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	<title>Virtual Journal Club &#187; Am Fam Physician</title>
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	<link>http://beckerinfo.net/JClub</link>
	<description>Division of Hospital Medicine Virtual Journal Club</description>
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		<title>Rivaroxaban vs. Warfarin for Stroke Prevention in Patients with Nonvalvular Atrial Fibrillation.</title>
		<link>http://beckerinfo.net/JClub/2012/04/27/rivaroxaban-vs-warfarin-for-stroke-prevention-in-patients-with-nonvalvular-atrial-fibrillation/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/27/rivaroxaban-vs-warfarin-for-stroke-prevention-in-patients-with-nonvalvular-atrial-fibrillation/#comments</comments>
		<pubDate>Fri, 27 Apr 2012 11:31:03 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

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		<description><![CDATA[Rivaroxaban vs. Warfarin for Stroke Prevention in Patients with Nonvalvular Atrial Fibril...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Rivaroxaban vs. Warfarin for Stroke Prevention in Patients with Nonvalvular Atrial Fibrillation.</b></p>
        <p>Am Fam Physician. 2012 Mar 15;85(6):577-86</p>
        <p>Authors:  Darby-Stewart A, Dachs R, Graber MA</p>
        <p>PMID: 22534269 [PubMed - in process]</p></body>]]></content:encoded>
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		<item>
		<title>Evaluation of nail abnormalities.</title>
		<link>http://beckerinfo.net/JClub/2012/04/27/evaluation-of-nail-abnormalities/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/27/evaluation-of-nail-abnormalities/#comments</comments>
		<pubDate>Fri, 27 Apr 2012 11:31:03 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

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		<description><![CDATA[Evaluation of nail abnormalities.
        Am Fam Physician. 2012 Apr 15;85(8):779-87
    ...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Evaluation of nail abnormalities.</b></p>
        <p>Am Fam Physician. 2012 Apr 15;85(8):779-87</p>
        <p>Authors:  Tully AS, Trayes KP, Studdiford JS</p>
        <p>Abstract<br/>
        Knowledge of the anatomy and function of the nail apparatus is essential when performing the physical examination. Inspection may reveal localized nail abnormalities that should be treated, or may provide clues to an underlying systemic disease that requires further workup. Excessive keratinaceous material under the nail bed in a distal and lateral distribution should prompt an evaluation for onychomycosis. Onychomycosis may be diagnosed through potassium hydroxide examination of scrapings. If potassium hydroxide testing is negative for the condition, a nail culture or nail plate biopsy should be performed. A proliferating, erythematous, disruptive mass in the nail bed should be carefully evaluated for underlying squamous cell carcinoma. Longitudinal melanonychia (vertical nail bands) must be differentiated from subungual melanomas, which account for 50 percent of melanomas in persons with dark skin. Dystrophic longitudinal ridges and subungual hematomas are local conditions caused by trauma. Edema and erythema of the proximal and lateral nail folds are hallmark features of acute and chronic paronychia. Clubbing may suggest an underlying disease such as cirrhosis, chronic obstructive pulmonary disease, or celiac sprue. Koilonychia (spoon nail) is commonly associated with iron deficiency anemia. Splinter hemorrhages may herald endocarditis, although other causes should be considered. Beau lines can mark the onset of a severe underlying illness, whereas Muehrcke lines are associated with hypoalbuminemia. A pincer nail deformity is inherited or acquired and can be associated with beta-blocker use, psoriasis, onychomycosis, tumors of the nail apparatus, systemic lupus erythematosus, Kawasaki disease, and malignancy.<br/></p><p>PMID: 22534387 [PubMed - in process]</p></body>]]></content:encoded>
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		<item>
		<title>Thrombocytopenia.</title>
		<link>http://beckerinfo.net/JClub/2012/04/27/thrombocytopenia/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/27/thrombocytopenia/#comments</comments>
		<pubDate>Fri, 27 Apr 2012 11:31:03 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

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		<description><![CDATA[Thrombocytopenia.
