General Information about Seroflo

One of the important thing advantages of Seroflo is its long-acting results. Unlike most inhalers which have short-term advantages, Seroflo can provide reduction for up to 12 hours after a single dose. This implies that patients can use it twice a day, once within the morning and as quickly as within the night, to keep their symptoms under control all through the day and evening. This helps in offering a consistent and handy therapy for these with busy schedules.

Seroflo is a drugs that combines two energetic elements, Fluticasone and Salmeterol, in an inhaler type. It is often used for the prevention and remedy of bronchial asthma and persistent lung illnesses. This inhaler offers effective aid for people who suffer from respiratory points, permitting them to manage and control their symptoms.

Moreover, Seroflo is appropriate for both youngsters and adults, making it a dependable option for the whole household. It is also obtainable in different strengths, allowing for personalized dosages relying on the severity of the condition. This makes it an effective therapy possibility for a variety of patients with varied respiratory conditions.

Seroflo has shown to be highly efficient in preventing and treating asthma assaults. In addition to its long-acting effects, it also helps to reduce the necessity for different medicines that patients could additionally be taking to control their signs. This can significantly enhance the quality of life for individuals affected by bronchial asthma, as they will go about their day by day actions without being restricted by their situation.

In conclusion, Seroflo is a highly efficient medication for the prevention and therapy of bronchial asthma and different persistent respiratory circumstances. Its combination of two lively ingredients provides long-lasting reduction for sufferers and improves their overall high quality of life. With correct utilization and monitoring, Seroflo helps people to handle and control their signs, allowing them to guide a extra lively and fulfilling life.

Fluticasone is an artificial corticosteroid that works by decreasing irritation and swelling within the airways. It helps to forestall bronchial asthma attacks and reduces the frequency and severity of symptoms corresponding to wheezing, coughing, and shortness of breath. Salmeterol however, is a long-acting beta-agonist that helps to open up the airways by stress-free the muscles round them. This permits the individual to breathe more simply, particularly during an asthma assault.

When utilizing Seroflo, it's important to follow the prescribed dosages and instructions from a healthcare professional. Some widespread side effects corresponding to headache, sore throat, and nausea could happen, but these are often gentle and momentary. In rare instances, more severe side effects corresponding to difficulty respiration, chest ache, or irregular heartbeat could occur, during which case quick medical consideration must be sought.

Seroflo is a unique mixture of those two medicines, providing a powerful and helpful treatment option for patients with continual respiratory situations. It is especially helpful for these who have issue managing their signs with just one medication or for these who need frequent rescue inhaler use.

