The Gastrointestinal Tract

Figure 7.1

Normal esophagus and stomach, gross

The normal esophagus on the left has the usual white to tan mucosa. The gastroesophageal junction with the lower esophageal sphincter, whose physiologic function is maintained by muscle tone, is in the center-left, and the normal stomach is on the right, opened along the greater curvature. The lesser curvature (↑) can be seen in the fundus. Just beyond the antrum is the pylorus (←) with thick surrounding muscle that empties into the first portion of duodenum on the lower right. The rugal folds of the normal stomach are prominent.

Figure 7.2

Normal esophagus, endoscopy

This normal upper GI endoscopic view shows the transition from pale pink squamous mucosa of the esophagus to darker pink columnar mucosa of the stomach at the gastroesophageal junction (▲). The lower esophageal sphincter (LES) is a physiologic sphincter maintained by normal muscle tone. Distention of the lower esophagus by food produces LES relaxation along with receptive relaxation of the proximal stomach through a vasovagal reflex with release of vasoactive intestinal peptide from postganglionic peptidergic vagal nerve fibers. Loss of LES tone allows reflux of acidic gastric contents into the lower esophagus that can produce burning retrosternal or substernal chest pain (heartburn). An abnormality of the esophageal sphincter can also produce difficulty in swallowing (dysphagia) . Lesions of the esophageal mucosa may cause pain on swallowing (odynophagia) . Abnormalities in intrinsic or extrinsic esophageal innervation may cause failure of LES relaxation, leading to achalasia and progressive dysphagia with esophageal dilation above the LES.

Figure 7.3

Normal esophagus, microscopic

The normal squamous mucosa (→) is on the left, with underlying submucosa containing minor mucous glands (↑) and a duct surrounded by lymphoid tissue (←). The muscularis (♦) is on the right. Predominantly voluntary striated muscle to initiate swallowing in the upper esophagus merges and changes to involuntary smooth muscle distally in the lower esophagus, which provides propulsive peristalsis of solid and liquid food boluses into the stomach. The physiologic lower esophageal sphincter smooth muscle with muscle tone provides an effective barrier to regurgitation. At the gastroesophageal junction, the squamous epithelium interdigitates with the glandular epithelium of the stomach.

Figure 7.4

Tracheoesophageal fistula, gross

Congenital anomalies involving the esophagus include atresia and fistula with the trachea. Embryologically, the lung buds off the esophagus, an endodermal derivative, so both are intimately associated in development. The esophageal atresia (▲) shown here is present in the mid esophagus in the right panel . The tracheoesophageal fistula (♦) is located below the carina in the left panel . Depending on the location of the atretic portion or the fistula, an infant at birth may exhibit vomiting or aspiration. Additional congenital anomalies are often present. Agenesis (complete absence) of the esophagus is very rare.

Figures 7.5 and 7.6

Esophageal stricture and Schatzki ring, barium swallow radiographs

The two panels on the left show stricture (♦) (stenosis) of the lower esophagus. This can occur from inflammation with reflux, scleroderma with submucosal fibrosis, radiation injury, or ingestion of caustic chemicals. The lateral view on the right reveals a Schatzki ring (▲) of the lower esophagus produced by an infolding of the muscular wall just above the diaphragm. With these conditions, there may be progressive dysphagia, more marked for solid foods than liquids initially.

Figure 7.7

Esophageal fibrosis with scleroderma, microscopic

Beneath the stratified squamous epithelium at the left, this trichrome stain emphasizes the blue collagenous submucosal fibrosis of the esophagus, with a few remaining fascicles of pink muscle. There is a minimal lymphocytic infiltrate. Systemic sclerosis is an autoimmune disease in which cytokines such as transforming growth factor-β and interleukin-13 (IL-13) from CD4 cells lead to progressive interstitial and perivascular fibrosis, and with the diffuse form multiple organ involvement, particularly gastrointestinal tract, lungs, and kidneys. Esophageal dysmotility with reflux, stricture, and dysphagia is common.