        Am Fam Physician. 2012 Mar 15;85(6):612-22
        Authors:  Ga...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Thrombocytopenia.</b></p>
        <p>Am Fam Physician. 2012 Mar 15;85(6):612-22</p>
        <p>Authors:  Gauer RL, Braun MM</p>
        <p>Abstract<br/>
        Thrombocytopenia is defined as a platelet count of less than 150 × 103 per µL. It is often discovered incidentally when obtaining a complete blood count during an office visit. The etiology usually is not obvious, and additional investigation is required. Patients with platelet counts greater than 50 × 103 per µL rarely have symptoms. A platelet count from 30 to 50 × 103 per µL rarely manifests as purpura. A count from 10 to 30 × 103 per µL may cause bleeding with minimal trauma. A platelet count less than 5 × 103 per µL may cause spontaneous bleeding and constitutes a hematologic emergency. Patients who present with thrombocytopenia as part of a multisystem disorder usually are ill and require urgent evaluation and treatment. These patients most likely have an acute infection, heparin-induced thrombocytopenia, liver disease, thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, disseminated intravascular coagulation, or a hematologic disorder. During pregnancy, preeclampsia and the HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome are associated with thrombocytopenia. Patients with isolated thrombocytopenia commonly have drug-induced thrombocytopenia, immune thrombocytopenic purpura, pseudothrombocytopenia, or if pregnant, gestational thrombocytopenia. A history, physical examination, and laboratory studies can differentiate patients who require immediate intervention from those who can be treated in the outpatient setting. Treatment is based on the etiology and, in some cases, treating the secondary cause results in normalization of platelet counts. Consultation with a hematologist should be considered if patients require hospitalization, if there is evidence of systemic disease, or if thrombocytopenia worsens despite initial treatment.<br/></p><p>PMID: 22534274 [PubMed - in process]</p></body>]]></content:encoded>
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		<item>
		<title>Pelvic inflammatory disease.</title>
		<link>http://beckerinfo.net/JClub/2012/04/27/pelvic-inflammatory-disease/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/27/pelvic-inflammatory-disease/#comments</comments>
		<pubDate>Fri, 27 Apr 2012 11:31:03 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=db7c90ddb69c27dc89761f256ee1f2e2</guid>
		<description><![CDATA[Pelvic inflammatory disease.
        Am Fam Physician. 2012 Apr 15;85(8):791-6
        Au...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Pelvic inflammatory disease.</b></p>
        <p>Am Fam Physician. 2012 Apr 15;85(8):791-6</p>
        <p>Authors:  Gradison M</p>
        <p>Abstract<br/>
        Pelvic inflammatory disease is a polymicrobial infection of the upper genital tract. It primarily affects young, sexually active women. The diagnosis is made clinically; no single test or study is sensitive or specific enough for a definitive diagnosis. Pelvic inflammatory disease should be suspected in at-risk patients who present with pelvic or lower abdominal pain with no identified etiology, and who have cervical motion, uterine, or adnexal tenderness. Chlamydia trachomatis and Neisseria gonorrhoeae are the most commonly implicated microorganisms; however, other microorganisms may be involved. The spectrum of disease ranges from asymptomatic to life-threatening tubo-ovarian abscess. Patients should be treated empirically, even if they present with few symptoms. Most women can be treated successfully as outpatients with a single dose of a parenteral cephalosporin plus oral doxycycline, with or without oral metronidazole. Delay in treatment may lead to major sequelae, including chronic pelvic pain, ectopic pregnancy, and infertility. Hospitalization and parenteral treatment are recommended if the patient is pregnant, has human immunodeficiency virus infection, does not respond to oral medication, or is severely ill. Strategies for preventing pelvic inflammatory disease include routine screening for chlamydia and patient education.<br/></p><p>PMID: 22534388 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Evaluation and treatment of the suicidal patient.</title>
		<link>http://beckerinfo.net/JClub/2012/04/27/evaluation-and-treatment-of-the-suicidal-patient/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/27/evaluation-and-treatment-of-the-suicidal-patient/#comments</comments>
		<pubDate>Fri, 27 Apr 2012 11:31:03 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=7cb89d20641101f250ace7384f9b2690</guid>
		<description><![CDATA[Evaluation and treatment of the suicidal patient.
