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Ulcerative colitis (UC) is a chronic, idiopathic inflammatory disease affecting the colon, and mostly afflicting adults ages 30-40. It is characterized by the relapsing and remitting mucosal inflammation that starts in the rectum and extends in an uninterrupted fashion to the proximal segments of the colon, but only affects the innermost layer of the colon (Ungaro, et. al, 2017). Mucosal inflammation leads to edema, ulcers, bleeding, and electrolyte derangements (McDowell, Farooq, & Haseeb, 2021). The exact cause of UC is unknown, however, colonic epithelial cells, mucus barrier, and epithelial barrier defects are strongly implicated in the pathogenesis of UC (Ungaro, et. al, 2017). The most common presenting symptoms of UC include urgency, incontinence, fatigue, increased bowel movement frequency, mucus discharge, nocturnal defecations, and abdominal cramps – although much less of a hallmark feature than in Crohn’s disease. Fever and weight loss may also be present in severe cases, and UC also makes one prone to iron deficiency. Additionally, presenting symptoms may vary depending on the extent of colonic involvement. Ulcerative proctitis is confined to the area closest to the anus and rectal bleeding may be the only sign, proctosigmoiditis involves the rectum and sigmoid colon and may include bloody diarrhea, abdominal cramps, and tenesmus as its symptoms, left-sided colitis afflicts the rectum up to the descending colon with presenting symptoms similar to proctosigmoiditis plus an urgency to defecate, and lastly, pancolitis affects the entire colon with symptoms similar to the other types of UC, but also includes fatigue and significant weight loss (Mayo Clinic, 2021). Extraintestinal manifestations are also present in 10-30% of patients and examples of such are scleritis, uveitis, peripheral arthropathies, erythema nodosum, pyoderma gangrenosum, sacroiliitis, and ankylosing spondylitis (Lynch & Hsu, 2021).
Colonic infection may be indistinguishable from UC, so microbiologic studies to rule out bacterial or parasitic infection must be part of the initial evaluation. Although not critical for diagnosis, a double-contrast barium enema will show a ‘stove-pipe’ sign for those with long-standing UC (Lynch & Hsu, 2021). Colonoscopy and proctosigmoidoscopy may also reveal loss of typical vascular pattern, granularity, friability, and erosions. Laboratory evaluation will reveal increased inflammatory markers such as ESR, CRP, and leukocytosis, especially during acute flares. Additionally, in 60-70% of patients, perinuclear antineutrophil cytoplasmic antibodies (pANCA) are found (Lynch & Hsu, 2021). The primary aim of medical management is to induce and maintain remission with long-term goals of preventing disability, colectomy, and colorectal cancer. The first-line treatment is sulfasalazine and 5-aminosalicylates given PO or PR. Moreover, glucocorticoids may be added for those who fail to achieve remission within two weeks. If still refractory, thiopurines (azathioprine, mercaptopurine) as well as biological drugs anti-TNF-alpha (infliximab, adalimumab, golimumab) are used. The newest class of biologics that have been added to the management of UC are the anti-adhesion molecule inhibitors (vedolizumab). Colectomy is the only curative treatment since the disease is restricted to the colon. Surgery is indicated for those who failed medical therapy, has intractable fulminant colitis, toxic megacolon, perforation, and uncontrollable bleeding, among many other reasons (Lynch & Hsu, 2021). Lastly, because of the risk of colon cancer, colonoscopy is recommended at regular intervals.
