Triamterene

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Biliary pain (2) pulmonary hypertension 60 mmhg order triamterene 75 mg line, acute cholecystitis (3), cholangitis (5), and pancreatitis (5) are the most common complications. Subsequent cholecystectomy *See Chapter 58 for a discussion of biliary pancreatitis. Some authorities recommend combined prophylactic splenectomy and cholecystectomy in young asymptomatic patients with hereditary spherocytosis if gallstones are present. Morbidly obese persons who undergo bariatric surgery are at high risk of complications of gallstones (see Chapters 7 and 8). Some investigators have proposed that patients with incidental cholelithiasis who are awaiting heart transplantation undergo a prophylactic cholecystectomy irrespective of the presence or absence of biliary tract symptoms because they are at increased risk of post-transplant gallstone complications. Only 50% of pigment stones and 20% of cholesterol stones contain enough calcium to be visible on a plain abdominal film. Because 80% of gallstones in the Western world are of the cholesterol type, only 25% of stones can be detected by simple radiographs. Plain abdominal films have their greatest usefulness in evaluating patients with some of the unusual complications of gallstones. It has the additional advantage of being portable and thus available at the bedside of a critically ill patient. The stones are mobile and generally congregate in the dependent portion of the gallbladder. Smaller stones may be missed or may be confused with biliary sludge (layering echogenic material that does not cast acoustic shadows). Rarely, advanced scarring and contraction of the gallbladder around gallstones make locating the gallbladder or the stones impossible, raising the possibility of gallbladder cancer. Table 65-3 shows the wide array of imaging techniques available to evaluate the biliary tract. Notably absent from the list of imaging studies of the biliary tract is the plain abdominal film. Unfortunately, in the critical care setting, these nonspecific findings are seen frequently in patients with no other evidence of gallbladder disease. Presence of the sign has a positive predictive value of greater than 90% for detecting acute cholecystitis if gallstones are present. With repositioning of the patient, stones will move, thereby excluding the possibility of a gallbladder polyp. Multiple gallstones can be seen within the gallbladder lumen, with associated acoustic shadowing. Cholescintigraphy Cholescintigraphy (hepatobiliary scintigraphy) is a radionuclide imaging test of the gallbladder and biliary tract that is most useful for evaluating patients with suspected acute cholecystitis. An abnormal or "positive" scan result is defined as nonvisualization of the gallbladder, with preserved excretion into the bile duct or small intestine. Cholescintigraphy demonstrating an obstructed cystic duct characteristic of acute cholecystitis. Sequential images show the isotope quickly entering the duodenum (at 45 minutes) and passing distally in the small intestine without ever being concentrated in the gallbladder. Failure of the gallbladder to be visualized as a hot spot within 30 to 60 minutes constitutes a positive result and implies obstruction of the cystic duct. An additional important role for cholescintigraphy is the noninvasive detection of bile leakage from the cystic duct as a complication of cholecystectomy (see Chapter 66). The reduction in gallbladder motility leads to greater water resorption, which results in a gelatinous bile. In critically ill patients, cholestasis and hepatocyte dysfunction result in reduced clearance of radionuclide imaging agents. Although nonvisualization of the gallbladder because of cystic duct obstruction is the hallmark of acute cholecystitis, pericholecystic hepatic uptake of radionuclide is a useful secondary sign. Morphine raises the pressure within the sphincter of Oddi, thereby leading to the preferential flow of bile into the gallbladder if the cystic duct is not obstructed. Another scan is obtained 30 minutes after injection of morphine, and if the gallbladder is visualized, cystic duct obstruction, and hence acute cholecystitis, is excluded. The gallbladder may not be visualized in approximately half of critically ill patients even after injection of morphine, thereby leading to false-positive cholescintigraphy results. In patients who present with a complication of gallstones, such as acute cholecystitis, a history of recurrent episodes of abdominal pain in the months preceding the complication is often elicited. Pathogenesis Biliary pain (conventionally referred to as biliary "colic," a misnomer) is caused by intermittent obstruction of the cystic duct by 1 or more gallstones.