        Am Fam Physician. 2012 Mar 15;8...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Evaluation and treatment of the suicidal patient.</b></p>
        <p>Am Fam Physician. 2012 Mar 15;85(6):602-5</p>
        <p>Authors:  Norris D, Clark MS</p>
        <p>Abstract<br/>
        Evaluation and treatment of a suicidal patient are challenging tasks for the physician. Because no validated predictive tools exist, clinical judgment guides the decision-making process. Although there is insufficient evidence to support routine screening, evidence shows that asking high-risk patients about suicidal intent leads to better outcomes and does not increase the risk of suicide. Important elements of the history that permit evaluation of the seriousness of suicidal ideation include the intent, plan, and means; the availability of social support; previous suicide attempts; and the presence of comorbid psychiatric illness or substance abuse. After intent has been established, inpatient and outpatient management should include ensuring patient safety and medical stabilization; activating support networks; and initiating therapy for psychiatric diseases. Care plans for patients with chronic suicidal ideation include these same steps, as well as referral for specialty care. In the event of a completed suicide, physicians should provide support for family members who may be experiencing grief complicated by guilt, while also activating their own support networks and risk management systems.<br/></p><p>PMID: 22534272 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Diagnosis and management of upper gastrointestinal bleeding.</title>
		<link>http://beckerinfo.net/JClub/2012/04/27/diagnosis-and-management-of-upper-gastrointestinal-bleeding/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/27/diagnosis-and-management-of-upper-gastrointestinal-bleeding/#comments</comments>
		<pubDate>Fri, 27 Apr 2012 11:31:03 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=5d60b04e942a4bd457772f71a4d7c892</guid>
		<description><![CDATA[Diagnosis and management of upper gastrointestinal bleeding.
        Am Fam Physician. 20...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Diagnosis and management of upper gastrointestinal bleeding.</b></p>
        <p>Am Fam Physician. 2012 Mar 1;85(5):469-76</p>
        <p>Authors:  Wilkins T, Khan N, Nabh A, Schade RR</p>
        <p>Abstract<br/>
        Upper gastrointestinal bleeding causes significant morbidity and mortality in the United States, and has been associated with increasing nonsteroidal anti-inflammatory drug use and the high prevalence of Helicobacter pylori infection in patients with peptic ulcer bleeding. Rapid assessment and resuscitation should precede the diagnostic evaluation in unstable patients with severe bleeding. Risk stratification is based on clinical assessment and endoscopic findings. Early upper endoscopy (within 24 hours of presentation) is recommended in most patients because it confirms the diagnosis and allows for targeted endoscopic treatment, including epinephrine injection, thermocoagulation, application of clips, and banding. Endoscopic therapy results in reduced morbidity, hospital stays, risk of recurrent bleeding, and need for surgery. Although administration of proton pump inhibitors does not decrease mortality, risk of rebleeding, or need for surgery, it reduces stigmata of recent hemorrhage and the need for endoscopic therapy. Despite successful endoscopic therapy, rebleeding can occur in 10 to 20 percent of patients; a second attempt at endoscopic therapy is recommended in these patients. Arteriography with embolization or surgery may be needed if there is persistent and severe bleeding.<br/></p><p>PMID: 22534226 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Acute respiratory distress syndrome: diagnosis and management.</title>
		<link>http://beckerinfo.net/JClub/2012/02/18/acute-respiratory-distress-syndrome-diagnosis-and-management/</link>
		<comments>http://beckerinfo.net/JClub/2012/02/18/acute-respiratory-distress-syndrome-diagnosis-and-management/#comments</comments>
		<pubDate>Sat, 18 Feb 2012 12:02:36 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=87f7bc6cf4f1d03ec3d893c5ac6f3cf2</guid>
		<description><![CDATA[Acute respiratory distress syndrome: diagnosis and management.
