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By: Jonathan Handy

  • Consultant in Intensive Care Medicine,Royal Marsden Hospital,Honorary Senior Lecturer,Imperial College London

The delay between the initiation of therapy and the clinical response is typically 3 to prostate 7 price flomax 0.4 mg otc 6 months prostate 84 buy 0.4 mg flomax free shipping. These drugs are used in patients who have active disease that is unresponsive to prostate oncology marina del rey cheap 0.2mg flomax with mastercard corticosteroids (refractory patients) and in corticosteroid-dependent patients androgen hormone production cheap flomax 0.4 mg online. Cyclosporine, given intravenously, is effective in reducing inflammation in patients with severe ulcerative colitis who are facing colectomy. Except in cases of overt sepsis, there is little role for antibiotics in the management of ulcerative colitis. Antibiotics do not affect the remission rate; moreover, the risk of inducing antibiotic-associated pseudomembranous colitis must be considered. The major side effect of metronidazole is peripheral neuropathy, which is dose dependent and usually resolves when the drug is discontinued. Ciprofloxacin at 500 mg twice a day for a few weeks is also effective in some patients. Another approach to proctitis or distal colitis is an oral aminosalicylate, although a response may not be evident for 3 to 4 weeks. For patients with colitis of mild to moderate activity and extension proximal to the sigmoid colon, the initial drug of choice is an oral aminosalicylate; efficacy increases with increasing doses. For patients with more active disease (>5-6 bowel movements per day), patients in whom a more rapid response is desired, or patients who have not responded to 3 to 4 weeks of aminosalicylates, the treatment of choice is oral prednisone. Patients with severe diarrhea, systemic symptoms, or significant amounts of blood in the stool should be started on 40 mg/day; most patients respond to oral corticosteroids within a few days. After the symptoms are controlled, prednisone can be gradually tapered by 5 to 10 mg every 1 to 2 weeks. Patients who respond to oral prednisone and can be fully withdrawn from it should be maintained on an aminosalicylate. Continuation of high-dose corticosteroid therapy for too long a time is the most common serious error in the management of ulcerative colitis. If the patient is on a substantial dose (>15 mg/day of prednisone) for more than 6 months, a trial of an immunomodulator or colectomy should be given serious consideration. The most common reason for hospitalization is intractable diarrhea, although blood loss is also a common problem. Patients with severe active ulcerative colitis should be evaluated for toxic megacolon. Anticholinergics and antidiarrheal agents are contraindicated in severe ulcerative colitis because of the risk of precipitating toxic megacolon. The mainstays of therapy for severe ulcerative colitis are bed rest, rehydration with intravenous fluids, and intravenous corticosteroids (hydrocortisone 300 mg/day; prednisolone, 60-80 mg/day, or methylprednisolone, 48-60 mg/day). Patients with peritoneal signs or signs of systemic infection should be treated with parenteral antibiotics. Patients who do not improve in 7 to 10 days should be considered for either colectomy or a trial of intravenous cyclosporine. Aminosalicylates reduce the incidence of recurrences in patients with ulcerative colitis; almost all patients 727 Figure 135-3 Treatment algorithm for ulcerative colitis. The efficacy of sulfasalazine at 3 to 4 g/day is greater than the efficacy of 2 g/day even though 2 g/day is the usual recommended maintenance dose. Response to therapy is monitored by empiric clinical assessment directed at the problem that is most troublesome for the patient. Patients with severe pain and diarrhea may have minimal findings on endoscopy or radiographic studies. Patients who have undergone ileal resections may have significant diarrhea on the basis of their surgery alone. Prednisone is the drug of choice for patients who have failed to respond to aminosalicylates or metronidazole, for patients with ileal disease, and for patients with highly active colonic or ileocolic disease. For patients who have been brought into clinical remission on corticosteroids, the rate at which the dose is tapered is arbitrary and not defined by controlled trials.