Figure 7.8

Hiatal hernia, CT image

Chest CT scan shows a dilated portion of gastric fundus (∗) sliding through a widened esophageal hiatus into the lower chest adjacent to heart (◼). About 95% of hiatal hernias are of this sliding type. About 9% of patients with hiatal hernias have associated symptoms of gastroesophageal reflux disease (GERD). Conversely, some cases of GERD are associated with a hiatal hernia. The widened esophageal hiatus interferes with maintenance of the normal lower esophageal sphincter function. Patients may have symptoms of “heartburn” from reflux of acidic gastric contents into the lower esophagus, with retrosternal burning pain, particularly after eating, and exacerbated by lying down after a meal.

Figure 7.9

Paraesophageal hernia, CT image

Chest CT scan without contrast enhancement reveals that much of the stomach (∗) is present in the left chest cavity adjacent to the heart. This is a complication of a hiatal rolling hernia known as paraesophageal hernia, an uncommon but serious form of hernia. Chest pain, epigastric pain, or vomiting may be present. The vascular supply to the stomach becomes compromised when the stomach herniates upward through the small opening, leading to incarceration, then strangulation with ischemia and infarction.

Figure 7.10

Esophageal pulsion diverticulum, barium swallow radiographs

These two views from an upper GI series with barium contrast material reveal a pulsion diverticulum (♦) in the upper esophagus. Bright contrast material fills this small outpouching. Such a diverticulum represents enlargement and protrusion of esophagus through a weak point in the muscular wall, typically between the constrictor muscles in the upper esophagus or through the muscularis just above the diaphragm. Such a lesion is also known as a Zenker diverticulum . An enlarging lesion can produce a mass effect, interfere with swallowing, and collect food that decays and produces marked halitosis.

Figure 7.11

Mallory-Weiss syndrome, CT image

Longitudinal tears in the esophagus leading to hemorrhage may occur from bouts of severe or forceful vomiting. The rare complication of rupture (Boerhaave syndrome) is shown on this chest CT scan with contrast enhancement that shows a dark lucency (♦) representing an air leak from the esophageal rupture into the mediastinum. The point of rupture in the lower esophagus lies just above the gastroesophageal junction. Leakage of esophageal contents into the mediastinum leads to infection with inflammation that can quickly spread to other areas of the chest cavity.

Figure 7.12

Esophageal varices, gross

These prominent purplish dilated veins (↓) near the gastroesophageal junction are a source of bleeding with hematemesis. Submucosal varices occur in patients with portal hypertension (usually from chronic liver disease: chronic alcohol abuse, viral hepatitis, or schistosomiasis) because the submucosal esophageal plexus of veins is a collateral channel for portal venous drainage. This plexus of veins also drains part of the upper stomach, but it is generically called the esophageal plexus of veins with esophageal variceal bleeding , which can be difficult to stop and life-threatening.

Figure 7.13

Esophageal varices, endoscopy

The dilated submucosal veins (▲) of the esophageal plexus appear to bulge into the lower esophageal lumen on upper GI endoscopy. This venous dilation is most often a complication of portal hypertension with hepatic cirrhosis. Eventually, about two thirds of patients with cirrhosis develop esophageal varices. With erosion and rupture of these delicate submucosal veins, there can be sudden, massive life-threatening hematemesis. Variceal ligation, octreotide infusion, and balloon tamponade have been employed as therapeutic measures to halt or prevent blood loss.

Figure 7.14

Esophagitis, microscopic

Reflux of acidic gastric contents into the lower esophagus from incompetence of the lower esophageal sphincter leads to gastroesophageal reflux disease (GERD) with esophagitis. Histologic findings in mild reflux esophagitis include epithelial hyperplasia with basal zone hyperplasia and lengthened papillae, and inflammation with neutrophils, eosinophils, and lymphocytes (eosinophils, especially in children, are a sensitive and specific indicator of reflux, as seen here with red cytoplasmic granules on Giemsa stain). Causes of GERD include hiatal hernia, neurologic disorders, scleroderma, lack of esophageal clearance, and delayed gastric emptying. Severe esophagitis can be complicated by ulceration and subsequent fibrosis with stricture.