        Am Fam Physician. ...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Acute respiratory distress syndrome: diagnosis and management.</b></p>
        <p>Am Fam Physician. 2012 Feb 15;85(4):352-8</p>
        <p>Authors:  Saguil A, Fargo M</p>
        <p>Abstract<br/>
        Acute respiratory distress syndrome manifests as rapidly progressive dyspnea, tachypnea, and hypoxemia. Diagnostic criteria include acute onset, profound hypoxemia, bilateral pulmonary infiltrates, and the absence of left atrial hypertension. Acute respiratory distress syndrome is believed to occur when a pulmonary or extrapulmonary insult causes the release of inflammatory mediators, promoting neutrophil accumulation in the microcirculation of the lung. Neutrophils damage the vascular endothelium and alveolar epithelium, leading to pulmonary edema, hyaline membrane formation, decreased lung compliance, and difficult air exchange. Most cases of acute respiratory distress syndrome are associated with pneumonia or sepsis. It is estimated that 7.1 percent of all patients admitted to an intensive care unit and 16.1 percent of all patients on mechanical ventilation develop acute lung injury or acute respiratory distress syndrome. In-hospital mortality related to these conditions is between 34 and 55 percent, and most deaths are due to multiorgan failure. Acute respiratory distress syndrome often has to be differentiated from congestive heart failure, which usually has signs of fluid overload, and from pneumonia. Treatment of acute respiratory distress syndrome is supportive and includes mechanical ventilation, prophylaxis for stress ulcers and venous thromboembolism, nutritional support, and treatment of the underlying injury. Low tidal volume, high positive end-expiratory pressure, and conservative fluid therapy may improve outcomes. A spontaneous breathing trial is indicated as the patient improves and the underlying illness resolves. Patients who survive acute respiratory distress syndrome are at risk of diminished functional capacity, mental illness, and decreased quality of life; ongoing care by a primary care physician is beneficial for these patients.<br/></p><p>PMID: 22335314 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Perioperative cardiac risk reduction.</title>
		<link>http://beckerinfo.net/JClub/2012/02/18/perioperative-cardiac-risk-reduction/</link>
		<comments>http://beckerinfo.net/JClub/2012/02/18/perioperative-cardiac-risk-reduction/#comments</comments>
		<pubDate>Sat, 18 Feb 2012 12:02:36 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=07e5c8f701e5b3f86b3c349a343df253</guid>
		<description><![CDATA[Perioperative cardiac risk reduction.
        Am Fam Physician. 2012 Feb 1;85(3):239-46
 ...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Perioperative cardiac risk reduction.</b></p>
        <p>Am Fam Physician. 2012 Feb 1;85(3):239-46</p>
        <p>Authors:  Holt NF</p>
        <p>Abstract<br/>
        Cardiovascular complications are the most common cause of perioperative morbidity and mortality. Noninvasive stress testing is rarely helpful in assessing risk, and for most patients there is no evidence that coronary revascularization provides more protection against perioperative cardiovascular events than optimal medical management. Patients likely to benefit from perioperative beta blockade include those with stable coronary artery disease and multiple cardiac risk factors. Perioperative beta blockers should be initiated weeks before surgery and titrated to heart rate and blood pressure targets. The balance of benefits and harms of perioperative beta-blocker therapy is much less favorable in patients with limited cardiac risk factors and when initiated in the acute preoperative period. Perioperative statin therapy is recommended for all patients undergoing vascular surgery. When prescribed for the secondary prevention of cardiovascular disease, aspirin should be continued in the perioperative period.<br/></p><p>PMID: 22335263 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Subacute management of ischemic stroke.</title>
		<link>http://beckerinfo.net/JClub/2012/01/11/subacute-management-of-ischemic-stroke/</link>
		<comments>http://beckerinfo.net/JClub/2012/01/11/subacute-management-of-ischemic-stroke/#comments</comments>
		<pubDate>Wed, 11 Jan 2012 13:02:46 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=dc25563f012d5862e5b90d732e1c546c</guid>
		<description><![CDATA[Subacute management of ischemic stroke.
