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Patients may take these or other laxatives as a manifestation of a psychiatric disorder womens health 85032 purchase discount fluoxetine online. Rapid transit of colonic contents and increased mucosal secretion occur in patients with active ulcerative colitis menstrual cycle age 7 buy cheap fluoxetine 20mg on-line. As in the other colonic causes of diarrhea pregnancy calculator conception date cheap 10mg fluoxetine otc, propagating contractions are increased in number and propagate into the rectum breast cancer kobe 9 buy 20mg fluoxetine with amex, accounting for the significant incidence of fecal incontinence. The rapid transit improves as the mucosal inflammation decreases after therapy for the underlying inflammation. When some of these drugs are used to treat other systemic diseases, they may precipitate gastrointestinal symptoms as a side effect. Excitatory Agents Drugs that excite the gastrointestinal tract should be used to treat decreased motility when the smooth muscle can functionally contract. In general, patients who benefit from these agents have an enteric neuropathy with decreased release of endogenous stimulatory neurotransmitters or an increased release of inhibitory neurotransmitters. When the smooth muscle is absent or severely damaged, the prokinetic drugs are rarely helpful. Acetylcholine analogues, such as bethanechol, stimulate both longitudinal and circular gastrointestinal smooth muscle by directly binding to the M2 muscarinic receptor to release inositol triphosphate or to open receptor-operated or voltage-dependent calcium channels. Drugs that block acetylcholinesterase increase endogenous acetylcholine concentration at the myoneural junction. These drugs have a theoretical advantage in regulating as well as in increasing motility, because the distribution of acetylcholine release is predetermined by the autonomic nervous system. Dopamine antagonists can variably increase motility throughout the gastrointestinal tract. Metoclopramide, a centrally and peripherally acting dopamine antagonist, increases gastric emptying and transit through the small intestine and the colon; it is useful in diabetic gastroparesis and constipation but has little therapeutic value in symptomatic patients with progressive systemic sclerosis or in many patients with pseudo-obstruction. Domperidone, a peripherally acting dopamine antagonist, mainly increases gastric emptying and has little therapeutic effect in small intestinal or colonic motility disorders. It stimulates gastric emptying, increases small intestinal transit, and stimulates colonic contractility. Cisapride may improve symptoms in patients with decreased gastric emptying, small intestinal pseudo-obstruction, or colonic inertia. Acetylcholine analogues Excitatory Neostigmine Metoclopramide Domperidone Cisapride Macrolide antibiotics Octreotide (low dose) Leuprolide acetate Atropine Secoverine Papaverine Calcium channel blockers Nitrate compounds Peppermint oil Cholecytokinin antagonists Erythromycin stimulates migrating motor complex activity, which is absent in many patients with neuropathic pseudo-obstruction, by binding at the motilin receptor on the small intestinal smooth muscle cell. Low dose octreotide (<100 mug) initiates phase 3 of the migrating motor complex, which also makes it useful in patients with pseudo-obstruction. Leuprolide acetate may improve symptoms secondary to functional disturbances of small intestinal motility. This drug is believed to work by decreasing the concentrations of the smooth muscle inhibitory hormones progesterone and relaxin. Inhibitory Agents Inhibitory drugs should be most useful for treating patients whose symptoms result from increased motility, which causes uncoordinated movement of the intestinal contents. The inhibitory drugs may block the receptors for excitatory neurotransmitters or block the increase in intracellular calcium necessary for normal smooth muscle contraction. Anticholinergic drugs, which inhibit muscarinic receptor stimulation, are sometimes effective for the small intestinal or colonic variants of the irritable bowel syndrome. The anticholinergics must be used with care in patients who may develop urinary retention. Several classes of calcium channel blockers, including verapamil and the dihydropyridines, such as nifedipine, inhibit the increase in intracellular calcium that is necessary for smooth muscle contraction and hence decrease smooth muscle contraction. These may be used in some patients with increased small intestinal or colonic motility. Nitrate compounds inhibit smooth muscle contraction, probably by increasing the intracellular concentration of cyclic guanosine monophosphate and decreasing calcium influx into the smooth muscle cell. Peppermint oil relaxes smooth muscle, which improves symptoms in some patients with the irritable bowel syndrome. Cholecystokinin antagonists may prove useful for treating multiple gastrointestinal motility disorders. Bueno L, Fioramonti J, Delvaux M, Frexinos J: Mediators and pharmacology of visceral sensitivity: From basic to clinical investigations.