CD is also a chronic relapsing inflammatory bowel disease that is characterized by transmural granulomatous inflammation that can affect any part of the GI tract, most commonly the ileum and colon. It has a peak age prevalence of 30-39 (Ha & Khalil, 2015). It affects the mouth, esophagus, stomach, entire layers of the small and large intestine, rectum, and anus. The pathophysiology of CD is multifactorial and involves genetics, infections, immunologic response, environment, and diet. The immune-mediated response in CD involves innate and acquired mechanisms by macrophages, neutrophils, and T-cells in the intestine while promoting pro-inflammatory mediators (Ranasinghe & Hsu, 2021). The main presentation of CD is chronic diarrhea with decreased fecal consistency for more than four weeks, abdominal pain, weight loss, as well as mucus and blood in the stool (Seyedian, Nokhostin, & Malamir, 2019). Malnutrition is also common with CD because the small intestine is responsible to nutrient absorption, subsequently, CD sufferers also have folate and vitamin D deficiency. Moreover, intestinal obstruction due to scarring and swelling and fistulas from the ulcers are common. Extraintestinal manifestations similar to UC are also possible with CD, with the addition of UTI, hydronephrosis, nephrolithiasis, cholangitis, and thromboembolic disease (Ranasinghe & Hsu, 2021).
There is no single definitive diagnostic investigation for the diagnosis of CD. A full ileocolonoscopy with biopsies is currently the most widely used (Ha & Khalil, 2015). A CT or MRE of the abdomen of pelvis can detect abscesses and fistulization as they give a high-definition image of the diseased intestine. MRI, however, can provide more details about fistulization and transmural inflammation. The use of video capsule endoscopy can also help visualize the small bowels as regular endoscopy and colonoscopy may not reach these areas. Plain x-ray films are ordered if bowel obstruction is suspected. Further, a small bowel follow-through is often used to assess terminal ileum involvement where the classic ‘string’ sign and spasm is seen. Blood tests including a CBC and MP can highlight the presence of anemia, and special serology such as negative perinuclear antineutrophil cytoplasmic antibodies (pANCA) combined with positive anti-saccharomyces cerevisiae (ASCA) can help distinguish CD from UC (Ha & Khalil, 2015). Lastly, stool tests to rule out infectious process must also be done such as cultures and sensitivities, ova and parasite, C. diff toxins, and leukocyte count. Medical treatment for mild to moderate cases of CD use PO mesalamine, immunomodulators such as thiopurines (mercaptopurines or azathioprine), methotrexate, and steroids. For moderate to severe cases, to include fistulizing disease, the combination of immunomodulators and biologics (infliximab, adalimumab, golimumab, vedolizumab) are used or biologics alone (Ranasinghe & Hsu, 2021). Surgical treatment is used for complications such as bowel obstructions, abscesses, fistulas, or perforated bowel.
#2 GERD, PUD, Gastritis
Pathophysiology: Gastroesophageal reflux disease (GERD) is a common gastrointestinal disease that can have complicated causes. Often GERD is caused by relaxation or incompetence of the esophageal sphincter that’s supposed to prevent stomach acid and contents from spilling back into the esophagus and more (McCance & Huether, 2014). The relaxation of the sphincter is also called transient lower esophageal sphincter relaxations (TLESR). It is said that the relaxation happens on its own aside from swallowing and can also be caused by pressure from hiatal hernia, impaired esophageal clearance, and delayed gastric emptying (Clarrett & Hachem, 2018). Infants also often get GERD because of their underdeveloped sphincter (McCance & Huether, 2014).
Clinical Manifestation: The most common symptom of GERD are heartburn and regurgitation. Other symptoms people report include water brash, chest pain or discomfort, dysphagia, belching, epigastric pain, nausea, and bloating (Sandhu & Fass 2018). Some people may report cough, hoarseness, throat clearing, throat pain or burning, wheezing, and sleep disturbances as well (Sandhu & Fass 2018).
Evaluation: GERD is usually diagnosed with heartburn symptoms alone. However, patients who don’t respond to medication treatment may need to have an endoscopic procedure done. The procedure is called upper gastrointestinal endoscopy or esophagogastroduodenoscopy (EGD). After an EGD, GERD is diagnosed, especially when Barrett’s esophagus is found, which is the erosion of the lower esophagus due to its consistent exposure to stomach acids (Clarrett & Hachem, 2018).
Treatment: Treatment includes proton pump inhibitors, which are usually enough as a monotherapy. Sometimes, receptor antagonists, prokinetics, and antacids are also prescribed as treatment. Lifestyle modifications are also included in the treatment plan, including weight management and stress reduction (McCance & Huether, 2014).