        Am Fam Physician. 2011 Dec 15;84(12):1383...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Subacute management of ischemic stroke.</b></p>
        <p>Am Fam Physician. 2011 Dec 15;84(12):1383-8</p>
        <p>Authors:  Bernheisel CR, Schlaudecker JD, Leopold K</p>
        <p>Abstract<br/>
        Ischemic stroke is the third leading cause of death in the United States and a common reason for hospitalization. The subacute period after a stroke refers to the time when the decision to not employ thrombolytics is made up until two weeks after the stroke occurred. Family physicians are often involved in the subacute management of ischemic stroke. All patients with an ischemic stroke should be admitted to the hospital in the subacute period for cardiac and neurologic monitoring. Imaging studies, including magnetic resonance angiography, carotid artery ultrasonography, and/or echocardiography, may be indicated to determine the cause of the stroke. Evaluation for aspiration risk, including a swallowing assessment, should be performed, and nutritional, physical, occupational, and speech therapy should be initiated. Significant causes of morbidity and mortality following ischemic stroke include venous thromboembolism, pressure sores, infection, and delirium, and measures should be taken to prevent these complications. For secondary prevention of future strokes, antiplatelet therapy with aspirin should be initiated within 24 hours of ischemic stroke in all patients without contraindications, and one of several antiplatelet regimens should be continued long-term. Statin therapy should also be given in most situations. Although permissive hypertension is initially warranted, antihypertensive therapy should begin within 24 hours. Diabetes mellitus should be controlled and patients counseled about lifestyle modifications to reduce stroke risk. Rehabilitative therapy following hospitalization improves outcomes and should be considered.<br/></p><p>PMID: 22230273 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Cirrhosis: diagnosis, management, and prevention.</title>
		<link>http://beckerinfo.net/JClub/2012/01/11/cirrhosis-diagnosis-management-and-prevention/</link>
		<comments>http://beckerinfo.net/JClub/2012/01/11/cirrhosis-diagnosis-management-and-prevention/#comments</comments>
		<pubDate>Wed, 11 Jan 2012 13:02:46 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=b051f78bcdfa8de8b6d5d111d9ca89e7</guid>
		<description><![CDATA[Cirrhosis: diagnosis, management, and prevention.