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If the immune active phase of hepatitis B remains untreated hypertension jnc 7 triamterene 75 mg line, cirrhosis can be anticipated to develop in at least 20% of cases. Clinical laboratories base their range of normal values on donors without known liver disease, but this population may include obese persons, alcohol consumers, and diabetics, each of whom tends to expand the supposedly upper limit of normal. Progression to cirrhosis should be suspected whenever hypersplenism, hypoalbuminemia (in the absence of nephropathy), or prolongation of the prothrombin time is found. The disease may be more severe in patients coinfected with other hepatitis viruses and in those with established underlying liver disease. These features generally abate before the manifestations of liver disease and peak serum aminotransferase elevations are observed. If acute liver failure develops, patients usually present within 4 weeks of the onset of symptoms and have associated multiorgan dysfunction, coagulopathy, encephalopathy, and high mortality rates if they are not treated by prompt antiviral therapy and liver transplantation. Patients older than 40 years appear to be more susceptible than younger persons to "lateonset" liver failure, which occurs several months after the onset of acute symptoms and is associated with encephalopathy and renal dysfunction. Extrahepatic Manifestations Although uncommon, extrahepatic syndromes can occur with acute or, more commonly, chronic hepatitis B and are important to recognize because they may occur without clinically apparent liver disease and can be mistaken for independent disease processes in other organ systems. The pathogenesis is not completely understood but likely involves an aberrant immunologic response to extrahepatic viral proteins. Serum complement levels are generally low, and antiviral therapy may be beneficial in reducing the amount of immunologically activating viral antigens. Typical features include arthralgias, fever, rash, abdominal pain, renal disease, hypertension, mononeuritis multiplex, and central nervous system abnormalities. Plasmapheresis may be useful, and therapeutic responses have also been observed with antiviral agents, given alone or in combination with plasmapheresis. When symptoms are present, fatigue tends to predominate over other constitutional symptoms, such as poor appetite and malaise. In decompensated cirrhosis, spider telangiectasias, jaundice, ascites, and peripheral edema are common. Cryoglobulinemia may be associated with systemic vasculitis (purpura, arthralgias, peripheral neuropathy, and glomerulonephritis) but is often paucisymptomatic or asymptomatic. Nucleos(t)ide analog therapy has been used successfully to treat symptomatic cryoglobulinemia. Acute Flares Chronic hepatitis B is often punctuated by sudden flares of disease activity that are characterized by a precipitous increase in serum aminotransferase levels. Flares are an important part of the natural history of hepatitis B because they can lead to histologic progression when they occur repeatedly and are moderate or severe. Acute flares in chronic hepatitis B occur in association with a number of circumstances and clinical situations (Table 79-1). Most flares are preceded by an increase in viral replication, which stimulates an enhanced cellular immune response that targets virusinfected hepatocytes. Periportal inflammation often leads to the disruption of the limiting plate of hepatocytes (interface hepatitis), and inflammatory cells often can be seen at the interface between collagenous extensions from the portal tracts and liver parenchyma (referred to as active septa). During reactivated hepatitis B, lobular inflammation is more intense and reminiscent of that seen in acute viral hepatitis. Steatosis is not a feature of chronic hepatitis B, as it is of chronic hepatitis C. When present in abundance, ground-glass hepatocytes often indicate active viral replication. During periods of intense hepatitis activity, cytoplasmic core antigen staining is generally observed. It is not clear if severe physical or emotional stress can weaken the immune system and lead to a secondary increase in viral replication. Note that the brownish inclusions correspond to the ground-glass inclusions seen in A. On discontinuation of immunosuppressive medications, as occurs with cancer chemotherapy, immune competence is restored and infected hepatocytes are rapidly destroyed. In general, the more potent the immunosuppression, the higher the level of viral replication and, thus, the greater the potential for serious clinical consequences. Postmortem studies of liver tissue from patients with severe liver injury have documented sparse staining of viral antigens, suggesting that the patients were in an active state of immune clearance. When reactivation occurs in the setting of cancer chemotherapy or systemic treatment for a severe autoimmune disorder, the patient may not be eligible for salvage liver transplantation. Clinical outcomes are much better when prophylaxis is provided as compared with on-demand antiviral therapy after reactivation has become clinically apparent.