Opiate receptor antagonists such as naloxone may be helpful for treatment of pruritus prostate cancer options for treatment cheap flomax 0.2 mg with visa. Patients with chronic cholestasis and fat maldigestion also require dietary fat restriction prostate cancer natural treatment purchase 0.2mg flomax with mastercard, fat-soluble vitamin supplements prostate 3d buy 0.4mg flomax visa, and calcium supplements prostate procedures cheap flomax 0.4mg visa. In contrast to chenodeoxycholic acid, it is a poor detergent because its 7-hydroxyl group projects toward the hydrophobic surface of the molecule, impeding hydrophobic interactions with other lipids. It was originally used for dissolution of cholesterol gallstones but was serendipitously found to improve cholestasis and liver injury in a variety of chronic cholestatic liver diseases. It reduces serum bilirubin, transaminase, and alkaline phosphatase levels and can improve clinical symptoms and liver histology. It also may have direct protective effects on the liver and may alter immunologic function. Indications for transplantation include intractable symptoms, complications of cirrhosis, or deterioration of prognostic indicators. The healthier the patient at the time of transplantation, the better the outcome; conversely, patients with complications of liver disease frequently die while awaiting transplantation. Obliteration 826 Figure 157-5 Cholangiographic appearance of cholestatic disorders. The tumor is obstructing the common bile duct and the pancreatic duct, producing proximal dilatation of both (double duct sign). A cannula extending from the endoscope has been passed through the area of obstruction and its tip lies in the proximal common hepatic duct. A large cholesterol gallstone in the common bile duct appears as a radiolucent shadow outlined by radiodense contrast material. Multiple strictures are present in both the intrahepatic and extrahepatic biliary tree. Beadlike areas of dilatation can be noted between areas of stricture, but the fibrotic process in the liver prevents generalized dilatation of the proximal biliary ducts. Cholestasis of metabolic origin may be seen commonly in severely ill patients and is associated with trauma, surgery, sepsis, and parenteral hyperalimentation. Numerous drugs and estrogen also can produce cholestasis either as a direct effect or as an idiosyncratic reaction (see Chapter 148). Cholestasis of pregnancy appears to reflect sensitivity to the direct cholestatic effects of estrogen. In sarcoidosis (see Chapter 81), an idiopathic disease characterized by non-caseating granulomas in lung and other tissues, liver involvement is common. Usually these patients are symptom free with mild abnormalities of liver function tests. Granulomas in the portal tracts may produce fibrotic obliteration of small bile ducts. Rarely, bile duct obliteration may be sufficiently 827 severe to produce biliary cirrhosis. Although some experts consider hepatic involvement in sarcoidosis to be an indication for glucocorticoid therapy, glucocorticoids have not been proven to alter the natural history of sarcoidosis involving the liver. Primary biliary cirrhosis (see Chapter 153) is a progressive cholestatic disorder characterized by autoimmune destruction of small interlobular bile ducts. Injury is thought to occur as a result of cytotoxic T cell-mediated immune attack directed against bile ductular epithelial cells. Progressive familial intrahepatic cholestasis typically presents as mild to moderate cholestasis in infancy or childhood. Liver biopsy specimens appear generally unremarkable except that bile ductules can be identified in fewer than 50% of portal tracts. Severity and prognosis are variable: some patients develop biliary cirrhosis requiring transplantation in childhood, whereas others have an indolent course. A variety of genetic defects in pathways of bile acid synthesis or biliary lipid secretion have been implicated in the pathogenesis of this disorder. Chronic graft-versus-host disease occurs when T cells from an allogenic source are infused into an immunodeficient patient, most typically at the time of bone marrow transplantation (see Chapter 182).