        Am Fam Physician. 2011 Dec 15;8...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Cirrhosis: diagnosis, management, and prevention.</b></p>
        <p>Am Fam Physician. 2011 Dec 15;84(12):1353-9</p>
        <p>Authors:  Starr SP, Raines D</p>
        <p>Abstract<br/>
        Cirrhosis is the 12th leading cause of death in the United States. It accounted for 29,165 deaths in 2007, with a mortality rate of 9.7 per 100,000 persons. Alcohol abuse and viral hepatitis are the most common causes of cirrhosis, although nonalcoholic fatty liver disease is emerging as an increasingly important cause. Primary care physicians share responsibility with specialists in managing the most common complications of the disease, screening for hepatocellular carcinoma, and preparing patients for referral to a transplant center. Patients with cirrhosis should be screened for hepatocellular carcinoma with imaging studies every six to 12 months. Causes of hepatic encephalopathy include constipation, infection, gastrointestinal bleeding, certain medications, electrolyte imbalances, and noncompliance with medical therapy. These should be sought and managed before instituting the use of lactulose or rifaximin, which is aimed at reducing serum ammonia levels. Ascites should be treated initially with salt restriction and diuresis. Patients with acute episodes of gastrointestinal bleeding should be monitored in an intensive care unit, and should have endoscopy performed within 24 hours. Physicians should also be vigilant for spontaneous bacterial peritonitis. Treating alcohol abuse, screening for viral hepatitis, and controlling risk factors for nonalcoholic fatty liver disease are mechanisms by which the primary care physician can reduce the incidence of cirrhosis.<br/></p><p>PMID: 22230269 [PubMed - in process]</p></body>]]></content:encoded>
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		<title>Evaluation of chronic diarrhea.</title>
		<link>http://beckerinfo.net/JClub/2012/01/05/evaluation-of-chronic-diarrhea/</link>
		<comments>http://beckerinfo.net/JClub/2012/01/05/evaluation-of-chronic-diarrhea/#comments</comments>
		<pubDate>Thu, 05 Jan 2012 16:33:09 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=a74d7ef93857164de993c36a7f23f604</guid>
		<description><![CDATA[Evaluation of chronic diarrhea.
        Am Fam Physician. 2011 Nov 15;84(10):1119-26
    ...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Evaluation of chronic diarrhea.</b></p>
        <p>Am Fam Physician. 2011 Nov 15;84(10):1119-26</p>
        <p>Authors:  Juckett G, Trivedi R</p>
        <p>Abstract<br/>
        Chronic diarrhea, defined as a decrease in stool consistency for more than four weeks, is a common but challenging clinical scenario. It can be divided into three basic categories: watery, fatty (malabsorption), and inflammatory. Watery diarrhea may be subdivided into osmotic, secretory, and functional types. Watery diarrhea includes irritable bowel syndrome, which is the most common cause of functional diarrhea. Another example of watery diarrhea is microscopic colitis, which is a secretory diarrhea affecting older persons. Laxative-induced diarrhea is often osmotic. Malabsorptive diarrhea is characterized by excess gas, steatorrhea, or weight loss; giardiasis is a classic infectious example. Celiac disease (gluten-sensitive enteropathy) is also malabsorptive, and typically results in weight loss and iron deficiency anemia. Inflammatory diarrhea, such as ulcerative colitis or Crohn disease, is characterized by blood and pus in the stool and an elevated fecal calprotectin level. Invasive bacteria and parasites also produce inflammation. Infections caused by Clostridium difficile subsequent to antibiotic use have become increasingly common and virulent. Not all chronic diarrhea is strictly watery, malabsorptive, or inflammatory, because some categories overlap. Still, the most practical diagnostic approach is to attempt to categorize the diarrhea by type before testing and treating. This narrows the list of diagnostic possibilities and reduces unnecessary testing. Empiric therapy is justified when a specific diagnosis is strongly suspected and follow-up is available.<br/></p><p>PMID: 22085666 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Anaphylaxis: Recognition and Management.</title>
		<link>http://beckerinfo.net/JClub/2011/11/17/anaphylaxis-recognition-and-management/</link>
		<comments>http://beckerinfo.net/JClub/2011/11/17/anaphylaxis-recognition-and-management/#comments</comments>
		<pubDate>Thu, 17 Nov 2011 14:01:53 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=4ff3c4669bcfa487d59e7f7efff19042</guid>
		<description><![CDATA[Anaphylaxis: Recognition and Management.
