GIT Bleeding Year 4 Internal Medicine Notes OmpathStudy

GIT Bleeding Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / I MED BEAUTIFUL NOTES / GIT -- ● Objectives: ● Identify presenting features of patients with suspected upper GI bleeding ● Appropriate identification and risk stratify patients with suspected upper GI bleeding. ● Appropriate resuscitation and initial management of patients. ● Appropriate medical management of patients with upper gastrointestinal bleeding and the\nappropriate alternatives to endoscopy based on the clinical situation.\n[ Color index: ​Important​ ​Notes ​ ​Extra​ ] [​ ​Editing file​ ​ ​ ​Feedback​ ​ ​Share your notes​ ​ ​Shared notes​ ​ ​Twitter​ ] ● Resources: ● 435 slides\n\n Check out this mind map​ ​here\n\n● Done by: ​Jwaher Alharbi ​Gassan almogbel Mohammed aldegaither ● Team sub-leader:​ Jwaher Alharbi ● Team leaders:​ ​Khawla AlAmmari & Fahad AlAbdullatif ● Revised by:​ Ahmad Alyahya \n\n Upper VS. lower GI bleeding \n❖ Anatomical landmarks and location of gastrointestinal bleeding:\n- Upper GI bleeding: a source of bleeding above the​ ligament of Treitz​ ​(​suspensory\nmuscle of duodenum).\n- Lower GI bleeding: bleeding below the ​ligament of Treitz\n\n ❖ Acute ​upper​ gastrointestinal bleeding:\n(Acute UGIB is a common medical emergency that has 11% hospital mortality rate)\nThe cardinal features are ​haematemesis​ (the vomiting of blood) and​ melaena ​(the passage of black tarry\nstools, the black colour being due to blood altered by passage through the gut). Melaena can occur with\nbleeding from any lesion ​proximal to the right colon.​ Rarely, melaena can also result from bleeding from the\nright colon. Following a bleed from the upper gastrointestinal tract, unaltered blood can appear per rectum, but\nthe bleeding must be massive​ and is almost always accompanied by shock. The passage of dark blood and\nclots without shock is always due to lower gastrointestinal bleeding.\n\n ❖ Acute ​lower​ gastrointestinal bleeding:\nMassive bleeding from the lower gastrointestinal tract is rare and is usually due to ​diverticular disease​ or\nischaemic colitis. Common causes of small bleeds are haemorrhoids and anal fissures. \n❖ Etiology:\n- The most common cause of ​upper GI bleeding ​is ​peptic ulcer disease\n- The most common cause of​ lower GI bleeding​ is ​Diverticulosis1 \nUpper GI bleeding Lower GI bleeding \n1. Peptic ulcer disease ​(duodenal ulcers ​25%\nand gastric ulcer ​20%​ )​. ​Most common 1. Diverticular disease​ ​(40%) most common source\n2. Esophagitis / Gastritis / duodenitis of GI bleeding in patients over age of 60, usually\n3. Variceal bleeding painless\n4. Mallory weiss tear ​and its severe form: 2. Angiodysplasia (AVM) ​(40%)​ ​second most\nBoerhaave syndrome (usually lethal) common source in patients over age of 60 Other uncommon causes: 3. IBD (UC, Crohn's disease)\n1. Arteriovenous malformation 4. Colorectal carcinoma\n2. Gastric antral vascular ectasia 5. Colorectal adenomatous polyps\n3. Dieulafoy's lesion2 ​(vessel that bleed and 6. Ischemic colitis\ndisappear) 7. Haemorrhoids, anal fissures\n4. Haemobilia3 8. Small intestinal bleeding ​diagnosed by excluding\n5. Aortoenteric fistula after aortic surgery upper GI and colonic bleeding\n6. Malignancy ​usually not an emergency\n\n 1\nDiverticulosis is the condition of having multiple pouches (diverticula) in the colon that are not inflamed. These are outpockets of the\ncolonic mucosa and submucosa through weaknesses of muscle layers in the colon wall.They typically cause no symptoms.Diverticular\ndisease occurs when diverticula become inflamed, known as diverticulitis, or bleed.\n2\nSubmucosal dilated arterial lesions that can cause massive GI bleeding.\n3\n​bleeding into the biliary tree \n\n❖ Vericeal UGIB: Defined as bleeding from the esophagus, stomach, or duodenum. Mortality decreased from 40 % to 15%. Fatality rate from 2.1 to 2.5% to 10%. ​ Portal HTN:\n● Pre-hepatic abnormalities (eg, portal or splenic vein thrombosis).\n● Post-hepatic abnormalities (eg, Budd–Chiari syndrome).\n● Intrahepatic noncirrhotic causes (eg, schistosomiasis, sinusoidal obstruction syndrome) or\ncirrhotic liver disease.\n● Portosystemic gradient (hepatic venous pressure gradient (HVPG) ):\n- wedged hepatic venous pressure (a measure of sinusoidal hepatic pressure) - the\nfree hepatic venous pressure\n- normal HVPG is 3 to 5 mmHg\n- HVPG than 5 mm Hg defines portal hypertension\n- HVPG 10 mmHg higher risk of: (varices, clinical decompensation “i.e.,\ndevelopment of ascites, variceal hemorrhage, and hepatic encephalopathy”,\nhepatocellular carcinoma). Clinically significant portal hypertension (CSPH):\n- presence of collaterals on imaging studies.\n- gastroesophageal varices on endoscopy.\n- the presence of ascites patient with decompensated cirrhosis. \n\n❖ Clinical features: \n1. Type of bleeding: \nHematemesis vomiting blood; suggests upper GI bleeding (bleeding proximal to ligament of Treitz).\nIndicates moderate to severe bleeding that may be ongoing. \