Patients typically present with complaints of diminished urine output, weight gain, and/or edema. Urine sodium concentrations (less than 20 mEq/L [mmol/L]) and fractional excretion of sodium (less than 1% [0. Nonnarcotic analgesics (eg, tramadol) may also be useful but do not provide antiinflammatory activity. Kidney injury is rarely severe, and kidney function generally recovers within 3 to 5 days. Cyclosporine and Tacrolimus the calcineurin inhibitors cyclosporine and tacrolimus have dramatically enhanced the success of solid-organ transplantation. As many as 94% of kidney transplant patients are prescribed a calcineurin inhibitor-based immunosuppressive regimen. Although delayed chronic interstitial nephritis has also been reported,69 acute hemodynamically mediated kidney injury is an important mechanism of calcineurin inhibitor-induced nephrotoxicity. Hypertension, hyperkalemia, sodium retention, oliguria, renal tubular acidosis, and hypomagnesemia are frequently observed in the absence of urine sediment abnormalities or morphologic lesions. Biopsy is most useful to distinguish acute calcineurin inhibitor nephrotoxicity from acute cellular rejection of the transplanted kidney, the latter being evidenced by interstitial infiltrates composed of activated lymphocytes (see Chapter 90). The mechanism of acute nephrotoxicity is generally thought to be dose related, since kidney function improves rapidly following dose reduction. Calcium channel blockers may antagonize the vasoconstrictor effect of cyclosporine by dilating glomerular afferent arterioles and preventing acute decreases in renal blood flow and glomerular filtration. Management Acute kidney injury usually improves with dose reduction and treatment of contributing illness or the discontinuation of interacting drugs. Nephrolithiasis, the formation of stones within the kidney, results from abnormal crystal precipitation in the renal collecting system, potentially causing urinary tract obstruction with kidney injury. Several medications that have been associated with development of obstructive nephropathy are listed in Table 46-1. Crystal Nephropathy Incidence the incidence of crystal nephropathy is unclear for most of the implicated agents because histologically confirmed cases are rare, and many drugs cause kidney injury via multiple mechanisms. For example, antineoplastic drugs may cause acute renal tubular obstruction indirectly by inducing tumor lysis syndrome, hyperuricemia, and intratubular precipitation of uric acid crystals. Uric acid precipitation can be prevented by vigorous hydration with normal saline, beginning at least 48 hours prior to chemotherapy, to maintain urine output 100 mL/h in adults. Administration of allopurinol 100 mg/m2 thrice daily (maximum of 800 mg/day) started 2 to 3 days prior to chemotherapy, and urinary alkalinization to pH 7 may also be of value. In patients at high risk of developing tumor lysis syndrome (ie, large tumor burden, pre-exisiting kidney disease, and older age), a single fixed dose of 3 mg rasburicase may be beneficial. Other risk factors included age, diabetes mellitus, hypertension, and cardiovascular disease. Precipitation of drug crystals is due primarily to supersaturation of a low urine volume with the offending drug or relative insolubility of the drug in either alkaline or acidic urine. Certain solutes can precipitate and obstruct the tubular lumen at this acid pH, particularly when urine is concentrated, such as for patients with volume depletion. The salt crystals may then secondarily precipitate in the renal tubules causing tubular necrosis. Low-grade proteinuria (less than 1 g/day), normocalcemia, and bland urinary sediment are usually observed. Extensive deposition of calcium phosphate in the distal tubules and collecting ducts without glomerular or vascular injury is the hallmark of acute phosphate nephropathy. Drug-induced nephrolithiasis can be the result of abnormal crystal precipitation in the renal collecting system, potentially causing pain, hematuria, infection, or, occasionally, urinary tract obstruction with kidney injury. The overall prevalence of drug-induced nephrolithiasis is estimated to be 1% to 2% of all cases of nephrolithiasis. Until the development of antiretroviral drugs, triamterene had been the drug most frequently associated with kidney stone formation, with a prevalence of 0. Numerous other drugs have been implicated in the development of nephrolithiasis, including the antibacterial agents ciprofloxacin, amoxicillin, and nitrofurantoin, and various products containing ephedrine, norephedrine, pseudoephedrine, and melamine. Moreover, nephrolithiasis has become a well known complication of antiretroviral agents, including the protease inhibitors indinavir, atazanavir, nelfinavir, amprenavir, saquinavir, ritonavir and darunavir. Glomerular injury associated with drug exposure is broadly classified into either direct cellular toxicity or immune mediated injury. Lesions from immune-mediated injury include vasculitis (see Renal Vaculitis section) and membranous nephropathy. It represents a pattern of glomerular injury, not a disease per se, and is the final common pathway by which normal glomerular components are replaced by fibrous scar tissue. Membranous Nephropathy Membranous nephropathy is the most common etiology of nephrotic syndrome in Caucasian adults. The pathogenesis may involve damage to proximal tubule epithelium with antigen release, antibody formation, and glomerular immune complex deposition. Patients who remain nephrotic after 6 months should be treated with a 6- to 12-month course of immunosuppressive therapy, which typically consists of prednisone with or without cyclophosphamide. The presentation may be acute and reversible with interstitial edema, rapid loss of kidney function, and systemic symptoms or chronic and irreversible, associated with interstitial fibrosis and minimal to no systemic symptoms. It usually manifests 2 weeks after exposure to a drug but may occur sooner if the patient was previously sensitized. Clinical signs present approximately 14 days after initiation of therapy and include (with their approximate incidence) fever (27%-80%), maculopapular rash (15%-25%), eosinophilia (23%-80%), arthralgia (45%), and oliguria (50%). However, it is now recognized that this constellation of findings is not consistently reliable as one or more are frequently absent. Tubular dysfunction may be manifested by acidosis, hyperkalemia, salt wasting, and concentrating defects.

