Stomach and duodenal diseases

    Last updated date: 11-Jul-2023

    Originally Written in English

    Stomach and duodenal diseases

    Stomach and duodenal diseases


    If you have symptoms like heartburn, nausea, vomiting, stomach pains, or difficulty swallowing, you may have an upper GI (gastrointestinal) tract problem. If you consistently have these symptoms, it may be time to seek the advice of a gastroenterologist for additional examination in order to successfully treat the underlying disease.


    What are organs of Upper GI Tract?

    The esophagus, stomach, and duodenum (initial section of the small intestine) comprise the upper GI tract, whereas the small intestine, large intestine (colon), rectum, and anus comprise the lower GI tract. Disorders of the GI tract are commonly referred to by the section of the tract in which they occur.



    Stomach and duodenal diseases Anatomy

    The upper GI tract contains the neck, esophagus, stomach, and the duodenum, the first section of the small intestine. Food and drink pass through the throat, esophagus, and stomach, where stomach acid breaks down solids into liquids that your body can digest and absorb.

    The lower esophageal sphincter is a muscle at the bottom of the esophagus that opens to enable food passage into the stomach and then shuts to prevent stomach acid from flowing back up the esophagus. After leaving your stomach, everything you ate enters the small intestine, where bile and digestive enzymes further break it down. The small intestine absorbs the majority of the nutrients from the food you've eaten. 


    Let's look at some of the most often treated upper GI tract illnesses and who you may talk to if you have any of these bothersome symptoms on a regular basis.




    Gastroenteritis is an inflammation of the stomach, small or large intestine that causes abdominal discomfort, cramps, nausea, vomiting, and diarrhea. Acute gastroenteritis is generally over in less than 14 days. In contrast, persistent gastroenteritis, which lasts 14 to 30 days, and chronic gastroenteritis, which lasts more than 30 days, are both rare. 

    Rotavirus and norovirus are the most common viral causes of acute gastroenteritis. It is estimated that 15 to 25 million bouts of viral gastroenteritis occur in the United States each year, resulting in 3 to 5 million office visits and 200,000 hospitalizations.

    Rotavirus produces a severe dehydrating gastroenteritis that primarily affects young children. Malnourishment exacerbates the severity of the illness, making rotavirus a substantial cause of mortality in children globally, accounting for nearly 500,000 fatalities each year. Rotavirus gastroenteritis has been reduced with the introduction of the rotavirus vaccination in the United States and Europe. Vaccination has resulted in a 67% drop in positive test diagnoses.

    Parasitic infections, medications, inflammatory bowel disease (ulcerative colitis, and Crohn disease), irritable bowel syndrome, eosinophilic gastroenteritis, celiac disease, lactose intolerance, colorectal cancer, bowel obstruction, malabsorption, and ischemic bowel are all causes of persistent or chronic gastroenteritis.


    Treatment of Gastroenteritis

    Treatment of Gastroenteritis

    Fluid replacement, with or without dietary restrictions, is the foundation of symptomatic therapy. There is no evidence that a clear liquid diet vs an unrestricted food affects the length or severity of symptoms because traveler's diarrhea is generally self-limiting, lasting 3 to 5 days. Although oral rehydration is preferable, intravenous hydration may be required in cases severe dehydration.

    Antibiotics may cut the course of treatment by 1 to 2 days. Travelers frequently seek a prescription for antibiotics to be taken as soon as symptoms appear. Although quinolone resistance is rising, particularly in Campylobacter jejuni, ciprofloxacin is usually adequate. Quinolones are not FDA-approved for use during pregnancy or in the treatment of traveler's diarrhea in children.

    Rifaximin has been proved to be effective, and as quinolone resistance increases, it is being used more frequently. Antimotility medicines, such as loperamide or diphenoxylate, can reduce stool frequency but have little effect on the infection's progression. In situations of fever or rectal bleeding, they should be avoided.




