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Necrotizing enterocolitis is a serious and yet incompletely understood gastrointestinal disease of infancy that predominately impacts premature neonates. Prevention is a key strategy for the management of necrotizing enterocolitis. Although postnatal risk factors have been the focus of prevention efforts, obstetric complications, including intrauterine inflammation and infection, growth restriction, preeclampsia, and prenatal medications, have been associated with an increased risk of necrotizing enterocolitis. This article reviews the evidence behind the prenatal risk factors for necrotizing enterocolitis, and discusses how these risk factors may elucidate the pathogenesis of necrotizing enterocolitis and provide insight into prevention and treatment.Infectious gastroenteritis is common after transplantation and can lead to increased morbidity and mortality. A wide range of organisms can lead to gastroenteritis in this patient population. Clostridioides difficile, cytomegalovirus, and norovirus are the most common pathogens. Newer diagnostic methods, especially multiplex polymerase chain reaction, have increased the diagnostic yield of infectious etiologies. In this review, we describe the epidemiology and risk factors for common infectious pathogens leading to gastroenteritis.Acute cholangitis, also referred to as ascending cholangitis, is an infection of the biliary tree characterized by fever, jaundice, and abdominal pain, which in most cases is the consequence of biliary obstruction. Diagnosis is commonly made by the presence of clinical features, laboratory tests, and imaging studies. The treatment modalities include administration of intravenous fluids, antimicrobial therapy, and prompt drainage of the bile duct. Early diagnosis and treatment of acute cholangitis are crucial to prevent unwanted clinical outcome of the disease. This article provides an update on early diagnosis and management of acute cholangitis.Nonhepatotropic viruses such as adenovirus, herpes simplex virus, flaviviruses, filoviruses, and human herpes virus, and bacteria such as Coxiella burnetii, can cause liver injury mimicking acute hepatitis. Most of these organisms cause a self-limited infection. However, in immunocompromised patients, they can cause severe hepatitis or in some cases fulminant hepatic failure requiring an urgent liver transplant. Hepatic dysfunction is also commonly seen in patients with severe acute respiratory syndrome coronavirus-2 infection. Patients with preexisting liver diseases are likely at risk for severe coronavirus disease 2019 (COVID-19) and may be associated with poor outcomes.Parasites have coevolved with humans. Several of them colonize the human body and establish a symbiotic relationship. Other parasites cause severe and lethal diseases. Prevalence of parasitic infections is decreased in highly industrialized countries, largely due to enforced hygienic practices. In contrast, parasites cause significant morbidity and mortality in parts of the world with barriers to effective public hygiene. Some parasites have emerged as potent pathogens in specific patient populations, such as immune suppressed individuals, regardless of sanitation. This article reviews common parasites encountered in clinical practice and, in the setting of host-parasite symbiosis, discusses their immune regulatory role.Gastrointestinal (GI) tuberculosis (TB) remains a significant problem worldwide, and may involve the luminal GI tract from oral cavity to perianal area in addition to associated viscera and peritoneum. Adenosine disodium triphosphate datasheet Although GI TB more commonly affects immunocompromised hosts, it can also occur in immunocompetent people. Diagnosis is difficult because it usually mimics a malignancy or inflammatory bowel disease. A high index of clinical suspicion and appropriate use of combined investigative methods help in early diagnosis, and reduce morbidity and mortality. Anti-TB therapy is the same as for pulmonary disease, and invasive and specialized interventions are reserved for selected complications.Antibiotic-associated diarrhea and Clostridioides difficile infection (CDI) occur frequently among adults. The pathophysiology of CDI is related to disruption of normal gut flora and risk factors include hospitalization, use of antibiotic therapy, and older age. Clinical manifestations can range from mild disease to toxic megacolon. Diagnosis is challenging and is based on a combination of clinical symptoms and diagnostic tests. Therapy includes cessation of antibiotics, or use of other agents depending on the severity of illness. Many novel agents for the treatment and prevention of CDI show promise and are under investigation.Viral acute gastroenteritis (AGE) is common and afflicts people of all ages. Nonviral causes of AGE are less common. Norovirus is a leading cause of sporadic cases and outbreaks of AGE across all ages. Universal rotavirus vaccination of infants has reduced frequency and severity of rotavirus AGE cases in children and indirectly reduced cases in older adults. Severe illness is more likely in persons at age extremes or with immunocompromising conditions. Viral causes of AGE can lead to protracted diarrheal illness in immunocompromised persons. Nucleic acid amplification tests are changing diagnostic testing algorithms.Acute bacterial gastroenteritis is among the most common infections worldwide, with millions of infections annually in the United States. Much of the illness is foodborne, occurring as both sporadic cases and large multistate outbreaks. Pathogen evolution through genetic exchange of virulence traits and antibiotic resistance determinants poses challenges for empiric therapy. Culture-independent diagnostic tests in clinical laboratories afford rapid diagnosis and expanded identification of pathogens. However, cultures remain important to generate sensitivity data and strain archiving for outbreak investigations. Most infections are self-limited, permitting judicious selection of antibiotic use in more severe forms of illness.Helicobacter pylori infection remains one of the most prevalent infections worldwide, causing significant morbidity and mortality from gastric malignancies and peptic ulcers. This article provides a summary of the microbiology and pathogenesis of this bacterium, emphasizing the complex and protean effects of H pylori on gastric epithelial cells, including stem and progenitor populations, and evasion of host immune defenses. Increasing antibiotic resistance has made management more challenging. This article discusses the appropriate diagnostic modality for different clinical scenarios, and the evolving treatment of H pylori infections, including the use of antibiotic susceptibility testing to aid regimen selection.
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