Peptic ulcer disease
Pathophysiology: Peptic ulcer disease is the visible erosion of the protective lining of the esophagus or stomach. Often this is caused by an imbalance in the gastric acid and protective linings or both structures. It was thought in the past that stress, environmental factors, and diet alone cause the imbalance, but a bacteria called Helicobacter pylori was discovered to add as a factor for peptic ulcer disease as well (Dunlap & Patterson, 2019). Other factors that can cause peptic ulcer disease are excessive alcohol, habitual use of NSAIDS, smoking, COPD, acute pancreatitis, cirrhosis, and age greater than 65 years (McCance & Huether, 2014).
Clinical Manifestation: Common symptoms include burning sensation and abdominal pain. Other symptoms include heartburn, nausea, intolerance to fatty foods, feeling of fullness, bloating, belching (Mayo Foundation, 2020). Patients often develop ulcers that can cause bleeding and make symptoms much worse. Worsening symptoms include vomiting blood, dark and tarry stools, feeling faint, unexplained weight loss, trouble breathing, nausea, vomiting, and appetite changes (Mayo Foundation, 2020).
Evaluation: Diagnosis includes testing for the bacteria H. pylori which are done by a blood test, breath, or stool sample. An upper endoscopy procedure called esophagogastroduodenoscopy is done with a scope to look at the upper GI tract to locate ulcers, and biopsy is done to test for H. pylori as well. Another diagnostic tool is a barium swallow, which is done with an x-ray. A patient swallows a white liquid with barium. This liquid coats the upper GI lining and makes it easier for ulcers to be seen in the x-ray (Mayo Foundation, 2020).
Treatment: Antibiotics are often given to help get rid of the bacteria H. pylori. These antibiotics include amoxicillin, metronidazole, tetracycline, and others. Other medications include PPIs, H2 blockers, and antacids to help reduce damage or ulcers and regulate acid production. Patients can also be given medications that help coat and protect the stomach lining or coat ulcerated areas of the stomach and upper GI tract. Sucralfate and misoprostol are the common medications prescribed. Lifestyle modifications are also prescribed, like weight loss, avoiding NSAIDs, and dietary changes (Mayo Foundation, 2020).
Pathophysiology: Gastritis is the inflammation of the mucus membranes in the stomach. Gastritis can often happen at the fundus, the round structure closest to the esophagus, the antrum, the part of the stomach closest to the small intestine, or both. Gastritis can be caused by H. pylori, NSAIDs, and chemicals. NSAIDs are known to cause gastritis because these medications block the production of protective mucus and inflammation suppression done by prostaglandins. Gastritis can also be acute and chronic. Acute usually resolves almost immediately with treatment, while chronic needs management (McCance & Huether, 2014).
Clinical Manifestation: symptoms include abdominal pain/discomfort, pain, nausea, vomiting, epigastric tenderness, and bleeding (McCance & Huether, 2014).
Evaluation: Diagnosis for gastritis is similar to peptic ulcer disease, which includes testing for H. pylori and EGD or a barium swallow (Mayo Foundation, 2020).
Treatment: treatment is also the same as peptic ulcer disease, including antibiotics to kill or suppress H. pylori. PPIs, H2 blockers, and antacids. Lifestyle management includes eating small meals but more frequent meals, avoiding foods that can cause irritations like fatty, acidic foods, and avoiding NSAIDs (Mayo Foundation, 2020).
TREND: I’ve noticed that more patients are being diagnosed with these types of upper gastrointestinal disorders, especially in the patients coming to the emergency department. This is most likely due to a combination of stress, eating habits, overuse of NSAIDs, and OTCs. People are more stressed now than ever. We are exposed to many different life stressors here and across the world because of technology. Dietary habits have been worse because of fast foods, diet fads, and the increasing volume of servings of food. So many people are overusing medications even when they don’t need them. Sharing medications is a huge problem because patients are taking medications that are meant for other people. Overusing over-the-counter medications like NSAIDs causes these upper GI issues as well.