Drugs with a high extraction ratio (high-extraction drugs) are dependent on blood flow for metabolism, and the rate of metabolism will be sensitive to changes in blood flow. Drugs with a low extraction ratio (low-extraction drugs) are dependent on intrinsic metabolic activity for metabolism, and the rate of metabolism will reflect changes in intrinsic clearance and protein binding. Phase I reactions involve the cytochrome P450 system and include hydrolysis, oxidation, dealkylation, and reduction reactions. Drugs metabolized by phase I reactions, especially oxidation, tend to be significantly impaired in patients with cirrhosis, whereas drugs eliminated by conjugation are relatively unaffected. The variability and complexity of the interaction between the extent and severity of liver disease and individual characteristics of the drug make it difficult to predict the degree of pharmacokinetic perturbation in an individual patient. Unfortunately, there are no sensitive and specific clinical or biochemical markers that allow us to quantify the extent of liver insufficiency or the degree of metabolic activity. In addition, renal insufficiency and alterations that commonly accompany cirrhosis further complicate empiric dosing recommendations in these patients. Dosing recommendations are most commonly nonspecific, with recommendations labeled for patients with mild to moderate liver impairment. Dosing information for patients with more severe liver impairment is not available. As a result, when patients with cirrhosis require therapy with drugs that undergo hepatic metabolism (eg, benzodiazepines), monitoring response to therapy and anticipating drug accumulation and enhanced effects is essential. In the case of benzodiazepines, selection of an agent such as lorazepam, an intermediate-acting agent that is metabolized via conjugation and has no active metabolites, is easier to monitor than a drug such as diazepam, a long-acting benzodiazepine that is oxidized in the liver and has an active metabolite with a long half-life of its own. Cirrhosis is generally a chronic progressive disease that requires aggressive medical management to prevent or delay common complications. Table 37-6 also lists monitoring criteria that need to be carefully followed in order to achieve the maximum benefit from the medical therapies employed and prevent adverse effects. A therapeutic plan including therapeutic end points for each medical and diet therapy needs to be developed and discussed with the patient. Hepatic stellate cells: Protean, multifunctional, and enigmatic cells of the liver. The management of portal hypertension: Rational basis, available treatments and future options. Garcia-Tsao G, Lim J, Members of the Veterans Affairs Hepatitis C Resource Center Program. Management and treatment of patients with cirrhosis and portal hypertension: Recommendations from the Department of Veterans Affairs Hepatitis C Resource Center Program and the National Hepatitis C Program. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Somatostatin, somatostatin analogues and other vasoactive drugs in the treatment of bleeding oesophageal varices. A meta-analysis of somatostatin versus vasopressin in the management of acute esophageal variceal hemorrhage. Transjugular intrahepatic portosystemic shunt versus endoscopic therapy in the secondary prophylaxis of variceal rebleeding in cirrhotic patients meta-analysis update. Meta-analysis: Isosorbide-mononitrate alone or with either -blockers or endoscopic therapy for the management of oesophageal varices. Meta-analysis: Combination endoscopic and drug therapy to prevent variceal rebleeding in cirrhosis. Liver enzyme assays in serum can help to determine if a particular type of liver damage is present. The number of drugs associated with adverse reactions involving the liver is extensive, but in clinical practice is dominated by alcohol, antibiotics, antiseizure medications and acetaminophen. The liver plays host to all of the cells that make up the innate immune response system in the body along with Kupffer cells, which are a type of macrophage. These cells sit in anticipation around the hepatocytes, in the space of Disse and elsewhere waiting for antigens (or neoantigens) to present themselves. The neoantigens serve as targets for cytolytic attack by killer T-cells, and others. Dantrolene, isoniazid, phenytoin, nitrofurantoin, trazodone, and methyldopa are associated with a type of autoimmune-mediated disease in the liver called chronic active hepatitis. It is a progressive disease with a high mortality rate and is more common in females than males. Idiosyncratic Reactions Idiosyncratic drug-related hepatotoxicity is rare and usually occurs in a small proportion of individuals. These adverse reactions are often categorized into allergic and nonallergic reactions. Allergic reactions represent 23% to 37% of all idiosyncratic drug-induce liver injuries and are characterized by fever, rash, eosinophilia, and granulomas. On re-exposure to the offending agent, there is a rapid recurrence of hepatotoxicity. Minocycline, nitrofurantoin, phenytoin, amoxicillin-clavulanate, sulfamethoxazole-trimethoprim, angiotensin-converting enzyme inhibitors, and allopurinol can cause allergic reactions. Dependent on the medication, the incident can be independent of dose or dose related. Amiodarone, isoniazid, and ketoconazole are associated with nonallergic drug-related hepatotoxicity. These reactive metabolites are capable of forming covalent bonds with cellular proteins (enzymes) and nucleic acids that lead to adduct formation. In the case of acute toxicity, the enzyme­drug adduct can cause cell injury or cell lysis. Acetaminophen, furosemide, and diclofenac are Individual genetic differences can play a role in the examples of this mechanism of liver injury. Stimulation of Apoptosis Apoptosis represents a distinct pattern of cell lysis that is characterized by cell shrinkage and fragmentation of nuclear chromatin.

