Gastroenterological emergencies

2019 ◽  
pp. 227-288
Author(s):  
Punit S. Ramrakha ◽  
Kevin P. Moore ◽  
Amir H. Sam
Keyword(s):  
Inflammatory Bowel Disease ◽  
Liver Failure ◽  
Biliary Obstruction ◽  
Gallstone Disease ◽  
Gi Bleeding ◽  
Drug Induced ◽  
Ulcer Disease ◽  
Liver Abscesses ◽  
Inflammatory Bowel ◽  
Upper Gastrointestinal

This chapter describes gastroenterological emergencies, including acute upper gastrointestinal (GI) bleeding, peptic ulcer disease, erosive gastritis/oesophagitis, variceal haemorrhage, Mallory–Weiss tear, gastroenteritis (acute, bacterial, viral), Clostridium difficile, giardiasis, travellers’ diarrhoea, bloody diarrhoea, dysentery (bacterial, amoebic), inflammatory bowel disease (IBD), jaundice, hepatitis (viral, alcoholic, drug-induced, autoimmune), acholuric jaundice, sepsis, ischaemic hepatitis, obstructive jaundice, gallstone disease, acute cholecystitis, biliary obstruction, ascites, acute liver failure, ‘acute-on-chronic’ liver failure, hepatic encephalopathy, liver abscesses, and acute pancreatitis.

Gastroenterology

2013 ◽  
Author(s):  
Victoria Stacey
Keyword(s):  
Inflammatory Bowel Disease ◽  
Liver Disease ◽  
Gastrointestinal Bleeding ◽  
Liver Failure ◽  
Upper Gastrointestinal Bleeding ◽  
Lower Gastrointestinal Bleeding ◽  
Acute Upper Gastrointestinal Bleeding ◽  
Inflammatory Bowel ◽  
Withdrawal Syndromes ◽  
Upper Gastrointestinal

Acute gastrointestinal bleeding - Acute upper gastrointestinal bleeding - Acute lower gastrointestinal bleeding - Vomiting - Diarrhoea - Inflammatory bowel disease (IBD) - Liver failure - Alcoholic liver disease/withdrawal syndromes - SAQs

Clostridium Difficile Infection and Biliary Obstruction

2021 ◽  
Vol 8 (1) ◽  
pp. 01-06
Author(s):  
Marilena Stoian
Keyword(s):  
Inflammatory Bowel Disease ◽  
Clostridium Difficile ◽  
Clostridium Difficile Infection ◽  
Crohn Disease ◽  
Bowel Disease ◽  
Biliary Obstruction ◽  
Hepatobiliary Disease ◽  
Protein Loss ◽  
Protein Losing Enteropathy ◽  
Inflammatory Bowel

We present a case of a 38-year -old man was admitted to the hospital with biliary obstruction and Clostridium Difficile infection. He presented with moderate increases in the aminotransferase and bilirubin levels suggesting the diagnosis of an autoimmune hepatobiliary disease; intestinal protein loss needs to evaluate an associated inflammatory bowel disease. The clinical diagnosis of autoimmune hepatobiliary disease associated with inflammatory bowel disease is based on the patients symptoms and the presence of a protein-losing enteropathy which are more suggestive of Crohn disease, while moderate increases in the aminotransferase levels in proportion to the increase in the bilirubin level suggesting the diagnosis of primary sclerosing cholangitis. The pathological and positive diagnosis needs an endoscopic retrograde cholangiopancreatography and a biopsy of gastric and duodenum mucosae who showed severe inflammation findings that are diagnostic of Crohn disease.

scholarly journals P586 Drug-induced lipid changes in patients with Inflammatory Bowel Disease: a single center, prospective study

2021 ◽  
Vol 15 (Supplement_1) ◽  
pp. S538-S538
Author(s):  
J Sleutjes ◽  
A C de Vries ◽  
J E Roeters van Lennep ◽  
C J van der Woude
Keyword(s):  
Inflammatory Bowel Disease ◽  
Prospective Study ◽  
Induction Therapy ◽  
Bowel Disease ◽  
Pearson Correlation ◽  
Lipid Lowering ◽  
Single Center ◽  
Lipid Levels ◽  
Drug Induced ◽  
Inflammatory Bowel

Abstract Background Drug use in the treatment of inflammatory bowel disease (IBD) might negatively impact lipid levels. In this study, we assessed drug-induced changes in the lipid profile after IBD induction therapy. Methods In this single center, prospective study IBD patients aged ≥17 years who started systemic drug therapy (corticosteroids, thiopurines, methotrexate, infliximab, adalimumab, vedolizumab, ustekinumab and tofacitinib) for IBD were included. Exclusion criteria were pregnancy, history of liver transplantation and use of lipid lowering drugs. Data on cardiovascular risk profile, disease activity (HBI, SCCAI, CRP, FCP) and concomitant medication use were collected. To calculate mean lipid changes after induction therapy, nonfasting lipid levels (total cholesterol (TC), HDL-c, LDL-c, triglycerides (TG)) were measured before and 8–10 weeks after start of therapy. Pearson correlation test was performed to assess the association between lipid changes and CRP. Results A total of 183 patients (87 males (48%), median age 36 years (IQR 28–48), 128 Crohn’s disease (70%), 46 CU (3%), 9 IBD-U (7%)) were included. (Table 1) Fourty-nine patients were on concomitant steroids at baseline (31%). Relative increases in TC, HDL-c and LDL-c were significant after treatment with corticosteroids and tofacitinib (+9%, +17%, +8% and +19%, +29%, +24%, respectively) and decrease in TG after treatment with corticosteroids, thiopurines, infliximab, adalimumab, ustekinumab and tofacitinib (-9%, -14%, -10%, -8%, -11%, -8%, respectively). (Table 2, Figure 1) A significant inverse relationship was found between CRP and TC (R -.171), HDL-c (R -.202), LDL-c (R -.153) but not with TG. Conclusion Serum lipid levels increased most after start of corticosteroids and tofacitinib as compared to other drug therapies. Whether these changes are explained by the control of inflammation or by the mechanism of action of these agents remains undetermined.

scholarly journals Applications and Pitfalls of Endoscopy in Inflammatory Bowel Disease

1990 ◽  
Vol 4 (7) ◽  
pp. 324-330
Author(s):  
BJ Salena ◽  
RH Hunt
Keyword(s):  
Inflammatory Bowel Disease ◽  
Early Detection ◽  
Bowel Disease ◽  
Endoscopic Surveillance ◽  
Clinical Strategies ◽  
Surveillance Programs ◽  
Inflammatory Bowel ◽  
Mass Lesions ◽  
Upper Gastrointestinal

The role of upper gastrointestinal and hepatobiliary endoscopy and colonoscopy in the diagnosis and management of patients with inflammatory bowel disease (IBD) is reviewed. The differentiation of IBD from other forms of colitis, mass lesions in the colon, strictures and polyps, and the management of the patient with dysplasia including clinical strategies for early detection are discussed. The role and value of endoscopic surveillance programs have yet to be defined.

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