Figure 7.15

Herpes esophagitis, gross

This lower esophagus, with stomach at right, shows sharply demarcated, oblong ulcerations (↓) that have a brown-red base, contrasted with the surrounding normal pale white esophageal squamous mucosa. These ulcerations have a “punched-out” appearance suggestive of herpes simplex virus (HSV) infection. Opportunistic infections like HSV are most often seen in immunocompromised patients. Odynophagia is a typical symptom. Herpetic esophagitis usually remains localized, rarely causes significant bleeding or obstruction, and is unlikely to become disseminated.

Figure 7.16

Candida esophagitis, gross

Tan-yellow plaques (◀) are seen in the lower esophagus, along with mucosal hyperemia. The same lesions also appear at the upper right in the upper gastric fundus. Candida infections involving the oral cavity (“oral thrush”) and upper GI tract tend to remain superficial, but invasion and dissemination occasionally occur in immunocompromised patients. A few Candida organisms can be part of the normal flora of the mouth. These lesions rarely cause significant hemorrhage or obstruction; larger lesions may coalesce to form pseudomembranes.

Figure 7.17

Barrett esophagus, gross

Islands of reddish metaplastic mucosa (↓) are shown in the lower esophagus, above the gastroesophageal junction, with remaining surrounding normal white squamous mucosa. Chronic gastroesophageal reflux disease with esophageal mucosal injury can lead to metaplasia of the normal esophageal squamous epithelium to columnar mucosa with intestinal-type goblet cells, known as Barrett esophagus . Ten percent of patients with chronic gastric reflux may develop Barrett esophagus. About 2% of adults (more men than women) have it. Ulceration may occur with bleeding and pain; inflammation with stricture may ensue.

Figure 7.18

Barrett esophagus, endoscopy

These endoscopic views of the lower esophagus just above the lower esophageal sphincter show areas of red metaplastic mucosa (↑) typical of Barrett esophagus along with remaining islands of normal pale esophageal squamous mucosa. If the area of Barrett mucosa extends less than 3 cm above the normal squamocolumnar junction, the condition is called short-segment Barrett esophagus . Risk of progression to adenocarcinoma is 0.5% per year.

Figure 7.19

Barrett esophagus, microscopic

Note the abnormal columnar epithelium on the left of this image and the normal squamous epithelium on the right. This is “typical” Barrett mucosa on the left because there is intestinal metaplasia with goblet cells (▼) in the columnar mucosa. Chronic reflux of gastric contents into the lower esophagus over many years predisposes to development of this metaplasia. Barrett esophagus is diagnosed on endoscopy with biopsy; average age is 55 to 65 years old, mostly men. There is a long-term risk (>30- to 40-fold compared with the general population) for development of esophageal adenocarcinoma when more than 3 cm of Barrett mucosa is present in the esophagus.

Figure 7.20

Barrett esophagus with dysplasia, microscopic

At the right is remaining squamous mucosa (▼) and to the left an area of dysplasia in the metaplastic columnar epithelium in the Barrett mucosa. Note the crowded, hyperchromatic nuclei (▶) in the columnar cells, a few remaining goblet cells at the upper surface on the left, and the glandular architectural irregularity. Because the columnar cell nuclei are basally oriented, this is a low-grade dysplasia; an apical orientation is part of high-grade dysplasia, which has a much greater likelihood of advancing to adenocarcinoma. Dysplasia may develop after years of untreated gastroesophageal reflux disease with Barrett esophagus.

Figure 7.21

Adenocarcinoma, gross

Normal pale tan upper esophageal mucosa at the far left contrasts with Barrett mucosa, producing a darker, slightly erythematous appearance. In the distal esophagus arising near the gastroesophageal junction is a large ulcerating adenocarcinoma with dark center that extends (←) into the upper stomach. Esophageal adenocarcinomas most often arise in Barrett esophagus, with frequent mutation of TP53 , followed by CDKN2A downregulation, then by nuclear translocation of β-catenin and ERBB2 (HER2) amplification. As with esophageal squamous cell carcinoma, there are often no early symptoms, so the cancer may be advanced at the time of diagnosis, with a poor prognosis.

