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09/Aug/2021

Duloxetine HCL

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 α1 adrenergic receptors. 5-HT2 and α1 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.

 


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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

 


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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-α 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

 


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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.

 


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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.

 


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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.

 


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09/Jul/2021

Esomeprazole Magnesium

Esomeprazole is an ulcer-healing drug, that inhibits gastric acid by blocking the proton-pump (Hydrogen-Potassium at pase enzyme system) of the gastric perital cells. Esomeprazole is used for the short-term treatment of gastric and duodenal ulcers and in gastro-oesophageal reflux disease with severe symptoms. Also used in combination with anti bacterial for the eradication of Helicobacter pylori.

Primary Characteristics

Esomeprazole Magnesium trihydrate is the derivative of Esomeprazole. It is of Synthetic origin and belongs to Sulphinyl Benzimidazol. . The Molecular Weight of Esomeprazole is 345.40.

Indications

Esomeprazole is indicated for the treatment of acid-reflux disorders including healing and maintenance of erosive esophagitis, and symptomatic gastroesophageal reflux disease (GERD), pepticulcer disease, Hpylorieradication, prevention of gastrointestinal bleeds with NSAID use, and for the long-term treatment of pathological hypersecretory conditions including Zollinger-Ellison Syndrome

Pharmacokinetics

Oral absorption of Esomeprazole found to 69.5% ±19.5. Plasma protien binding is 97%. and metabolism is reported Liver. Renal Excretion accounts for Urine and plasma half life is 1.2hour.

Mechanism of action

Esomeprazole exerts its stomach acid-suppressing effects by preventing the final step in gastric acid production by covalently binding to sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of esomeprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, esomeprazole’s duration of anti secretory effect that persists longer than 24 hours.

Side Effects

The severe or irreversible adverse effects of Esomeprazole, which give rise to further complications include Liver damage.

The signs and symptoms that are produced after the acute over dosage of Esomeprazole include Ataxia, Tremor, Change in respiratory frequency, Intermediate Chronic Convulsion.

The symptomatic adverse reactions produced by Esomeprazole are more or less tolerable and if they become severe, they can be treated symptomatically, these include Flatulence, Dizziness, Headache, Fatigue, Diarrhea, Myalgia, Constipation, Abdominal pain, Dry mouth, Blurred vision, Rashes, Pruritus, Malaise, Arthralgia, Nausea and vomiting, Musculoskeletal pain, Dry mouth, dizziness, subacute myopathy, athralgia.

Warning / Precautions

Esomeprazole should be given with caution in patients with renal impairment, liver disease, in pregnancy and in breast-feeding. Proton-pump inhibitors may mask symptoms of gastric cancer, particular care required in those whose symptoms change and in those over 45 years of age the presence of gastric malignancy should excluded before treatment.

 

Storage Conditions

Store at room temperature, . Protect from Sunlight

 


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05/Jul/2021

Dexlansoprazole (DDR)

 

Dexlansoprazole is a new generation proton pump inhibitor (PPI) used for the management of symptoms associated with gastroesophageal reflux disease (GERD) and erosive esophagitis. Dexlansoprazole the R-enantiomer of Lansoprazole, which is composed of a racemic mixture of the R- and S-enantiomers. Compared to the older generation of PPIs (which includes Pantoprazole, Omeprazole, and Lansoprazole) , dexlansoprazole MR has a unique pharmacokinetic profile due to its delayed-release and dual-delivery release system. The active ingredient is released in two phases at different pH values and at different time points, resulting in two peak concentrations in the blood; 25% of the dose is released at pH 5.5 in the proximal duodenum, while the remaining 75% is released at pH 6.75 in the distal small intestine . As a result, dexlansoprazole has a peak concentration within 1-2 hours after dosing and another within 4-5 hours . Dexlansoprazole’s unique pharmacokinetics addresses limitations of the older generation PPIs including short plasma half-life, break-through symptoms, and need for meal-associated dosing . These characteristics make dexlansoprazole a good option for people who struggle with adherence and strict dosage timing before meals.

More about Dexlansoprazole

Dexlansoprazole exerts its stomach acid-suppressing effects in the same way as other drugs in the PPI family by inhibiting the final step in gastric acid production. Dexlansoprazole targets the (H+, K+)-ATPase enzyme, which is involved in the secretion of hydrochloric acid through the exchange of H+ ions from the cytoplasm for K+ ions. Normally functioning (H+, K+)-ATPase stimulates hydrochloric acid secretion into the gastric lumen thereby increasing stomach acidity and lowering pH. Once absorbed into circulation, dexlansoprazole covalently binds to the sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells, which leads to inhibition of both basal and stimulated gastric acid secretion. Despite dexlansoprazole’s unique pharmacokinetic profile, efficacy in management of GERD symptoms is considered similar to other medications within the PPI class including Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole, and Rabeprazole.