    Gastritis is defined by histological characteristics of the gastric mucosa. It is not erythema seen through a gastroscopy, and it has no distinct clinical manifestations or symptoms. Gastritis is now classified based on its temporal course (acute vs chronic), histological characteristics, anatomic distribution, and underlying pathogenic processes. If not treated, acute gastritis will progress to chronic gastritis.

    Gastritis can be acute or chronic. The causes of gastritis can be summarized as follows:

    1. H. pylori-associated gastritis: This is the most common cause of gastritis worldwide. 
    2. H. pylori-negative gastritis: The patients should fulfill all four of these criteria 
    • A negative triple staining of gastric mucosal biopsies, 
    • A negative H. pylori culture, 
    • A negative IgG H. pylori serology, and
    • No self-reported history of H. pylori treatment. 

    The etiology of gastritis in these people may be related to cigarette usage, alcohol intake, and/or the use of NSAIDs or steroids.

        3. Autoimmune gastritis: This is a chronic inflammatory condition characterized by chronic atrophic gastritis and elevated anti-parietal and anti-intrinsic factor antibodies in the blood. The loss of parietal cells reduces stomach acid output, which is required for inorganic iron absorption. As a result, iron insufficiency is a typical observation in autoimmune gastritis patients. Iron insufficiency frequently comes before vitamin B12 deficiency in these people. Young women are more vulnerable to the sickness.

        4. Gastritis can be caused by organisms other than Helicobacter pylori, including Mycobacterium avium-intracellulare, enterococcal infection, Herpes simplex, and CMV. Infection with cryptosporidium, Strongyloides stercoralis, or anisakiasis can cause parasitic gastritis.

        5. Gastritis may result from bile acid reflux.

        6. Radiation gastritis.

        7. Crohn disease-associated gastritis: This is an uncommon cause of gastritis.

        8. Collagenous gastritis: This is an uncommon cause of gastritis. The condition is distinguished by prominent subepithelial collagen deposition, which is accompanied by a mucosal inflammatory infiltrate. The actual cause and pathophysiology of collagenous gastritis remain unknown.

        9. Eosinophilic gastritis: This is another another uncommon cause of gastritis. The disease could be classified as eosinophilic gastrointestinal disorders, which are distinguished by the lack of known causes of eosinophilia (not secondary to an infection, systematic inflammatory disease, or any other causes to explain the eosinophilia).


    Gastritis has no conventional clinical symptoms. Acute gastritis has been associated with the sudden development of epigastric discomfort, nausea, and vomiting. Many people are asymptomatic or just have minor dyspeptic symptoms. If not addressed, the condition might progress to chronic gastritis. Smoking history, alcohol usage, NSAID or steroid use, allergies, radiation, or gall bladder diseases should all be considered. If no obvious cause of gastritis is found, a history of therapy for inflammatory bowel disease, vasculitic illnesses, or eosinophilic gastrointestinal disorders may necessitate further investigation.


    H. pylori-associated gastritis

    The first line of treatment is a 14 to 21-day course of clarithromycin/proton-pump inhibitor/amoxicillin. Clarithromycin is favored over metronidazole because it has a lower recurrence rate when compared to metronidazole triple treatment. In locations where clarithromycin resistance is known, metronidazole is the preferred treatment. Quadruple bismuth treatment might be beneficial, especially if metronidazole was used.




    Gastroparesis literally translates to "stomach paralysis." Gastroparesis is a disorder characterized by a combination of nausea and vomiting, bloating, and early satiety, as well as upper abdominal discomfort, produced by delayed stomach emptying in the absence of mechanical restriction.

    Gastric stasis can develop in the absence of mechanical blockage owing to anomalies in the process of normal gastrointestinal motor activity. It involves a sequence of complicated actions that need coordination of the parasympathetic and sympathetic nervous systems, neurons, and pacemaker cells inside the stomach and intestine, together with the smooth muscle cells of the gut.