Figure 7.22

Adenocarcinoma, CT image

Abdominal CT scan with contrast enhancement shows a mass (♦) surrounding the central dark esophageal lumen and extending into the upper stomach. This malignant neoplasm arose in a Barrett mucosa that followed chronic gastroesophageal reflux disease (GERD). Preexisting high-grade dysplasia further increases the risk for development of subsequent adenocarcinoma. By the time an adenocarcinoma arises, untreated GERD has been present for years, and the patient is typically older than 40 years. The increased epithelial cell turnover with increased proliferative activity in Barrett mucosa is the background for mutations to arise with subsequent loss of cell cycle control.

Figure 7.23

Adenocarcinoma, endoscopy

Endoscopy of the lower esophagus shows irregular pale reddish mucosa representing Barrett mucosa. A pale, polypoid, exophytic mass (↑) extends into and partially obstructs the esophageal lumen. On biopsy this is a moderately differentiated adenocarcinoma. The patient had a long history of poorly controlled gastroesophageal reflux disease. Clinical findings with esophageal carcinomas include hematemesis, dysphagia (solids more than liquids), chest pain, and weight loss.

Figure 7.24

Squamous cell carcinoma, gross

An irregular reddish, ulcerated, exophytic mid-esophageal mass (↓) projects from the mucosal surface. The distensibility of the esophagus partly ameliorates the mass effect so that early symptoms are uncommon, and by the time a diagnosis is made, there is often extensive mediastinal invasion that precludes a surgical cure. The overall prognosis for this malignancy is poor. Risk factors for esophageal squamous carcinoma in the United States include smoking and alcohol abuse. In other parts of the world, dietary factors, such as a high nitrate/nitrosamine content and deficiency of zinc or molybdenum, and human papillomavirus infection may play a role.

Figure 7.25

Squamous cell carcinoma, endoscopy

On upper GI endoscopy there is an ulcerated mid-esophageal squamous cell carcinoma causing luminal stenosis (→). Pain and dysphagia are typical presenting problems. Interference with swallowing leads to cachexia with weight loss. Most of these carcinomas have a higher stage with invasion and spread to adjacent mediastinal tissues by the time of diagnosis, complicating treatment.

Figure 7.26

Squamous cell carcinoma, microscopic

At the lower right is a small remnant of normal squamous esophageal mucosa (←) that merges into abnormal, thick, invasive squamous cell carcinoma. Solid nests (↓) of neoplastic cells are infiltrating down through the submucosa to the left. These carcinomas often spread to surrounding structures, making surgical removal difficult. Half of these cancers have TP53 tumor suppressor gene mutations. The p16/CDKN2A tumor suppressor gene is abnormal in some cases, whereas cyclin D1 may be amplified in others. These mutations can arise in the setting of carcinogen exposure with chronic inflammation producing increased epithelial cell proliferation.

Figure 7.27

Normal gastric mucosa, microscopic

The fundal mucosa has short gastric pits (♦), beneath which are long glands (◼) with pale cuboidal mucous neck cells that secrete mucus to protect the mucosa against the acid and enzyme secretions. These fundic glands contain pink parietal cells (▲) secreting hydrochloric acid and intrinsic factor. Acid is secreted through the H + ,K + ATPase (“proton pump”) mechanism in parietal cells under the influence of acetylcholine secreted from the vagus nerve acting on muscarinic receptors, via histamine from mast cells acting on histamine-2 (H2) receptors, and gastrin from mucosal G cells. Fundic glands also contain chief cells secreting pepsinogen activating to pepsin by contact with hydrochloric acid (HCl) and initiating protein digestion.