Due to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as dexlansoprazole have been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal C. difficile), reduced absorption of micronutrients including iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life  PPIs such as dexlansoprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary .

Dexlansoprazole doses should be slowly lowered, or tapered, before discontinuing as rapid discontinuation of PPIs such as dexlansoprazole may cause a rebound effect and a short term increase in hypersecretion .

Weight

Average: 369.36
Monoisotopic: 369.075882366

Chemical Formula

C16H14F3N3O2S

Indication

Dexlansoprazole is indicated for healing all grades of erosive esophagitis (EE), maintaining and healing of EE and relief of heartburn, and treating heartburn associated with symptomatic non-erosive gastroesophageal reflux disease (GERD).

 

Pharmacodynamics

Dexlansoprazole is a proton pump inhibitor (PPI) and is included in the drug class of antisecretory compounds. It blocks the final step of gastric acid secretion by specific inhibition of the (H+, K+)-ATPase at the secretory surface of the parietal cells on gastric mucosa.

 

Mechanism of action

Dexlansoprazole inhibits the H/K ATPase enzyme, which is involved in the secretion of hydrochloric acid, hydrolyzing ATP and exchanging H+ ions from the cytoplasm for K+ ions in the secretory canaliculus, which results in HCl secretion into the gastric lumen. Dexlansoprazole inhibits this effect of H/K ATPase by demonstrating a high degree of activation in the acidic environment. After passing through the liver and reaching the gastric parietal cells activated by a meal, PPIs undergo protonation in the acidic pH environment, followed by conversion to sulphenamide which represents the active form of the drug. Sulphenamide inhibits the activity of the proton pump and hence the transport of hydrogen ions into the gastric lumen via covalent binding to the SH groups of the cysteine residues of H/K ATPase 2. The delivery technology of dexlansoprazole MR is designed to release the drug in two separate pH-dependent phases, the first in the proximal duodenum (25% of total drug dose) and the second (75% of total drug dose) in the more distal small intestine. Dexlansoprazole reduces both basal and stimulated gastric acid secretion.

Route of elimination

Dexlansoprazole is cleared from the body by either fecal excretion (50.7%) or renal excretion (47.6%) following oral ingestion, with no unchanged drug detected in the urine.

Half-life

Dexlansoprazole is eliminated with a half-life of approximately one to two hours in healthy subjects and in patients with symptomatic GERD.

 

Clearance

Apparent clearance (CL/F) in healthy subjects was 11.4 to 11.6 L/hour, respectively, after five days of 30 or 60 mg once daily administration

Adverse Effects

Most commonly reported adverse reactions are diarrhea, abdominal pain, nausea, upper respiratory tract infection, vomiting, and flatulence. There are no reports of significant overdose but serious adverse events of hypertension have been reported in association with twice daily doses of DEXILANT 60 mg. Nonclicnial toxicology of dexlansopraole was assessed using lansoprazole studies. In two 24-month carcinogenicity studies involving rats, lansoprazole induced dose-related gastric ECL cell hyperplasia and ECL cell carcinoids and increased the incidence of intestinal metaplasia of the gastric epithelium in both sexes of rats. Dexlansoprazole is expected to have no effect on fertility and the reproductive system.


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02/Jul/2021

Ciprofloxacin

Overview

Ciprofloxacin is a fluoroquinolone antimicrobial agent with a broad spectrum of activity against both gram-negative and gram-positive bacteria. It relatively non-toxic and well tolerated broad spectrum agent. Excellent bioavailability permits its use for treatment of variety of serious bacterial infections. 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. For Ciprofloxacin (HCl) it important to take the drug for the full time period as prescribed. If you discontinue the therapy it may result in ineffective treatment.
Ciprofloxacin (HCl) is the monohydrated hydrochloride salt of ciprofloxacin. Ciprofloxacin (HCl) is effective against many gram positive and gram negative bacteria, including some strains resistant to penicillins, cyclosporins and aminoglycosides.

Primary Characteristics

Ciprofloxacin (HCl) is the derivative of Ciprofloxacin. It is of Semi Synthetic origin and belongs to Quinoline Carboxylic Acid. It belongs to DNA Gyrase inhibitor pharmacological group on the basis of mechanism of action and also classified in Antibiotics pharmacological group. The Molecular Weight of Ciprofloxacin is 346.00. Its pKa is 6-8.8.