Seroflo Dosage and Price

Seroflo 250mcg

• 1 inhalers - $88.87
• 2 inhalers - $152.34
• 3 inhalers - $215.82
• 4 inhalers - $279.29
• 5 inhalers - $342.77
• 6 inhalers - $406.25
• 7 inhalers - $469.72
• 8 inhalers - $533.20

Secondly, reflux may occur following transient increases in intra-abdominal pressure (stress reflux). The other natural defense mechanisms (anatomic factors, esophageal clearance, mucosal resistance, and other gastric factors) must be evoked to explain this phenomenon. Although anatomic factors are still considered significant by some, the diagnosis of hiatal hernia is currently considered a separate entity with which gastroesophageal reflux may simultaneously occur. Contact time is dependent on the rate at which the esophagus clears the noxious material, as well as the frequency of reflux. Saliva contains bicarbonate that buffers the residual gastric material on the surface of the esophagus. The production of saliva decreases with increasing age, making it more difficult to maintain a neutral intraesophageal pH. Mucosal Resistance Within the esophageal mucosa and submucosa there are mucus-secreting glands that may contribute to the protection of the esophagus. Bicarbonate moving from the blood to the lumen can neutralize acidic refluxate in the esophagus. In theory, mucosal resistance may be related not only to esophageal mucus but also to tight epithelial junctions, epithelial cell turnover, nitrogen balance, mucosal blood flow, tissue prostaglandins, and the acid­base status of the tissue. Gastric Emptying/Increased Intra-abdominal Pressure Delayed gastric emptying can contribute to gastroesophageal reflux. An increase in gastric volume may increase both the frequency of reflux and the amount of gastric fluid available to be refluxed. Gastric volume is related to the volume of material ingested, rate of gastric secretion, rate of gastric emptying, and amount and frequency of duodenal reflux into the stomach. Factors that increase gastric volume and/or decrease gastric emptying, such as smoking and high-fat meals, are often associated with gastroesophageal reflux. Patients with gastroesophageal reflux, particularly infants, may have a defect in gastric antral motility. If the pH of the refluxate is less than 2, esophagitis may develop secondary to protein denaturation. In addition, pepsinogen is activated to pepsin at this pH and may also cause esophagitis. Duodenogastric reflux esophagitis, or "alkaline esophagitis," refers to esophagitis induced by the reflux of bilious and pancreatic fluid. The term alkaline esophagitis may be a misnomer in that the refluxate may be either weakly alkaline or acidic in nature. Although bile acids have both a direct irritant effect on the esophageal mucosa and an indirect effect of increasing hydrogen ion permeability of the mucosa, symptoms are more often related to acid reflux than to bile reflux. Specifically, the percentage of time that the esophageal pH is less than 4 is greater for patients with severe disease as compared with that for patients with mild disease. Nevertheless, the combination of acid, pepsin, and/or bile is a potent refluxate in producing esophageal damage. Strictures are common in the distal esophagus and are generally 1 to 2 cm in length. The severity of the symptoms of gastroesophageal reflux does not always correlate with the degree of esophageal tissue injury, but it does correlate with the duration of reflux. Diagnostic Tests the most useful tool in the diagnosis of gastroesophageal reflux is the clinical history, including presenting symptoms and associated risk factors. Patients presenting with typical symptoms of reflux, such as heartburn or regurgitation, do not usually require invasive esophageal evaluation. These patients generally benefit from an initial