        Am Fam Physician. 2011 Nov 15;84(10):111...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Anaphylaxis: Recognition and Management.</b></p>
        <p>Am Fam Physician. 2011 Nov 15;84(10):1111-1118</p>
        <p>Authors:  Arnold JJ, Williams PM</p>
        <p>Abstract<br/>
        Anaphylaxis is a severe, life-threatening, systemic allergic reaction that is almost always unanticipated and may lead to death by airway obstruction or vascular collapse. Anaphylaxis occurs as the result of an allergen response, usually immunoglobulin E-mediated, which leads to mast cell and basophil activation and a combination of dermatologic, respiratory, cardiovascular, gastrointestinal, and neurologic symptoms. Dermatologic and respiratory symptoms are most common, occurring in 90 and 70 percent of episodes, respectively. The three most common triggers are food, insect stings, and medications. The diagnosis of anaphylaxis is typically made when symptoms occur within one hour of exposure to a specific antigen. Confirmatory testing using serum histamine and tryptase levels is difficult, because blood samples must be drawn with strict time considerations. Allergen skin testing and in vitro assay for serum immunoglobulin E of specific allergens do not reliably predict who will develop anaphylaxis. Administration of intramuscular epinephrine at the onset of anaphylaxis, before respiratory failure or cardiovascular compromise, is essential. Histamine H1 receptor antagonists and corticosteroids may be useful adjuncts. All patients at risk of recurrent anaphylaxis should be educated about the appropriate use of prescription epinephrine autoinjectors.<br/></p><p>PMID: 22085665 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Causes and evaluation of mildly elevated liver transaminase levels.</title>
		<link>http://beckerinfo.net/JClub/2011/11/04/causes-and-evaluation-of-mildly-elevated-liver-transaminase-levels/</link>
		<comments>http://beckerinfo.net/JClub/2011/11/04/causes-and-evaluation-of-mildly-elevated-liver-transaminase-levels/#comments</comments>
		<pubDate>Fri, 04 Nov 2011 10:31:32 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=4fc29c703897eddff34decca93b23c94</guid>
		<description><![CDATA[Causes and evaluation of mildly elevated liver transaminase levels.
        Am Fam Physic...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Causes and evaluation of mildly elevated liver transaminase levels.</b></p>
        <p>Am Fam Physician. 2011 Nov 1;84(9):1003-8</p>
        <p>Authors:  Oh RC, Hustead TR</p>
        <p>Abstract<br/>
        Mild elevations in levels of the liver enzymes alanine transaminase and aspartate transaminase are commonly discovered in asymptomatic patients in primary care. Evidence to guide the diagnostic workup is limited. If the history and physical examination do not suggest a cause, a stepwise evaluation should be initiated based on the prevalence of diseases that cause mild elevations in transaminase levels. The most common cause is nonalcoholic fatty liver disease, which can affect up to 30 percent of the population. Other common causes include alcoholic liver disease, medication-associated liver injury, viral hepatitis (hepatitis B and C), and hemochromatosis. Less common causes includea1-antitrypsin deficiency, autoimmune hepatitis, and Wilson disease. Extrahepatic conditions (e.g., thyroid disorders, celiac disease, hemolysis, muscle disorders) can also cause elevated liver transaminase levels. Initial testing should include a fasting lipid profile; measurement of glucose, serum iron, and ferritin; total iron-binding capacity; and hepatitis B surface antigen and hepatitis C virus antibody testing. If test results are normal, a trial of lifestyle modification with observation or further testing for less common causes is appropriate. Additional testing may include ultrasonography; measurement of a1-antitrypsin and ceruloplasmin; serum protein electrophoresis; and antinuclear antibody, smooth muscle antibody, and liver/kidney microsomal antibody type 1 testing. Referral for further evaluation and possible liver biopsy is recommended if transaminase levels remain elevated for six months or more.<br/></p><p>PMID: 22046940 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Diagnosis and management of osteomyelitis.</title>
		<link>http://beckerinfo.net/JClub/2011/11/04/diagnosis-and-management-of-osteomyelitis/</link>
		<comments>http://beckerinfo.net/JClub/2011/11/04/diagnosis-and-management-of-osteomyelitis/#comments</comments>
		<pubDate>Fri, 04 Nov 2011 10:31:32 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=83d080eb61cd9dbe96ae3f11ba00c852</guid>
		<description><![CDATA[Diagnosis and management of osteomyelitis.