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Successful bone marrow transplantation with amelioration of enteropathy has been reported in some cases arrhythmia 4279 diagnosis discount triamterene 75 mg visa. Affected patients are also at increased risk for autoimmune and neoplastic diseases. Symptoms are associated with stunting of intestinal villi or their complete absence. The pathophysiology of malabsorption is unknown, and the syndrome usually fails to respond to antimicrobial treatment. Mechanisms of malabsorption include periampullary duodenal tumors, which are mainly somatostatin-containing neuroendocrine tumors, and pancreatic carcinomas with resultant pancreatic duct obstruction; tumors can cause exocrine pancreatic insufficiency and biliary obstruction. Severe diarrhea and malabsorption occur as a result of diffuse villus atrophy, and ulcerations may be present in the small and large intestine. Two patients with autoimmune enteropathy unresponsive to steroids have been reported to respond to infusion of mesenchymal stromal cells. Duodenal biopsy specimen from a patient with nongranulomatous chronic idiopathic enterocolitis. A, Histopathologic features include villus atrophy, diffuse infiltration of lamina propria with inflammatory cells, and crypt abscesses (arrow). Chromogranin A immunohistochemical staining of enteroendocrine cells in duodenal biopsy specimens obtained from a normal subject (A) and from a patient with malabsorption associated with autoimmune polyglandular syndrome type 1 (B). Motility studies in hyperthyroid patients (including patients with and without diarrhea) have demonstrated accelerated small intestinal and whole-gut transit times315; fecal fat values were not reported in these patients. It can be hypothesized that more pronounced disturbances of intestinal transit can lead to decreased mixing of food and digestive secretions and reduced intestinal absorption of nutrients. Some of the steatorrhea in hyperthyroid patients might result from hyperphagia with increased dietary intake of fat. The prevalence of celiac disease in patients with autoimmune thyroid disease is approximately 2% to 4%. In patients with diabetes mellitus type 1, a high prevalence (3% to 8%) of celiac disease has been reported from screening studies, but most of these patients are asymptomatic. In 40% of diabetic patients with reduced fecal elastase levels, fat malabsorption with fecal fat output of more than 10 g/day was detected. Foods recommended to diabetics because they contain poorly absorbable carbohydrates such as fructose or sorbitol can result in bloating and diarrhea. Metabolic Bone Disease Special consideration has to be given to osteoporosis and osteomalacia in malabsorptive diseases. Patients with these metabolic bone diseases usually do not present with suggestive symptoms or abnormalities either on physical examination or on routine laboratory examinations. Reduced bone mineral density is a common finding in patients with gastric resection,328 celiac disease,329 and lactose malabsorption. Vitamin D malabsorption is Diabetes Mellitus Chronic diarrhea is common in patients with diabetes mellitus, especially in those with long-standing diabetes mellitus type 1. Although up to one half of patients on a gluten-free diet have osteoporosis,330 some studies have shown significant improvement in bone mineral density 1 year after starting a gluten-free diet. In addition to treating the underlying cause of malabsorption, calcium supplementation is needed to ensure a daily intake of 1500 mg of calcium. In patients with home parenteral nutrition, catheterrelated bloodstream infections remain the major threat. A prevention strategy using taurolidine, which is a potent antimicrobial agent, has been shown to reduce the risk of these infections. Using breath tests wisely in a gastroenterology practice: An evidence-based review of indications and pitfalls in interpretation. The reader is referred to the relevant chapters of this book for discussion about treatment of specific diseases and their nutritional management. In patients with abdominal bloating and gas-related complaints due to sugar malabsorption, a diet with reduced content of poorly absorbable carbohydrates.

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• Folate works with vitamin B12 to help form red blood cells. It is needed for the production of DNA, which controls tissue growth and cell function. Any woman who is pregnant should be sure to get enough folate. Low levels of folate are linked to birth defects such as spina bifida. Many foods are now fortified with folic acid.