Figure 7.28

Normal gastric mucosa, microscopic

The gastric antral epithelium has long pits (♦) with shorter glands (◼) than the fundus. In the more distal gastric antrum and pyloric regions, there are columnar mucous cells in pits and glands. Mucosal cells produce prostaglandins that favor production of mucus and bicarbonate, and increase mucosal blood flow to protect the mucosa from the effects of gastric acid. Peristaltic movements in the stomach mix the chyme. The rate of gastric emptying is partially controlled by the amount of H + and nutrient density (fat and some amino acids) entering the duodenum. Duodenal fat increases the secretion of cholecystokinin, which slows the rate of gastric emptying.

Figures 7.29 and 7.30

Normal upper GI, endoscopy

The normal appearance of the gastric fundus with rugal folds is shown on the left, and the normal duodenal appearance with circular folds is shown on the right . The folds are regular and have smooth mucosal surfaces.

Figure 7.31

Congenital diaphragmatic hernia, gross

The left diaphragmatic dome is absent here, allowing herniation of abdominal contents into the chest cavity during fetal development. The metal probe is positioned behind the left lung, which has been displaced into the right chest by the herniated stomach. Seen next to white stomach is a dark spleen (▼) that overlies the left lobe of the liver herniating upward. Incursion of abdominal contents into the chest during development results in pulmonary hypoplasia. Although diaphragmatic hernia may be an isolated congenital anomaly that is potentially reparable, most are associated with multiple anomalies and often with chromosomal abnormalities such as trisomy 18.

Figure 7.32

Pyloric stenosis, gross

Note the thick hypertrophied muscle (▲) and lengthened pyloric canal at the gastric outlet. Pyloric stenosis is uncommon, but is a cause of gastric outlet obstruction with “projectile” nonbilious vomiting in infants 2 to 6 weeks old. Muscular hypertrophy may be so prominent that there is a palpable mid-abdominal mass. Pyloric stenosis manifests the genetic phenomenon of “threshold of liability,” above which the disease is manifested when more multifactorial genetic and environmental risks are present. The incidence is 1 in 300 to 900 live births, with boys affected more often than girls because more risks must be present in girls for the disease to occur. Myotomy is curative.

Figure 7.33

Gastropathy-gastritis, gross

Larger irregular areas of gastric hemorrhage (▼) are shown, which could best be termed erosions because the superficial mucosa is eroded away, but not completely gone. The clinical term gastropathy describes several different patterns of gastric mucosal epithelial or endothelial injury with mucosal damage without significant inflammation. Causes of gastropathy are similar to those for acute gastritis and include nonsteroidal antiinflammatory drugs, alcohol, stress, bile reflux, uremia, portal hypertension, radiation, and chemotherapy. The prominent erosions here suggest gastritis with inflammation.

Figure 7.34

Acute gastritis, gross

The gastric mucosa of the fundus is diffusely hyperemic, with multiple petechiae, and with small erosions (▲) but no ulcerations. Acute gastritis (also called hemorrhagic gastritis, or acute erosive gastritis if mucosal erosions are present) can be caused by ischemia (shock, burns, or trauma), or toxins, such as alcohol, salicylates, or nonsteroidal antiinflammatory drugs. Damage to the gastric mucosal barrier allows back-diffusion of acid. It may be asymptomatic or lead to massive hemorrhage. The lesions can progress to more extensive erosions or to ulcerations. The stress of burn injuries (Curling ulcer) or central nervous system trauma (Cushing ulcer) can cause acid hypersecretion.

Figure 7.35

Acute gastritis, microscopic

Microscopic findings include hemorrhage, edema, and variable degrees of acute inflammation with neutrophilic infiltrates. The gastric mucosa here shows infiltration of glands and lamina propria by neutrophils. Typical clinical findings range from mild to severe epigastric pain, nausea, and vomiting. In severe cases, there can be significant hematemesis, particularly in patients with a history of chronic alcohol abuse; this can be termed acute hemorrhagic gastritis . Although the presence of gastric acid is a necessary antecedent to mucosal injury and ulceration, the amount of acid is not typically the determining factor for development of most gastric ulcerations.