Focal Segmental Ischemia of the Small Bowel Vascular insults to short segments of small bowel produce a broad spectrum of clinical features without the life-threatening complications associated with more extensive ischemia menstruation 10 purchase genuine fluoxetine. Focal segmental ischemia usually is caused by atheromatous emboli menopause irregular bleeding buy discount fluoxetine 10 mg on-line, strangulated hernias menstruation for dummies order fluoxetine now, vasculitis atraso menstrual 02 dias purchase fluoxetine 10mg without a prescription, blunt abdominal trauma, radiation, or oral contraceptives. Colon Ischemia Colon ischemia is the most common ischemic injury to the gastrointestinal tract. A spectrum of colon ischemic injury is recognized, including reversible colopathy (submucosal or intramural hemorrhage) (at least 30 to 40%); transient colitis (at least 15-20%); chronic ulcerating colitis (20-25%); stricture (10-15%); gangrene (15-20%); and fulminant universal colitis (<5%). In most cases, no specific cause is identified, and what finally triggers the presenting episode is usually unknown. However, colonic blood flow is lower than that of any other intestinal segment, decreases with functional motor activity, and is greatly affected by autonomic stimulation-a combination that may make the colon especially susceptible to ischemia. More than 90% of patients are older than age 60, although colon ischemia has been documented in young individuals with vasculitis (especially systemic lupus erythematosus), sickle cell disease, coagulopathies, medication-induced reactions (estrogens, danazol, vasopressin, gold, psychotropic drugs), 734 Figure 137-1 Algorithm for managing patients with suspected acute mesenteric ischemia. B, Intra-arterial infusion of papaverine (30 to 60 mg/hr) resulted in vasodilation. Five to 10 per cent of patients with colon ischemia have had a distal and potentially obstructing colonic or rectal lesion, including carcinoma, diverticulitis, stricture, or fecal impaction. Colon ischemia is a complication of elective aortic surgery in 1 to 7% of cases, but after surgery for ruptured abdominal aortic aneurysm it may be as high as 60%. Mildest changes include mucosal and submucosal hemorrhage and edema with or without partial mucosal necrosis. Hemorrhages are subsequently resorbed or the overlying mucosa sloughs, forming an ulcer. With more severe injury, the mucosa and submucosa are replaced by granulation tissue. Later, the mucosa may regenerate over the edematous submucosa, which contains granulation and fibrous tissue and iron-laden macrophages. Moderately severe colon ischemia can produce chronic ulcerations separated by normal bowel, a picture that mimics inflammatory bowel disease. With more severe and prolonged ischemia, the muscularis propria is damaged and replaced by fibrous tissue, thus forming a stricture. In contrast to acute mesenteric ischemia, most colon ischemia is not associated with either a major vascular occlusion or a period of low cardiac output. Colon ischemia usually presents with sudden, crampy, mild, left lower abdominal pain, an urge to defecate, and passage of bright red or maroon blood mixed with the stool within 24 hours. Bleeding is not vigorous, and blood loss requiring transfusion suggests another diagnosis. Physical examination usually reveals only mild to moderate abdominal tenderness over the involved segment of bowel. Any part of the colon may be affected, but the splenic flexure and sigmoid are most commonly involved. Systemic low flow states usually involve the right colon; local non-occlusive ischemic injuries involve the "watershed" areas of the colon. If colon ischemia is suspected and the patient has no signs of peritonitis and an unrevealing abdominal plain film, colonoscopy or the combination of sigmoidoscopy and a gentle barium enema should be performed on the unprepared bowel within 48 hours of the onset of symptoms; colonoscopy is more sensitive in diagnosing mucosal abnormalities, and biopsy specimens may be obtained. Hemorrhagic nodules seen at colonoscopy represent submucosal bleeding and appear as filling defects called "thumbprints" on barium enema examination. The initial diagnostic study should be performed within 48 hours, because thumbprinting disappears as the submucosal hemorrhages are resorbed or the overlying mucosa sloughs. Studies performed 1 week after the initial study should reflect evolution of the injury: normalization of the colon or replacement of the thumbprints with segmental ulceration. Mesenteric angiography usually is not indicated in colon ischemia, because by the time of presentation colonic blood flow has returned to normal. In such situations, because untreated acute mesenteric ischemia rapidly becomes irreversible and because optimal management requires angiography, acute mesenteric ischemia must be excluded before barium studies, which would preclude an adequate angiographic examination. In general, symptoms of colon ischemia subside within 24 to 48 hours, and healing is seen within 2 weeks.