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The utility of theophylline is limited by its toxicity and by wide variations in the rate of its metabolism prostate ejaculaton order flomax 0.4 mg without prescription, both in a single individual over time and among individuals in a population prostate supplement reviews purchase flomax 0.2 mg on line. As a result of this variability prostate ultrasound procedure generic 0.4 mg flomax overnight delivery, monitoring of plasma theophylline levels is indicated to prostate lab test order 0.4mg flomax with visa ensure that patients are treated appropriately. Acceptable plasma levels for therapeutic effects are between 10 and 20 mug/mL; higher levels are associated with gastrointestinal, cardiac, and central nervous system toxicity, including anxiety, headache, nausea, vomiting, diarrhea, cardiac arrhythmias, and seizures. These last catastrophic complications may occur without antecedent mild side effects when plasma levels exceed 20 mug/mL. Because of these potentially life-threatening complications of treatment, plasma levels need to be measured with great frequency in hospitalized patients receiving intravenous aminophylline and less frequently in stable outpatients receiving one of the long-acting theophylline preparations. Most asthma care providers use dosing amounts and intervals to achieve steady-state theophylline levels of 10 to 14 mug/mL, thereby avoiding the toxicity associated with decrements in metabolism. Treatment with theophylline is recommended only for patients with moderate or severe persistent asthma who are receiving controller medications, such as inhaled steroids or antileukotrienes, but whose asthma is not adequately controlled. Systemic corticosteroids are effective for the treatment of moderate to severe persistent asthma as well as occasional severe exacerbations of asthma that occur in a patient with otherwise mild asthma. No consensus has been reached on the specific type, dose, or duration of corticosteroid to be used in the treatment of asthma. In nonhospitalized patients with asthma refractory to standard therapy, a steroid "pulse" with initial doses of prednisone on the order of 40 to 60 mg/day, tapered to zero over 7 to 14 days, is recommended. For patients who cannot stop taking steroids without having recurrent uncontrolled bronchospasm despite the addition of multiple other controller treatments, alternate-day administration of oral steroids is preferable to daily treatment. For patients whose asthma requires in-hospital treatment but is not considered life-threatening, an initial intravenous bolus of 2 mg/kg of hydrocortisone, followed by continuous infusion of 0. In attacks of asthma that are considered life-threatening, the use of intravenous methylprednisolone (125 mg every 6 hours) has been advocated. In each case, as the patient improves, oral steroids are substituted for intravenous steroids, and the oral dose is tapered over 1 to 3 weeks; addition of inhaled steroids to the regimen when oral steroids are started is strongly recommended. Available in 2 strengths; prescription must indicate strength Beclomethasone Beclovent 42 Vanceril Budesonide Flunisolide Fluticasone Triamcinolone AeroBid Flovent Pulmicort 200 44, 110, or 220 2 puffs b. Cromolyn sodium and nedocromil sodium are nonsteroid inhaled treatments that have proven beneficial in the management of mild to moderate persistent asthma. They appear to be most useful in pediatric populations or when an identifiable stimulus (such as exercise or allergen exposure) elicits an asthmatic response. The use of systemic gold (as in rheumatoid arthritis), methotrexate, or cyclosporine has been suggested as adjunctive treatment for patients with severe chronic asthma who cannot otherwise discontinue high-dose corticosteroid treatment. In some patients, acute exacerbations of asthma may be due to concurrent infection, which will require targeted therapy (see Chapters 75, 77, and 82). Approximately 5% of patients with moderate to severe persistent asthma develop asthma when they ingest agents that inhibit cyclooxygenase, such as aspirin and other nonsteroidal anti-inflammatory drugs. Such patients quite often have difficult-to-manage asthma, with nasal polyposis and chronic sinusitis even in the absence of exposure to agents that inhibit cyclooxygenase. It has been established that all the physiologic manifestations of aspirin sensitivity can be attributed to leukotriene excess; thus, the treatment of choice for such individuals is a leukotriene pathway inhibitor. If the attack has been prolonged and failed to respond to treatment with bronchodilators and high-dose inhaled steroids before arrival at the emergency department, intravenous steroids (40 to 60 mg of methylprednisolone) should be administered. If this point is not reached within 2 hours, admission to the hospital for further treatment is strongly advocated. If significant improvement takes place in the emergency department, such patients can usually be treated as outpatients with inhaled beta2 -agonists and an additional controller agent. Frequent treatments with inhaled beta-agonists, intravenous aminophylline (at doses yielding maximal plasma levels), and high-dose intravenous steroids are indicated. Oxygen should be administered by face mask or nasal cannula in amounts sufficient to achieve Sa O2 values between 92% and 94%; a higher Fi O2 promotes absorption atelectasis and provides no therapeutic benefit. If objective evidence of an infection is present, appropriate treatment for that infection should be given. If no improvement is seen with treatment, and respiratory failure appears imminent, bronchodilator treatment should be intensified to the maximum tolerated by the patient.