Figure 7.36

Chronic gastritis, microscopic

Chronic nonspecific (antral) gastritis is typically the result of Helicobacter pylori infection. Other causes include bile reflux and drugs (salicylates and alcohol). The inflammatory cell infiltrates are composed mainly of lymphocytes and plasma cells, and occasionally some neutrophils, seen here mostly at the left. Mucosal atrophy and intestinal metaplasia are sequelae that can be the first step toward development of gastric adenocarcinoma. An autoimmune form of gastritis can occur when anti-parietal or anti-intrinsic factor antibodies are present, leading to atrophic gastritis and pernicious anemia. Fasting serum gastrin levels are inversely proportional to gastric acid production, and a high serum gastrin suggests atrophic gastritis.

Figure 7.37

Helicobacter pylori, microscopic

H. pylori is a small, spiral, rod-shaped, gram-negative bacterium residing under microaerobic conditions in a neutral microenvironment between the overlying secreted mucus and superficial columnar mucosal cells. The organisms appear as pale pink rods (▲) with hematoxylin and eosin (H&E) staining. These organisms do not invade or directly damage the mucosa, but rather change the microenvironment of the stomach to promote mucosal damage. H. pylori strains that possess the cagA pathogenicity island induce more severe gastritis and augment the risk for developing peptic ulcer disease and gastric cancer. H. pylori organisms elaborate urease to produce a protective surrounding cloud of ammonia to resist gastric acid. The urea breath test can be used to detect the presence of H. pylori.

Figure 7.38

Helicobacter pylori, microscopic

H. pylori organisms (▲) shown here as short, thin rods with methylene blue stain stimulate cytokine production by gastric epithelial cells to recruit and activate immune and inflammatory cells in the underlying lamina propria. H. pylori is often identified in the surface epithelial mucus of most patients with active gastritis. This infection is thought to be acquired starting in childhood, but inflammatory changes progress throughout life. Colonization rates vary from 10% to 80% around the world. Only a subset of persons infected with H. pylori develop the complications of chronic gastritis, gastric ulcers, duodenal ulcers, mucosa-associated lymphoid tissue lymphoma, or adenocarcinoma.

Figure 7.39

Acute gastric ulcer, gross

This 1-cm, shallow and sharply demarcated acute gastric ulcer (▼) with surrounding hyperemia is in the upper fundus. An ulcer is focal full-thickness loss of the mucosa (an erosion is a partial-thickness loss). Ulcers can be complicated by hemorrhage, penetration (extension into an adjacent organ), perforation (communication with the peritoneal cavity), and stricture (owing to scarring). Isolated gastric ulcers may be seen with chronic atrophic gastritis; they are usually located in the antrum and lesser curve or at the junction of antrum and body. Helicobacter pylori infection is the most common cause, followed by nonsteroidal antiinflammatory drug use. Though acid is required for ulceration, most patients are normochlorhydric or hypochlorhydric.

Figures 7.40 and 7.41

Acute gastric ulcers, endoscopy

The left panel shows a small prepyloric ulcer (▲), and the right panel shows a larger antral ulcer (◀). All gastric ulcers found on endoscopy undergo biopsy because gross inspection alone cannot reliably differentiate a malignancy from a benign process. Smaller, more sharply demarcated gastric ulcerations are more likely to be benign.

Figure 7.42

Acute gastric ulcer, microscopic

Note the loss of the gastric epithelium and extension of the ulcer downward to the muscularis. This ulcer is sharply demarcated, with normal gastric mucosa on the lower right falling away into a deep ulcer crater whose base contains inflamed, necrotic debris (◼). A small arterial branch (▼) at the ulcer base is eroded. Ulcers may penetrate more deeply over time if they remain active and do not heal. Penetration leads to pain. If the ulcer penetrates through the muscularis and through adventitia, the ulcer is said to “perforate,” leading to an acute abdomen with peritonitis, and an abdominal radiograph may show free air.

