision

13/Jul/2021

Omeprazole

Omeprazole is a an oral antiulcer agent. Omeprazole is characterized as a gastric acid pump inhibitor because it blocks the final step of gastric acid production. It has a long duration of action and is very potent, allowing for once-daily administration. Despite its potency, it must be used in combination with antibiotics to be effective against Helicobacter pylori. Due to concern regarding long-term use, it was originally approved by the FDA in September 1989 for acute treatment only. In December 1994, an FDA advisory committee recommended it be approved for maintenance therapy of healed erosive esophagitis. In April 1996, it was approved for the treatment of H. pylori-associated duodenal ulcer. Belongs to a new class of ant secretory agents, the substituted benzimidazoles, which suppress gastric acid secretion by inhibiting the H+/K+ ATPase enzyme system of parietal cells. it, following activation in an acidic pH, binds irreversibly to the H+/K+ ATPase pump on the secretory surface of the parietal cell membrane. Subsequently, the secretion of hydrogen ions into the gastric lumen is inhibited. it inhibits both basal and stimulus-induced acid secretion.

Primary Characteristics

Omeprazole is also known as Proton pump Inhibitor. It is of Synthetic origin and belongs to Benzimidazol. It belongs to H/K At pase proton pump inhibitor pharmacological group on the basis of mechanism of action and also classified in Antacids pharmacological group. The Molecular Weight of Omeprazole is 345.40.

Its pKa is 4.0, 8.7.

Indications

Omeprazole is primarily indicated in conditions like Acid reflux disease (long-term management), Benign gastric and duodenal ulceration, Benign gastric and duodenal ulcers, Benign gastric ulcer associated with H.pylori, Duodenal errosions, Duodenal or benign gastric ulcer associated with H.pylori, Duodenal ulcer, Duodenal ulcer associated with h. Pylori, Gastric acid reduction during anaesthesia, Gastric acid reduction during general anesthesia, Gastric ulcer, Gastro-esophageal reflux disease, Gastro-o esophageal reflux disease, Gastro-esophageal reflux disease (refractory to other treatment), Maintenance of recurrent duodenal ulcers, Non-ulcer dyspepsia, NSAID-associated gastric and duodenal ulcers, NSAID-associated gastric and duodenal ulcers (prophylaxis), NSAID-associated gastric and duodenal ulcers and duodenal erosions, NSAID-associated gastric or duodenal ulcers, NSAID-associated gastric or duodenal ulcers (prophylaxis), Prevention of relapse in duodenal ulcer, Prophylaxis for NSAID-associated gastric and duodenal ulcers, Prophylaxis of acid aspiration, Reflux esophagitis, Resistant ulcers, Severe or recurrent duodenal and gastric ulceration, Zollinger-Ellison syndrome, and can also be given in adjunctive therapy as an alternative drug of choice in Acid aspiration syndrome prevention, GI bleeding.

Pharmacokinetics

Oral absorption of Omeprazole is found to be 57.5% ±7.5. Volume of distribution is found to be 0.3 – 0.4 l/kg and plasma proteins binding is 95%. Pre systemic metabolism is noted to be 20% and metabolism is reported Hepatic. Renal Excretion accounts for 80% and plasma half life is 1 hr.

Mechanism of action

Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump , expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid) .

Omeprazole is a member of a class of anti secretory compounds, the substituted benzimidazoles, that stop gastric acid secretion by selective inhibition of the H+/K+ ATPase enzyme system. Proton-pump inhibitors such as omeprazole bind covalently to cysteine residues via disulfide bridges on the alpha subunit of the H+/K+ ATPase pump, inhibiting gastric acid secretion for up to 36 hours . This anti secretory effect is dose-related and leads to the inhibition of both basal and stimulated acid secretion, regardless of the stimulus .