    As indicated below, a wide range of neurologic illnesses can impair gastrointestinal motility by affecting the parasympathetic or sympathetic nerve supply to the gastrointestinal (GI) tract. The following are the etiologies of gastroparesis:

    • Idiopathic - most common cause present in about half of patients 
    • Diabetes mellitus (DM) - most common and severe in type 1 diabetics
    • Rheumatological diseases - amyloidosis, scleroderma
    • Autoimmune - autoimmune gastrointestinal dysmotility causing delayed emptying
    • Neurological conditions - stress, Parkinson disease, multiple sclerosis, brainstem CVA and tumors, autonomic neuropathy
    • Postsurgical - vagal nerve injury during fundoplication and partial gastric resection
    • Trauma - spinal cord injury
    • Viral infections including Norwalk virus and rotavirus 
    • Medications - narcotics, cyclosporine, phenothiazines, dopamine agonists, octreotide, alpha-2-adrenergic agonists (e.g. clonidine), tricyclic antidepressants, calcium channel blockers, GLP-1 agonists exenatide or analogs liraglutide, lithium, progesterone


    Gastroparesis is a complex illness whose origin influences symptoms and severity. Patients with gastroparesis may exhibit a variety of symptoms. The primary symptom may differ depending on the underlying cause. Overall, nausea is present in around 93 percent of patients, vomiting in 68 to 84 percent of cases, stomach discomfort in 46 to 90 percent of cases, and early satiety in 60 to 86 percent of cases.

    In severe and chronic cases, further symptoms include postprandial fullness, bloating, and weight loss. Vomitus may include food that was consumed some hours before. The clinical aspects of diabetic gastroparesis and idiopathic gastroparesis are similar and dissimilar. Idiopathic gastroparesis patients reported higher sensations of early satiety, postprandial fullness, and abdominal discomfort than diabetic gastroparesis patients. Diabetic gastroparesis was associated with more acute retching and vomiting.

    Although stomach discomfort is a common complaint in gastroparesis patients, it is rarely the primary symptom (present in about 18 percent). Other explanations should be considered in patients whose primary symptom is stomach discomfort. Providers may detect epigastric distention or discomfort on physical examination, but no guarding or stiffness. Patients may have symptoms of the underlying illness that is producing gastroparesis.

    Management of gastroparesis should include a holistic approach to target different aspects of the disease such as nutritional status assessment, measures to correct fluid, electrolyte, and nutritional deficiencies, relief of gastroparesis symptoms, improving gastric emptying, recognizing and correcting the underlying cause of gastroparesis to prevent disease progression, e.g., tight glycemic control in diabetes, stopping causative medications 


    Peptic Ulcer Disease

    Peptic Ulcer Disease

    Peptic ulcer disease (PUD) is defined by a break in the inner lining of the GI tract caused by stomach acid secretion or pepsin. It penetrates the stomach epithelium's muscularis propria layer. It is most commonly found in the stomach and proximal duodenum. It can affect the lower esophagus, the distal duodenum, or the jejunum. In individuals with a stomach ulcer, epigastric pain normally develops within 15-30 minutes of eating; whereas, discomfort with a duodenal ulcer usually occurs 2-3 hours after eating.

    Helicobacter pylori infection or nonsteroidal anti-inflammatory medications are frequently used (NSAIDs). Rarely fatal sickness, Zollinger-Ellison syndrome, glucocorticoids in conjunction with NSAIDs, or other medications (potassium chloride, bisphosphonates, mycophenolate mofetil).

    1. pylori infection causes more than half of all duodenal and stomach ulcers. H. pylori may thrive in the gastrointestinal environment because it produces urease, which breaks urea and releases ammonia, which neutralizes gastric acid and generates a less acidic milieu within the gastric mucus layer.