Figure 7.43

Perforated gastric ulcer, radiograph

This anterior to posterior (AP) portable upright chest radiograph shows free air (▲) under the right diaphragmatic dome. This patient had a perforation of a duodenal peptic ulcer. The intraluminal air released from a perforated viscus can be detected as free peritoneal air, and a good place to detect it is under a diaphragmatic leaf on an upright abdominal plain film radiograph. Such patients have an “acute abdomen” with pain and sepsis. The pathogenesis of duodenal ulcers is hyperacidity. These ulcers occur in the proximal duodenum and are associated with peptic duodenitis. Almost all duodenal ulcers are associated with Helicobacter pylori infection in the stomach.

Figure 7.44

Ménétrier disease, CT image

The gastric rugal folds (◀) are markedly thickened and irregular from excessive secretion of transforming growth factor-α binding to a growth factor receptor. There is diffuse hyperplasia of the foveolar epithelium of the body and fundus, but not the antrum. There is diminished acid, excess mucus production, and loss of protein from the epithelium, leading to diarrhea and weight loss. Hypoproteinemia is indicative of this form of protein losing enteropathy. In children with cytomegalovirus (CMV) infection, this condition is usually self-limited. In adults it can persist and there is increased risk for adenocarcinoma. If severe, gastrectomy may be performed.

Figure 7.45

Hyperplastic polyp, microscopic

Gastric Helicobacter pylori infection may predispose to development of chronic gastritis with reactive hyperplasia and growth of inflammatory and hyperplastic polyps. Treatment of H. pylori may lead to their regression, while growth greater than 1.5 cm increases risk for dysplasia and carcinoma. Their smooth surfaces may become eroded. Microscopically there are irregular, cystically dilated, and elongated glands with edematous lamina propria containing acute and chronic inflammation (right panel) . There is foveolar hyperplasia with tall columnar mucinous epithelium (left panel) .

Figure 7.46

Fundic gland polyp, microscopic

Proton pump inhibitor therapy to reduce gastric acid secretion may increase gastrin production, leading to gastric glandular hyperplasia and polyps. These polyps are more common in women, at an average age of 50 years; they may be asymptomatic or associated with nausea, vomiting, or epigastric pain. Grossly they are circumscribed and smooth. When sporadic they are single; when multiple they can be associated with familial polyposis. Microscopically there are many dilated, irregular glands (left panel) lined by pink parietal and chief cells (right panel) with minimal to absent inflammation.

Figure 7.47

Adenocarcinoma, gross

The shallow gastric ulcer (▼) is 2 × 4 cm in size. This ulcer on biopsy proved to be malignant, so the stomach was resected. In the United States, most gastric cancers are discovered at a late stage when invasion or metastases are present, while in Japan screening programs detect more early gastric cancers. All gastric ulcers and all gastric masses must undergo biopsy because it is impossible to determine malignancy from their endoscopic appearances. In contrast, virtually all duodenal peptic ulcers are benign. Worldwide, gastric carcinoma is among the most common causes for cancer deaths, but the incidence has been declining for decades in the United States.

Figure 7.48

Adenocarcinoma, CT image

Abdominal CT scan with contrast enhancement reveals an irregular dark exophytic mass (▲) lesion distorting the gastric antrum. Manifestations include nausea, vomiting, abdominal pain, hematemesis, weight loss, altered bowel habits, and dysphagia. Early gastric cancers confined to the mucosa are usually asymptomatic and detected by endoscopic screening. This patient had Helicobacter pylori infection with chronic gastritis for many years, but only a few persons with H. pylori infection develop gastric cancer. Dietary risks for development of the intestinal type of gastric cancer include ingestion of pickled or smoked foods, nitrosamines derived from ingested nitrites, and excessive salt intake; changes in dietary patterns can lead to a steady decrease in the incidence of this form of cancer. Risk factors for the diffuse form of gastric carcinoma are less well defined.

Figure 7.49

Adenocarcinoma, microscopic

This intestinal type of gastric adenocarcinoma has irregular shapes and sizes of neoplastic glands infiltrating into the submucosa. Some of the cells show mitoses (▲). The cells have an increased nuclear-to-cytoplasmic ratio and nuclear hyperchromatism. There is a desmoplastic stromal reaction to these infiltrating glands. Genetic abnormalities in the intestinal type of gastric cancer include TP53 mutation, abnormal E-cadherin expression, and instability of transforming growth factor- β and BAX genes.

