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Introduction
1. Anatomy
2. Microbiology
3. Physiology
4. Pathology
4.1 General pathology
4.2 Central and peripheral nervous system
4.3 Cardiovascular system
4.4 Respiratory system
4.5 Hematology and oncology
4.6 Gastrointestinal pathology
4.6.1 Salivary gland pathology
4.6.2 Esophageal disorders
4.6.3 Diverticula of the esophagus
4.6.4 Stomach
4.6.5 Small intestine
4.6.6 Mesenteric ischemia
4.6.7 Large intestine
4.6.8 Ischemic colitis
4.6.9 Benign and malignant growths of the colon
4.6.10 Rectum and anal canal
4.6.11 Disorders of the liver
4.6.12 Cirrhosis and portal hypertension (PHT)
4.6.13 Benign masses in the liver
4.6.14 Disorders of the gallbladder and bile ducts
4.6.15 Cholangitis
4.6.16 Cholangiocarcinoma
4.6.17 Disorders of the pancreas
4.6.18 Additional information
4.7 Renal, endocrine and reproductive system
4.8 Musculoskeletal system
5. Pharmacology
6. Immunology
7. Biochemistry
8. Cell and molecular biology
9. Biostatistics and epidemiology
10. Genetics
11. Behavioral science
Wrapping up
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4.6.4 Stomach
Achievable USMLE/1
4. Pathology
4.6. Gastrointestinal pathology

Stomach

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  1. Melena: Hematemesis, melena, and hematochezia are symptoms of acute gastrointestinal bleeding.

Melena is the passage of black, tarry stools. Hematemesis is vomiting of blood, which may be bright red or may look like coffee grounds. Hematochezia is the passage of fresh blood per anus, usually in or with stools.

Melena is typically seen in upper gastrointestinal bleeding. More than 50 mL of blood is usually required to make stools tarry.

Common causes of melena

  • Bleeding gastric/peptic ulcer
  • Gastritis or esophagitis
  • Esophageal or gastric varices
  • Mallory Weiss syndrome
  • Gastric tumors
  1. Gastritis: Gastritis is inflammation of the lining of the stomach. It may be acute or chronic.

    Acute gastritis may be caused by drugs like aspirin, NSAIDS, steroids, iron tablets, alcohol, H.pylori, viruses like Hepatitis viruses, infectious mononucleosis, stress etc. It presents with upper abdominal discomfort or pain, bloating, nausea and vomiting.

    Chronic gastritis is seen in H.pylori infections, post gastric surgery, autoimmune disorders like atrophic gastritis, Crohn’s disease, HIV/AIDs etc. It is frequently asymptomatic; when symptoms occur, they may result from anemia due to Vit. B12 deficiency.

    Classification of chronic gastritis

    Type A gastritis
    • Involves fundus and body
    • Autoimmune disorder caused by antibodies to parietal cells and intrinsic factor
    • Hypochlorhydria, hypergastrinemia, hypertrophy of G cells, pernicious anemia
    Type B gastritis
    • Involves antrum, more common
    • Caused by chronic H.pylori infection
    • Hypersecretion of gastric acid
    • Associated with peptic ulcer disease

    Microscopic examination shows infiltration of the mucosa with lymphocytes, plasma cells, neutrophils and sometimes eosinophils, along with mucosal atrophy and intestinal metaplasia. In chronic erosive gastritis caused by NSAIDS, superficial mucosal erosions are seen. Granulomas are present in Crohn’s disease, TB, sarcoidosis and other granulomatous disease. Predominantly eosinophilic infiltrate is seen in eosinophilic gastritis associated with food allergies.

  2. Dyspepsia: Dyspepsia is a common symptom described as an uncomfortable feeling in the epigastrium. It may include upper abdominal pain, bloating, heartburn, nausea, vomiting and/or indigestion.

It can be due to peptic ulcer disease, gastritis, GERD, alcohol, drugs like NSAIDS or aspirin, stress, spicy or fatty foods, caffeine, or gastric cancers.

  1. Peptic ulcer: A peptic ulcer is ulceration of the epithelial lining of the stomach and/or duodenum due to the action of pepsin and HCl, along with loss of the protective mucous layer.

It may be caused by H.pylori infections, NSAIDS, stress, burns, TB, Crohn’s disease, cirrhosis, renal failure, sarcoidosis, CMV, surgery, critical illness or smoking. Multiple ulcers are seen in Zollinger-Ellison syndrome. Duodenal ulcers are more common than gastric ulcers.