        Am Fam Physician. 2011 Nov 1;84(9):102...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Diagnosis and management of osteomyelitis.</b></p>
        <p>Am Fam Physician. 2011 Nov 1;84(9):1027-33</p>
        <p>Authors:  Hatzenbuehler J, Pulling TJ</p>
        <p>Abstract<br/>
        The incidence of chronic osteomyelitis is increasing because of the prevalence of predisposing conditions such as diabetes mellitus and peripheral vascular disease. The increased availability of sensitive imaging tests, such as magnetic resonance imaging and bone scintigraphy, has improved diagnostic accuracy and the ability to characterize the infection. Plain radiography is a useful initial investigation to identify alternative diagnoses and potential complications. Direct sampling of the wound for culture and antimicrobial sensitivity is essential to target treatment. The increased incidence of methicillin-resistant Staphylococcus aureus osteomyelitis complicates antibiotic selection. Surgical debridement is usually necessary in chronic cases. The recurrence rate remains high despite surgical intervention and long-term antibiotic therapy. Acute hematogenous osteomyelitis in children typically can be treated with a four-week course of antibiotics. In adults, the duration of antibiotic treatment for chronic osteomyelitis is typically several weeks longer. In both situations, however, empiric antibiotic coverage for S. aureus is indicated.<br/></p><p>PMID: 22046943 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Evaluation of syncope.</title>
		<link>http://beckerinfo.net/JClub/2011/09/16/evaluation-of-syncope/</link>
		<comments>http://beckerinfo.net/JClub/2011/09/16/evaluation-of-syncope/#comments</comments>
		<pubDate>Fri, 16 Sep 2011 19:58:14 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am Fam Physician]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=64e8b3d8073c3d23eb104a5d1a339892</guid>
		<description><![CDATA[
        Evaluation of syncope.
        Am Fam Physician. 2011 Sep 15;84(6):640-50
        Authors:  Gauer RL
        Abstract
        Syncope is a transient and abrupt loss of consciousness with complete return to preexisting neurologic function. It i...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Evaluation of syncope.</b></p>
        <p>Am Fam Physician. 2011 Sep 15;84(6):640-50</p>
        <p>Authors:  Gauer RL</p>
        <p>Abstract<br>
        Syncope is a transient and abrupt loss of consciousness with complete return to preexisting neurologic function. It is classified as neurally mediated (i.e., carotid sinus hypersensitivity, situational, or vasovagal), cardiac, orthostatic, or neurogenic. Older adults are more likely to have orthostatic, carotid sinus hypersensitivity, or cardiac syn- cope, whereas younger adults are more likely to have vasovagal syncope. Common nonsyncopal syndromes with similar presentations include seizures, metabolic and psychogenic disorders, and acute intoxication. Patients presenting with syncope (other than neurally mediated and orthostatic syncope) are at increased risk of death from any cause. Useful clinical rules to assess the short-term risk of death and the need for immediate hospitalization include the San Francisco Syncope Rule and the Risk Stratification of Syncope in the Emergency Department rule. Guidelines suggest an algorithmic approach to the evaluation of syncope that begins with the history and physical examination. All patients presenting with syncope require electrocardiography, orthostatic vital signs, and QT interval monitoring. Patients with cardiovascular disease, abnormal electrocardiography, or family history of sudden death, and those presenting with unexplained syncope should be hospitalized for further diagnostic evaluation. Patients with neurally mediated or orthostatic syncope usually require no additional testing. In cases of unexplained syncope, further testing such as echocardiography, grade exercise testing, electrocardiographic monitoring, and electrophysiologic studies may be required. Although a subset of patients will have unexplained syncope despite undergoing a comprehensive evaluation, those with multiple episodes compared with an isolated event are more likely to have a serious underlying disorder.<br>
        </p><p>PMID: 21916389 [PubMed - in process]</p>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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