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However blood pressure medication and weight gain buy triamterene overnight delivery, physical exercise, perhaps through increased sympathetic tone, decreases colonic motility. Colchicine increases the frequency of spontaneous bowel movements and accelerates colonic transit in patients with chronic constipation. In the rat, colchicine given into the small intestine stimulates myoelectric activity. Activation of ClC2 increases intestinal chloride secretion and results in increased intraluminal fluid accumulation, which accelerates intestinal transit, softens stools, and increases spontaneous stool frequency in patients with constipation. In constipated patients, use of the drug has resulted in slight improvement over placebo, but there are notable side effects, including nausea and headache. Although this class of drug shows promise for the treatment of constipation, tegaserod was withdrawn from the market because of concerns about adverse cardiovascular events. Opiates are known to inhibit presynaptic and postsynaptic enteric neural circuitry. The reduction in neurally dependent propagating contractions and the enhancement of myogenic mixing movements and fluid absorption contribute to the constipating effect of the drug. Specific constipation syndromes like opiate-induced constipation or postsurgical ileus might respond to opiate antagonists such as methylnaltrexone and alvimopan (see Chapter 124). For example, the irritant laxative bisacodyl and the bile acid chenodeoxycholic acid both stimulate high-amplitude colonic propagating pressure wave sequences, thereby leading to mass movements. Bisacodyl exerts its motor effect through mucosal afferent nerve fibers; the response can be blocked by Nonpharmacologic Probiotics are living organisms that, when ingested in adequate amounts, are claimed to exert a health benefit to the host (see Chapter 130). In the colon, probiotics are likely to modulate the inflammatory response through activation of signals with the epithelium and immune system. Probiotics may well influence colonic motility, but this has not yet been systematically evaluated. Electrical stimulation of the S3 sacral root alters motor patterns in patients with slow transit constipation40 and patients with fecal incontinence,12 although the precise mode of actions remains unknown. The substantial latency between stimulus and pelvic floor or colonic contractile responses is longer than would be expected via a polysynaptic efferent pathway, which suggests possible involvement of extrinsic sensory pathways. An uncontrolled study utilizing sacral nerve stimulation in patients with constipation has shown some promise in alleviating symptoms. Acupuncture reportedly improved stool frequency in children, but these results were not replicated in adults; this warrants further study. Diarrhea Detailed scintigraphic studies in patients with diarrhea have shown the dominant feature to be early and rapid transit through the ascending and transverse colon. Normally, propagating sequences are more frequent in these proximal regions than elsewhere. Manometric data from the entire colon in patients with diarrhea might help explain these observations but have not yet been reported. A relative lack of distal colonic segmenting activity, perhaps in combination with increased proximal colonic propagating pressure waves, might explain this preferential acceleration of proximal colonic transit, but proof of this hypothesis is awaited. It is useful, however, to consider how disturbances in the mechanisms of colonic motility described in this chapter might relate to symptoms or pathophysiologic phenomena. Colonic Motility Disturbances Secondary to Nonmotor Intestinal Disorders Altered motility secondary to underlying inflammation or a hormonal disturbance can contribute to the colonic symptoms of a nonmotor disease. For example, exposure of the healthy proximal colon to supranormal concentrations of bile salts, such as from terminal ileal disease or resection, not only stimulates net colonic secretion but also initiates high-amplitude propagating pressure waves, thereby accelerating colonic transit. Sometimes this is true, but in the distal colon at least, the converse may be true. An increase in nonpropagating (segmenting) contractions and myoelectrical short spike-bursts has been reported in the rectosigmoid region in constipated patients, which until recently has seemed paradoxical. As discussed earlier, much of this nonpropagating activity probably consists of short-extent retrograde-propagating pressure waves. If this motor pattern retards flow, then increased frequency may contribute to constipation in some patients. Conversely, patients with diarrhea have hypomotility in this region, indicating that a normal physiologic brake (retrograde propagating sequences) has been removed, allowing content to be propelled unheeded into the rectum. In severe slow-transit constipation, prolonged manometric studies have confirmed a reduction in the overall number of high-amplitude propagating pressure waves,45 but the overall number of propagating pressure waves of all magnitudes is often normal or increased. Modulation of cholinergic neuromuscular transmission by nitric oxide in canine colonic 1712 Section X SmallandLargeIntestine circular smooth muscle.

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