    H pylori produces acute gastritis in the prepyloric area, which advances to chronic gastritis after a few weeks; H pylori also causes hypergastrinemia, which leads to increased production of hydrochloric acid, which plays an essential part in the pathophysiology of duodenal ulcers. 

    All NSAIDs, including acetylsalicylic acid (ASA) (even at moderate dosages used for cardiovascular reasons), harm the GI mucosa, principally by lowering prostaglandin synthesis as a result of cyclooxygenase-1 (COX-1) inhibition, and are linked to ulcer formation.

    The degree to which NSAIDs harm the mucosa varies by type, but they all raise the chance of peptic ulceration; also, they suppress platelet function and, to varying degrees, increase the risk of bleeding from those ulcers. With selective cyclooxygenase-2 (COX-2) inhibitors or diclofenac, the risk of major upper GI events (including bleeding) is doubled, and with naproxen or ibuprofen, the risk is quadrupled. 


    Diagnosis of Peptic Ulcer Disease

    Diagnosis of Peptic Ulcer Disease

    PUD diagnosis necessitates a medical history, physical examination, and invasive/non-invasive medical testing. A thorough history should be collected and any difficulties should be documented. Patient reports of epigastric stomach discomfort, early satiety, and fullness after eating suggest the possibility of PUD.

    Gastric ulcer pain increases 2 to 3 hours after a meal and may result in weight loss, but duodenal ulcer discomfort reduces after a meal and may result in weight gain. Any patient who presents with anemia, melena, hematemesis, or weight loss should be evaluated further for PUD consequences, most notably bleeding, perforation, or malignancy. A physical examination may indicate epigastric belly discomfort and anemia.


    1. Esophagogastroduodenoscopy (EGD): The gold standard and most reliable diagnostic test for identifying stomach and duodenal ulcers, with sensitivity and specificity up to 90%. The American Society of Gastrointestinal Endoscopy has issued guidelines on the use of endoscopy in patients with upper abdomen discomfort or dyspeptic symptoms indicative with PUD. Patients over the age of 50 who have recently developed dyspeptic symptoms should get an EGD. Anyone, regardless of age, who has alarm symptoms should get an EGD.

    Esophagogastroduodenoscopy (EGD)

         2. Barium swallow: It is indicated when EGD is contraindicated.

         3. Complete blood work, liver function, and levels of amylase and lipase.

         4. Serum gastric is ordered if Zollinger-Ellison syndrome is suspected.

         5. Helicobacter pylori testing:

      • Serologic testing
      • Urea breath testHigh specificity and sensitivity. It can be utilized to confirm eradication 4 to 6 weeks after discontinuing therapy. The radiolabeled carbon dioxide generated by the stomach is exhaled by the lungs in the presence of urease, an enzyme produced by H.pylori.
      • Antibodies to H.pylori can also be measured.
      • Stool antigen test
      • Urine-based ELISA and rapid urine test
      • Endoscopic biopsy: Culture is typically not suggested since it is costly, time-consuming, and intrusive. It is recommended if eradication therapy fails or if antibiotic resistance is suspected. Biopsies from at least 4-6 different locations are required to enhance sensitivity. Gastric ulcers are most typically seen on the minor curvature of the stomach between the antrum and fundus. The majority of duodenal ulcers are found in the duodenum's initial section.
    1. Computerized tomography of the abdomen with contrast is of limited value in the diagnosis of PUD itself but is helpful in the diagnosis of its complications like perforation and gastric outlet obstruction.


    Peptic Ulcer Disease Management

    Peptic Ulcer Drug

    Medical Treatment

    H2-receptor antagonists and proton pump inhibitors are antisecretory medications used to treat peptic ulcer disease (PUD) (PPIs). Because of their greater healing and effectiveness, PPIs have essentially supplanted H2 receptor blockers. PPIs inhibit stomach acid production, relieving discomfort and promoting recovery. Because long-term use of PPIs might raise the risk of bone fractures, treatment may include calcium supplements.