Indications

Ciprofloxacin primarily indicated in conditions like Acromegaly (short-term treatment before pituitary surgery), Chronic prostatitis, GI infections, Gonorrhoea, Iron-deficiency anaemia prophylaxis or for mild iron deficiency, Iron-deficiency anaemia with chronic renal failure, Most other infections, Muscle relaxation (long duration) for surgery and intubation, , Osteomyelitis, Pseudomonal lower+RTI in cystic fibrosis, Respiratory tract infections, Sexually transmitted disease, Sexually transmitted infections, Skin infections, Skin structure infections, Status epilepticus (unlicensed use), Surgical prophylaxis, Urinary tract infection.

 

Pharmacokinetics

Oral absorption of Ciprofloxacin is found to be 67% ±17. Volume of distribution is found to be 177-217 litre and plasma protien binding 30%. and metabolism reported 5% via liver. Renal Excretion accounts for 70% unchanged, 10% metabolites of IV dose and plasma half life is 3-4 hr.

 

 Mechanism of action

Ciprofloxacin acts on bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. Ciprofloxacin’s targeting of the alpha subunits of DNA gyrase prevents it from supercoiling the bacterial DNA which prevents DNA replication.

Metabolism

Ciprofloxacin is primarily metabolized by CYP1A2. The primary metabolites oxociprofloxacin and sulociprofloxacin make up 3-8% of the total dose each. Converted to the minor metabolites desethylene ciprofloxacin and formylciprofloxacin. These 4 metabolites account for 15% of a total oral dose.

There a lack of available data on the enzymes and types of reactions involved in forming these metabolites.

Contraindications

Ciprofloxacin is contraindicated in conditions like Epilepsy, and Hypersensitivity.

Side Effects

The severe or irreversible adverse effects, which give rise to further complications include Hearing loss, Seizures and Pseudomembranous colitis.

Produces potentially life-threatening effects which include Anaphylactoid reactions, Stevens Johnson syndrome, Acute Renal Failure, Epidermal necrolysis, Fluminant hepatic failure. which are responsible for the discontinuation of Ciprofloxacin therapy.

The symptomatic adverse reactions produced by Ciprofloxacin are more or less tolerable and if they become severe, they can treated symptomatically, these include Dizziness, Headache, Nausea, Vomiting, Diarrhoea, Tachycardia, Nervousness, Tremors, Rashes, Urticaria, Pruritus, Photosensitivity, Elevation of liver enzymes, Thrombocytopenia, Eosinophilia, Increased intracranial pressure, nervousness, joint symptoms, agranulocytosis.

Warning / Precautions

Ciprofloxacin used with caution in patients with known or suspected central nervous system (CNS) disorders, renal impairment or hepatic disease, with a history of GI disease especially colitis or who dehydration. Do not exceed the recommended dose. Take appropriate measures if secondary infections occur.

 

Storage Conditions

Eye Solution/ Eye ointment

Store at room temperature, Below 30°C or in refrigerator. Do not Freeze. Protect from Sunlight.

Injection (reconstituted solutions)

Store at room temperature, Below 25°C or in refrigerator. Do not Freeze. Protect from Sunlight. Use within 2 weeks if kept at room temperature.

Store .

 

Interference in Pathology

Elevations of SGPT and SGOT

Serum creatinine raised

Elevation in ALT or AST

blood urea raised.


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01/Jul/2021

Cyclobenzaprine HCL

Overview

Cyclobenzaprine hydrochloride is a tricyclic amine salt with the empirical formula C20H21N•HCl. Cyclobenzaprine is a central nervous system (CNS) muscle relaxant intended for short-term use in the treatment of pain, tenderness, and limitation of motion caused by muscle spasms. It is thought to act within the CNS at the brain stem rather than spinal cord levels, although action at the spinal cord level may contribute to some of its skeletal muscle relaxant action.

Primary Characteristics

. It belongs to Muscle Relaxants pharmacological group on the basis of mechanism of action. The Molecular Weight of cyclobenzaprine hydrochloride is 311.90. Its pKa is 8.47.

Indication

Cyclobenzaprine is indicated as a short-term (2-3 weeks) adjunct therapy, along with rest and physical therapy, for relief of muscle spasm associated with acute, painful musculoskeletal conditions. It not been found effective in the treatment of spasticity originating from cerebral or spinal cord disease, or spasticity in children with cerebral palsy. Cyclobenzaprine is also occasionally used off-label for reducing pain and sleep disturbances in patients with fibromyalgia.