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Continuing oral anticoagulant prophylaxis beyond the initial 6 months following an acute episode of venous thromboembolism must be weighed against continued exposure of the individual patient to the significant risk of bleeding complications menstruation in animals cheap fluoxetine amex. Patients with primary hypercoagulable states who have suffered two or more thrombotic events should receive lifelong prophylactic anticoagulation with warfarin breast cancer options order generic fluoxetine line. In fact women's health center danvers ma cheap fluoxetine line, indefinite or lifelong anticoagulation is probably indicated for individuals with recurrent thrombosis even in the absence of identifiable primary hypercoagulable states women's health center dickson tn generic fluoxetine 10mg with mastercard. The decision to continue prophylactic oral anticoagulation beyond the initial period following the initial episode of thrombosis is more difficult. Recent data indicate that the risk of recurrent thrombosis up to 8 years after an initial episode in patients heterozygous for Factor V Leiden is significantly greater than in genetically unaffected individuals. Furthermore, despite the increased risk of thrombosis recurrence over several years in individuals with Factor V Leiden and the clear efficacy of prophylactic warfarin therapy, it is not yet clear whether the protection afforded by oral anticoagulation outweighs the risk of serious bleeding complications associated with it. Following a single episode of thrombosis, patients with inherited hypercoagulable states should probably receive indefinite or lifelong anticoagulation if their initial episodes were life threatening or occurred in unusual sites. In the absence of these characteristics, particularly if the initial episode was precipitated by a transient acquired prothrombotic situation. Asymptomatic individuals with known thrombophilia who have not had previous thrombotic complications do not require prophylactic anticoagulation except during periods of high risk for thrombosis. Because about half of the first-degree relatives of a patient with a primary hypercoagulable state should be affected, such individuals should be counseled about the implications of making a diagnosis. The management of pregnancy in women with primary hypercoagulable states requires special consideration because of the high risk of thrombosis, particularly in the puerperium. Women with thrombophilia who have had previous thrombosis-and probably also asymptomatic women with thrombophilia-should receive prophylactic anticoagulation throughout pregnancy and for 4 to 6 weeks postpartum, a particularly high-risk period. Heparin is presently the anticoagulant of choice because of the risk of embryopathy in the first trimester and bleeding late in pregnancy with the use of warfarin. Most cases can be avoided by not initiating warfarin therapy with high loading doses and by concomitant coverage with heparin. When the complication does occur, as manifested by painful red and subsequently dark, necrotic skin lesions within a few days of starting warfarin, warfarin therapy must be immediately discontinued, vitamin K administered, and heparin started. The use of fresh-frozen plasma or purified protein C concentrate to rapidly normalize protein C levels can improve results. Despite this rare complication, warfarin is an effective, long-term prophylactic anticoagulant in patients with inherited protein C or protein S deficiency. Antithrombin concentrate infusion can also be considered in some perioperative or obstetric settings in which anticoagulation poses an unacceptable bleeding risk. Purified protein C concentrate has been used to initiate warfarin therapy in severe protein C deficiency and in the initial treatment of neonatal purpura fulminans. It is not clear at this time whether comparable guidelines for anticoagulation are applicable to patients with hyperhomocysteinemia and venous thrombosis. Vitamin supplementation with folate, pyridoxine, and cobalamin can normalize elevated blood levels of homocysteine, but it is not known whether such treatment reduces the risk of thrombosis. Until such information becomes available, the safety and low cost of supplementation make this treatment advisable for patients with hyperhomocysteinemia associated with thrombosis. Many of these conditions also represent the acquired precipitating stimuli for clinical thrombotic events in individuals with a genetic predisposition (primary hypercoagulable states). Although each disorder causes thrombosis primarily through abnormalities in blood flow (rheology), blood composition (coagulation factors and platelet function), or the vessel wall, multiple overlapping mechanisms are operative in many of them. For example, the leukocytes of patients with acute promyelocytic leukemia produce tissue factor-like procoagulant activity. The thrombotic tendency of patients with cancer may also be related to mechanical factors such as immobility or a bulky tumor mass compressing vessels, as well as to co-morbid conditions such as liver dysfunction secondary to metastases, sepsis, surgery, and the prothrombotic effects of certain antineoplastic agents. The incidence of thrombotic complications in cancer patients depends in part on the type of malignancy. Hypercoagulability appears to be most prominent in patients with pancreatic cancer, adenocarcinomas of the gastrointestinal tract or lung, and ovarian cancers. The presence of underlying malignancy compounds the independent risk of thrombosis in the postoperative state. Although thrombosis most commonly occurs in patients with established malignancy, it can also antedate the diagnosis by months or even years (see Chapters 69 and 197).

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