    PUD caused by NSAIDs can be managed by discontinuing the NSAIDs or moving to a lower dosage. If at all feasible, corticosteroids, bisphosphonates, and anticoagulants should be stopped. Prostaglandin analogs (misoprostol) are occasionally used to prevent NSAID-induced peptic ulcers. A triple regimen of two antibiotics plus a proton pump inhibitor is used as first-line therapy for H. pylori-induced PUD.

    Pantoprazole, clarithromycin, metronidazole, or amoxicillin are prescribed for a period of 7 to 14 days. Antibiotics and PPIs act together to eliminate H. pylori. The antibiotic used should account for the occurrence of antibiotic resistance in the environment. If first-line therapy is unsuccessful, triple therapy with bismuth and other antibiotics is utilized.


    Stomach (Gastric) Cancer

    Stomach (Gastric) Cancer

    Stomach cancer, also known as gastric cancer, is a kind of cancer that arises from the stomach lining. The majority of stomach malignancies are gastric carcinomas, which can be further subdivided into gastric adenocarcinomas. In the stomach, lymphomas and mesenchymal tumors can form. Heartburn, upper abdomen discomfort, nausea, and loss of appetite are common early symptoms.

    Weight loss, yellowing of the skin and whites of the eyes, vomiting, trouble swallowing, and blood in the stool are some of the later signs and symptoms. The cancer may spread from the stomach to other regions of the body, including the liver, lungs, bones, abdominal lining, and lymph nodes.

    Infection with the bacteria Helicobacter pylori is the most prevalent cause, accounting for more than 60% of cases. Certain strains of H. pylori are more dangerous than others. Other risk factors include smoking, dietary variables such as pickled vegetables, and obesity. Approximately 10% of instances run in families, and 1% to 3% of cases are caused by genetic disorders inherited from one's parents, such as hereditary diffuse gastric cancer.

    Stomach cancer usually develops in stages over time. Typically, a sample performed during an endoscopy is used to make the diagnosis. Following this, medical imaging is used to evaluate whether the illness has spread to other regions of the body. Screening for stomach cancer is done in Japan and South Korea, two nations with high prevalence of the illness.

    A Mediterranean diet, as well as quitting smoking, reduces the risk of stomach cancer. Preliminary research suggests that treatment H. pylori reduces future risk. Stomach cancer can be cured if treated early. Treatment options may include surgery, chemotherapy, radiation treatment, and targeted therapy. Cancer immunotherapy is also a possibility for certain subtypes of gastric cancer. Palliative care may be recommended if treated late. Some kinds of lymphoma can be healed by removing H. pylori from the body.

    Outcomes are frequently dismal, with advanced patients having a five-year survival rate of fewer than 10% in the Western world. This is primarily due to the fact that the majority of patients with the syndrome come with advanced disease. Five-year survival in the United States is 31.5%, but it is over 65% in South Korea and over 70% in Japan, owing in part to screening efforts.


    Duodenal Adenocarcinoma

    Duodenal Adenocarcinoma

    Although the duodenum is the site of the bulk of small bowel adenocarcinomas, duodenal adenocarcinoma (DA) accounts for fewer than 1% of all gastrointestinal malignancies. Not surprisingly, given the disease's rarity, there is little evidence to guide therapy recommendations. When addressing treatment possibilities, early studies lumped DA alongside other periampullary cancers (pancreatic, ampullary, and distal bile duct).

    In general, DA has a better outcome. For example, as compared to other periampullary malignancies, DA is more likely to be curable and has better long-term prognosis. As a result, therapeutic approaches have favored aggressive surgical excision.



    Peptic ulcer disease is one of the most frequent disorders that affects the stomach and duodenum. Untreated peptic ulcers might lead to additional health issues. They occasionally bleed. They can break through your stomach if they get too deep. Ulcers can be treated using a combination of lifestyle modifications and medications. Surgery is only required in rare cases.