Pharmacokinetics

Oral absorption of cyclobenzaprine hydrochloride is found to be 44% ±11. Plasma protein binding is high. and metabolism is reported P-450 3A4, 1A2, and, to a lesser extent, 2D6. Renal Excretion accounts for as glucuronides and plasma half life is 18 Hours.

 

Contraindications

Cyclobenzaprine hydrochloride is contraindicated in conditions like Hyperthyroidism, Congestive heart failure, Hypersensitivity to any component of product.

Pharmacodynamics

Cyclobenzaprine is a skeletal muscle relaxant that works on areas of the brainstem to reduce skeletal muscle spasm, though its exact pharmacodynamic behavior is currently unclear. Despite its long half-life, it is relatively short-acting with a typical duration of action of 4-6 hours. Cyclobenzaprine has been reported to contribute to the development of serotonin syndrome when used in combination with other serotonergic medications. Symptoms of serotonin syndrome may include autonomic instability, changes to mental status, neuromuscular abnormalities, or gastrointestinal symptoms. treatment with cyclobenzaprine should be discontinued immediately if any of these reactions occur during therapy.

Mechanism of Action

The exact mechanism of action of cyclobenzaprine has not been fully elucidated in humans, and much of the information available regarding its mechanism has been ascertained from early animal studies. There is some evidence that cyclobenzaprine exerts its effects at the supraspinal level, specifically within the locus coeruleus of the brainstem, with little-to-no action at neuromuscular junctions or directly on skeletal musculature. Action on the brainstem is thought to result in diminished activity of efferent alpha and gamma motor neurons, likely mediated by inhibition of coeruleus-spinal or reticulospinal pathways, and ultimately depressed spinal cord interneuron activity.

More recently it has been suggested that inhibition of descending serotonergic pathways in the spinal cord via action on 5-HT2 receptors may contribute to cyclobenzaprine’s observed effects.

Metabolism

Cyclobenzaprine is extensively metabolized in the liver via both oxidative and conjugative pathways. Oxidative metabolism, mainly N-demethylation, is catalyzed primarily by CYP3A4 and CYP1A2 (with CYP2D6 implicated to a lesser extent) and is responsible for the major metabolite dimethyl cyclobenzaprine. Cyclobenzaprine also undergoes N-glucuronidation in the liver catalyzed by UGT1A4 and UGT2B1, and has been shown to undergo enterohepatic circulation

Half-life

The effective half-life of cyclobenzaprine in young healthy subjects is approximately 18 hours. These values are extended in the elderly and those with hepatic insufficiency, with a mean effective half-life of 33.4 hours and 46.2 hours in these groups, respectively

Side Effects

The severe or irreversible adverse effects of cyclobenzaprine hydrochloride, which give rise to further complications include Irregular heart beat.

cyclobenzaprine hydrochloride produces potentially life-threatening effects which include Hypersensitivity reactions. which are responsible for the discontinuation of cyclobenzaprine hydrochloride therapy.

The signs and symptoms that are produced after the acute over dosage of cyclobenzaprine hydrochloride include Nausea, Tachycardia, Hallucinations, Drowsiness, Changes in ECG, Slurred speech, Dizziness, Coma, Severe hypotension, Seizures, Cardiac dysrhythmias, Confusion, Tremor, Vomiting, Ataxia, Agitation, Hypertension.

The symptomatic adverse reactions produced by cyclobenzaprine hydrochloride are more or less tolerable and if they become severe. They can be treated symptomatically, these include Headache, Drowsiness, Fatigue, Nausea, Diarrhea, Constipation, Abdominal pain, Dry mouth, Acid regurgitation.

Warning / Precautions

Use of Cyclobenzaprine Hydrochloride for periods longer than two or three weeks is not recommended. Less frequent dosing should be considered for hepatically impaired or elderly patients. It is contraindicated in acute recovery phase of myocardial infarction, and patients with arrhythmias, heart block or conduction disturbances, or congestive heart failure. Used with caution in elderly patients with reduced doses. It should be used with caution in patients with a history of urinary retention. Angle closure glaucoma, increased intraocular pressure, and in patients taking anticholinergic medication. Used with caution in subjects with mild hepatic impairment starting with a 5 mg dose and titrating slowly upward. In subjects with moderate to severe impairment is not recommended. Safety and effectiveness of cyclobenzaprine hydrochloride in pediatric patients below 15 years of age have not been established.

 

Storage Conditions

Store Between 15°C-30°C.

 






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