Mechanism of H. pylori eradication

Peptic ulcer disease (PUD) is frequently associated with Helicobacter pylori bacterial infection (NSAIDs) . The treatment of H. pylori infection may include the addition of omeprazole or other proton pump inhibitors as part of the treatment regimen. H. pylori replicates most effectively at a neutral pH . Acid inhibition in H. pylori eradication therapy, including proton-pump inhibitors such as omeprazole, raises gastric pH, discouraging the growth of Pylori . It is generally believed that proton pump inhibitors inhibit the urease enzyme, which increases the pathogenesis of H. pylori in gastric-acid related conditions .

Side Effects

The severe or irreversible adverse effects of Omeprazole, which give rise to further complications include Interstitial nephritis.

Omeprazole produces potentially life-threatening effects which include Anaphylaxis. which are responsible for the discontinuation of Omeprazole therapy.

The signs and symptoms that are produced after the acute over dosage of Omeprazole include Tachycardia, Drowsiness, Drowsiness, Headache.

The symptomatic adverse reactions produced by Omeprazole are more or less tolerable and if they become severe, they can be treated symptomatically, these include Flatulence, Dizziness, Headache, Fatigue, Nausea, Diarrhea, Myalgia, Constipation, Insomnia, Abdominal pain, Dry mouth, Urticaria, Pruritus, Photosensitivity, Skin rash, Impotence, Depression, Arthralgia, Myopathy, Gynecomastia, Agitation, Dry mouth, dizziness.

pharmavision

06/Nov/2020

Drug Pellet formation may appear as semicircular granules to an unaided eye. But is it the same plain, old, bitter tastings medicinal stuff, nay! It indeed a marvelous of modern pharmaceutical research. We at Vision Pharmaceutical put literally our heart and soul with critical Thinking brains and expert hands into making drug palletization a reality and its wider availablity to local as well as international consumers.

Vision Pharmaceutical with its focused and result oriented R&D makes the formation of nearly spherical particles into final, pellitized product possible undergoing the process of fine particulating ,tumble drying, addition of binders and additives in various pellitization equipment.

Our unique pellitization techniques make us not only on par with any standardized international pellet manufacturers but give us un upper hand in economically competitive market as well. Drug Pellets manufacturing an art in itself and undergoes stages of production under uber scientific principles. What factors work deep down in these processing and how complicated it ,let us have a look.

At first moist content of dried particles is reduced to form an effective air water interface. Make a granulation of particles possible with the help of both physical and applied forces. Physical forces impart tensile strength and liquid bridging among particles, changing capillary and surface tension of granules.

At Vision Pharmaceutical purpose built fully automated manufacturing unit makes tumbling motion of the particles possible and applied forces. That arise as a result bring individual wetted particles close to each other and uniform distribution of active ingredients. This mechanism makes it possible to initiate pellitization process and subsequent growth of individual pellets under the following factors.

Nucleation

Nucleation the Formation of nuclei and the process of particles formation from the continuos phase via interaction within the physical environment. In this stage liquid bridges created making formation of three dimensional water-air-liquid bonding possible, this give particles specific physical appearance and properties. Vision Pharmaceuticals makes sure that particles size must kept smaller for better bonding strength.

Coalescence:

The second stage is coalescence, its a transition stage. This region affected by growth factors of coalescence and drug layering. Very important indeed so it needs to be closely supervised and Our R&D strives to make the process up to date. Coalescence brings discreet changes to size and no of particles but not to their mass.

Layering

Layering is a third and final factor in manufacturing process of pellet formation. It is a continuous phase where both size and properties of particulate matter changes with drug layering. Vision Pharmaceutical advanced, fully automated production facility. Makes its possible to layer single or multiple active drugs on a single granule. Masking of bitter tastings drugs with addition of layers of Tasteless additives also ensured in this process.

All these Physical and Chemical processes work simultaneously in delicate ways to make scientifically quantified, tasteless, single/multi ingredient active drug pellets a reality and Vision as a pioneer in the science of pellitization.

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