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If the obstruction has been present for a long time prostate cancer home remedies buy 0.4mg flomax visa, bowel sounds are quieter or absent prostate health flomax 0.4 mg generic. If the ileus is associated with a severe abdominal insult mens health get back in shape flomax 0.2mg sale, such as peritonitis or surgery prostate cancer 4 plus 3 buy generic flomax 0.4 mg online, bowel sounds are absent. An alteration in bowel habit (diarrhea or constipation) is the cardinal symptom of motor disorders of the gastrointestinal tract, but these alterations do not specifically identify the pattern of motility. In the absence of a defect in mucosal absorption, diarrhea results from more rapid transit of intestinal contents through either the small intestine or the colon (see Chapter 133). The mechanism of rapid transit through the small intestine is unclear, but diarrhea due to altered colonic motility is associated with an increased frequency of propagating contractions. Constipation generally results from slow colonic transit due to either colonic inertia or increased segmenting contractions, which impede the forward movement of the intraluminal contents. Propagating contractions are markedly decreased or absent in patients with constipation. The frequency, character, and volume of bowel movements should be carefully defined in each patient. Stool volume is increased in small bowel-mediated diarrhea, whereas low-volume stools result from disordered colonic motility. The constipated stool generally has a lower volume (weight) and is firmer than normal stools, since more water has been absorbed. These strict definitions may exclude the patient who complains of constipation and who has stools of normal size and consistency but who strains to defecate. The patient who has only increased straining may have a functional anal outlet obstruction (Chapter 143). Gastric emptying can be performed simultaneously using different radionuclides to tag the liquid and the solid phases. Bedside assessment of the gastric transit of a bolus of isotonic saline may be a useful and inexpensive screening test. After 30 minutes, the residual should be less than 40% of an oral volume of 750 mL administered. Estimating gastric emptying from an upper gastrointestinal barium study often does not provide useful information. A breath test measures both liquid and solid gastric emptying using non-radioactive isotopes of carbon (13 C or 14 C) bound to octanoic acid. With an enteric neuropathy, the migrating motor complex is absent, whereas with a myopathy, contractions are present but their amplitude is decreased. Small intestinal transit can be measured by breath tests to estimate small intestinal transit by reflecting the bacterial metabolism of non-absorbable carbohydrate marker to H2, or the bacterial release of a radionuclide label from a bile salt conjugate, both of which increase in the breath after the substrates reach the colon. These tests are invalid if the patient has small intestinal bacterial overgrowth resulting from the motility dysfunction or a blind loop of intestine, because the bacteria release the marker proximal to the ileocecal valve. The appearance in the right lower quadrant (cecum) of a radionuclide-labeled non-absorbable marker ingested with a meal also provides an estimate of small intestinal transit. Intraluminal pressures measured in the small intestine may document abnormalities in the fasting migrating motor complex and the postprandial motility response. As in the stomach, concomitant use of transit and manometric studies allows the contribution of the enteric nerves and smooth muscle to the motility disorder to be estimated objectively. Global colonic transit can be easily measured by orally administering radiopaque markers and measuring the distribution of the markers throughout the colon 5 days later. If no markers are then present within the colon, the patient probably is not constipated. In the constipated patient, localization of the markers to the rectosigmoid region suggests a rectoanal outlet dysfunction. If the markers are distributed throughout the colon, a colonic motility disturbance exists. Once the motility defect has been localized to the colon, more specific transit and motility tests, measuring increases in intraluminal pressure and segment transit times with radionuclide markers, are available in specialized centers. The absence of a postprandial increase in segmenting contractions suggests a neural lesion, whereas low amplitude or absent postprandial contraction suggests disturbed smooth muscle function.

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