Clinical features include episodic gnawing pain or burning epigastric pain. Pain is aggravated by food intake in gastric ulcers and relieved by food intake in duodenal ulcers. Other symptoms include indigestion, nausea, vomiting, weight loss and loss of appetite.

Gastric ulcers are typically located on the lesser curvature, while duodenal ulcers are located at the duodenal bulb.

On gross examination, the ulcer is a round or oval, “punched-out” lesion. It may be superficial (involves only mucosa) or deep (penetrates the muscularis layer). Microscopic examination shows a necrotic base, a zone of fibrocollagenous tissue, and overlying granulation tissue.

Obstruction and malignant change are more common in gastric ulcers than duodenal ulcers, while perforation is more common in duodenal ulcers.

Treatment includes eradication of H.pylori, H2 blockers, PPIs (first choice), sucralfate and rarely surgery (vagotomy, partial gastrectomy).

  1. GIST or gastrointestinal stromal tumors: GIST tumors arise from the interstitial cells of Cajal. They are typically seen in adults between 40-70 years of age. They can be benign or malignant.

Many cases are asymptomatic. When symptoms occur, presentation may include abdominal pain, nausea, fatigue, GI bleeding and weight loss. Skin changes like urticaria pigmentosa or cutaneous mastocytosis (itchy brown macules and papules) may be seen.

Mutations in the KIT and PDGFRA genes are associated with GIST. These mutations lead to persistent activation of signalling pathways, causing abnormally increased cell proliferation and survival. Some cases have SDH mutations and are deficient in the enzyme succinate dehydrogenase, resulting in excess accumulation of succinate in the mitochondria.

GIST may develop in cases of neurofibromatosis type 1. Tumors may be single or multiple.

Biopsy findings include spindle-shaped, epithelioid or mixed cells arranged in fascicles or syncytia, resembling muscle cells. GIST tumors are CD117 and DOG1 marker +.

Treatment is by surgical excision or imatinib.

  1. Adenocarcinoma of stomach: This is the most common type of gastric cancer. It has a high incidence in Japan, South America and Eastern Asia.

Diets rich in salt, smoked or poorly preserved foods, nitrates, nitrites and secondary amines are associated with an increased risk of gastric cancer. Most cases are sporadic. Familial cases are associated with mutations in p53, BRCA2 and the gene coding E-cadherin (high risk). Gastric cancer is seen as part of HNPCC, familial adenomatous polyposis and Peutz-Jeghers syndrome.

H.pylori infection, especially in blood group A individuals, is associated with high risk. Chronic atrophic gastritis with pernicious anemia, obesity and Menetrier’s disease are other risk factors.

Patients may remain asymptomatic until late in the disease. Symptoms include dyspepsia, anorexia, vague abdominal pain, early satiety, weight loss and GI bleeding.

Distant metastases may present as:

  • Enlarged supraclavicular lymph node (Virchow’s node)
  • Periumbilical lymph node (Sister Mary Joseph’s node)
  • Left axillary lymph node (Irish’s node)

Peritoneal seeding may cause Krukenberg tumors (bilateral ovarian tumors with signet-ring cells).

Gross examination shows a polypoid, fungating mass, an ulcerative lesion, or a diffusely infiltrative lesion. Locally advanced cancers invade the muscularis propria.

Linitis plastica is a type of diffusely infiltrative, scirrhous-type, gastric adenocarcinoma. It presents as thickened gastric folds and extensive submucous fibrosis with poor distensibility seen on endoscopic ultrasound.

Treatment of gastric cancer is surgical with subtotal or total gastrectomy. Chemotherapy with cisplatin, 5FU, etoposide and/or leucovorin, radiotherapy or immunotherapy may be used in advanced cases.

Signet cell cancer
Signet cell cancer
  1. Dumping syndrome: Dumping syndrome is caused by rapid gastric emptying. It is most commonly seen following gastric bypass surgery, partial gastrectomy, fundoplication etc.

It presents with early and late symptoms:

  • Early dumping syndrome occurs 10-30 minutes after a meal. Hyperosmolar gastric contents reach the small intestines and cause bloating, nausea, abdominal cramps and explosive diarrhea.
  • Late dumping occurs 1-3 hours after a meal and presents with flushing, dizziness, palpitations and fatigue, with marked changes in blood pressure and heart rate. It results from reactive hypoglycemia due to oversecretion of insulin.

Management is by dietary modifications like eating smaller, more frequent meals, avoiding drinking water with meals, post-meal short naps, and medications like octreotide, propranolol and tolbutamide.

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