Figure 7.50

Adenocarcinoma, gross

This is linitis plastica, a diffuse infiltrative gastric adenocarcinoma, giving the stomach a shrunken “leather bottle” appearance with extensive mucosal erosion, ulceration (♦), and a markedly thickened gastric wall (↑). This type of gastric carcinoma has a very poor prognosis. More localized gastric cancers are most likely to arise on the lesser curvature and show ulceration. The intestinal type of gastric cancer is more likely to arise from precursor lesions and to be related to Helicobacter pylori infection. The declining incidence of intestinal-type gastric cancers in the United States is probably related to diminishing prevalence of H. pylori infection. The incidence of the diffuse type of gastric cancer shown here has remained more constant over time.

Figure 7.51

Adenocarcinoma, endoscopy

The endoscopic view of the linitis plastica appearance of the diffuse type of gastric adenocarcinoma reveals extensive reddish irregular mucosal erosion (◀). Exposure to ingested carcinogens may play a role in the development of diffuse gastric adenocarcinomas. Some arise at an earlier age (fourth decade) in hereditary diffuse gastric cancer syndrome with mutations in the E-cadherin ( CDH1 ) gene, with high risk for stomach and lobular breast carcinoma. Preventive measures include diets rich in fruits and vegetables that reduce the risk for carcinoma.

Figure 7.52

Adenocarcinoma, microscopic

This gastric adenocarcinoma is so poorly differentiated that just a few clusters and many single infiltrating neoplastic cells with marked pleomorphism are seen. Most of the neoplastic cells are distended by cytoplasm filled with clear vacuoles of mucin (▶) displacing the cell nucleus to the periphery. This is the “signet ring” cell pattern typical for the diffuse type of gastric adenocarcinoma, which tends to be highly infiltrative and has a poor prognosis. Mutations in CDH1 that encode E-cadherin involved in epithelial intercellular adhesion are found with some diffuse gastric carcinomas, including familial forms.

Figure 7.53

Normal small intestine and mesentery, gross

A loop of bowel attached by the mesentery is seen here. Note the extensive venous outflow (▲), which collects into the portal venous system draining into the liver. Arcades of arteries supplying blood to the bowel run in the same mesenteric location. The small and large bowel are supplied by branches and collaterals from the celiac axis, superior mesenteric artery, and inferior mesenteric artery, providing an extensive anastomosing arterial blood supply to the bowel, making it more difficult to infarct. Note the smooth, glistening peritoneal surfaces of the small intestine.

Figure 7.54

Normal small intestine, gross

Normal terminal ileum shown in the upper frame displays the ileocecal valve (♦), along with several darker oval Peyer patches (▲) on the mucosal surface. In the lower frame, the prominent darker oval Peyer patch (▶) is a concentration of submucosal lymphoid tissue. In the duodenum, the lamina propria and the submucosa have proportionately more lymphoid tissue than the rest of the GI tract. The ileum has prominent submucosal lymphoid tissue concentrated into small nodules or elongated ovoid Peyer patches. Gut-associated lymphoid tissue is present from the back of the tongue all the way to the rectum and is collectively the largest lymphoid organ of the body.

Figure 7.55

Normal small intestine, microscopic

The small intestinal mucosa has surface villi lined by columnar cells (♦) and scattered goblet cells (▲). The villi terminate in the lamina propria as glandular lumina known as crypts of Lieberkühn (◼). The villi greatly increase the surface digestive and absorptive area. The jejunum has more prominent mucosal folds (plicae) to increase absorptive area. Each intestinal villus contains a blind-ended lymphatic channel known as a lacteal . The major immunoglobulin secreted by plasma cells of the GI tract (and respiratory tract) is IgA, so-called secretory IgA. This IgA is bound to protein on the glycocalyx overlying the microvilli of the brush border to neutralize harmful agents such as infectious organisms.

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Dec 29, 2020 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on The Gastrointestinal Tract
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