empiric trial of acid-suppression therapy. It should be performed in patients not responding to twice daily proton pump inhibitor therapy, and those with dysphagia or unexplained weight loss. The wireless pH monitoring involves attaching a radiotelemetry capsule to the esophageal mucosa. The advantages of this method are that a longer period of monitoring is possible (48 hours), it may demonstrate superior recording accuracy compared with some catheter designs, and it is more comfortable for the patient because a nasogastric tube is unnecessary. However, when testing for nonacid reflux, only impedance­pH monitoring should be performed and testing should be done while patient is still on a proton pump inhibitor. Manometry is useful for patients who are candidates for antireflux surgery and for ensuring proper placement of pH probes. Therapy is directed at augmenting defense mechanisms that prevent reflux and/or decrease the aggressive factors that worsen reflux or mucosal damage. A step-down approach, starting with a proton pump inhibitor, instead of an H2-receptor antagonist, and then stepping down to the lowest dose of acid suppression (either an H2-receptor antagonist or proton pump inhibitor) needed to control symptoms, is most often advocated. The clinician should determine the most appropriate approach for the individual patient. Acid Suppression Therapy ·Therapy of choice for symptom relief and healing of erosive esophagitis is an 8-week proton pump inhibitor course. High, Strong ·For maximal pH control, delayed-release proton pump inhibitors should be Moderate, Strong administered 30-60 minutes before meals. Level of Evidence and Strength of Evidencea Low, Strong Low, Strong ·Increasing to twice daily dosing or switching proton pump inhibitor may be Low, Conditional beneficial in partial responders to proton pump inhibitor therapy. Moderate, Strong Moderate, Conditional Moderate, Conditional Moderate, Conditional Moderate, Conditional Moderate, Moderate Moderate, Conditional High, Strong ·The lowest effective dose should be used when long-term proton pump inhibitor therapy is indicated for maintenance. Strategies such as on-demand Low, Conditional and intermittent therapy may be beneficial. Note: Most patients will require standard doses for maintenance therapy Cimetidine (off-label use) 400 mg four times daily or Tagamet 800 mg twice daily Recommended Treatment Regimen Famotidine Nizatidine Ranitidine Brand Name Pepcid Axid Zantac Oral Dose 20 mg twice daily 150 mg twice daily 150 mg twice daily Comments Prescription-strength proton pump inhibitors (for 4-8 weeks) For typical symptoms, treat empirically with prescription-strength acid suppression therapy Dexlansoprazole Dexilant 30 mg once daily for 4 weeks Patients with moderate to severe symptoms should receive a proton pump inhibitor as initial therapy If symptoms recur, consider maintenance therapy Esomeprazole Lansoprazole Omeprazole Omeprazole/sodium bicarbonate Nexium Prevacid Prilosec Zegerid 20-40 mg once daily 15mg once daily 20 mg once daily 20 mg once daily Pantoprazole (Off-label 40 mg once Protonix use) daily Rabeprazole Aciphex 20 mg once daily Healing of erosive esophagitis or treatment of patients with moderate to severe symptoms or complications (individualized lifestyle modifications + high-dose H2-receptor antagonists or proton pump inhibitors or antireflux surgery) Individualized lifestyle modifications Lifestyle modifications should be individualized for each patient. Proton pump inhibitors (up to twice daily for up to 8 weeks) Dexlansoprazole Dexilant 60 mg daily For extraesophageal or alarm symptoms, Recommended Treatment Regimen Brand Name Oral Dose Comments obtain endoscopy with biopsy to evaluate mucosa If symptoms are relieved, consider maintenance therapy.