The Gastrointestinal System

Chapter 12 The Gastrointestinal System



Ivan Damjanov, MD, PhD, Anamarija Morović, MD




1 What is the basic structure of the gastrointestinal (GI) system?


The entire GI tract has a relatively uniform structure and consists of four layers:


image Mucosa composed of epithelium lining the lumen of the cavity

image Submucosa composed of loose connective tissue, blood vessels, and nerves

image Muscle layer (muscularis propria) composed predominantly of smooth muscle cells responsible for the peristaltic movement of these hollow organs

image Adventitia or serosa forming the outer layer (In the esophagus, the adventitia is a connective tissue structure linking it with other thoracic organs. The external surface of the stomach and small and large intestines is covered with serosa, a layer of peritoneum continuous with the peritoneum covering the other parts of the abdominal cavity and other organs, such as the liver and the spleen.)


2 What are the main diseases of the GI system?



image Developmental disorders

image Inflammatory diseases, usually caused by infections but often of unknown etiology (e.g., inflammatory bowel disease)

image Functional disorders affecting the digestion, absorption of nutrients, or motility of the intestines

image Circulatory disturbances

image Tumors


3 Discuss the possible consequences of abnormal development of the GI system



image Atresia (absence of lumen; The normal GI system is a tube that develops from cords of embryonic cells. The cells forming the central part of these cords undergo apoptosis, and a lumen is thus formed. If the centrally located cells do not undergo apoptosis, the lumen never forms, and the affected part of the GI system will be atretic, i.e., unpassable.)

image Stenosis (narrowing)

image Diverticulosis (formation of outpouchings)

image Fistula (a connection between the lumen of the GI tract and another tubular system; e.g., an esophageal–tracheal fistula)


Key Points: Most Important Symptoms and Signs Pertaining to the GI System



1. Dysphagia

2. Vomiting

3. Hematemesis

4. Hematochezia and melena

5. Colics, diarrhea, and constipation


ESOPHAGUS



4 What are the main clinical symptoms and signs of esophageal disease?



image Dysphagia: Difficulty in swallowing. It may be caused by anatomic lesions (e.g., stricture, webs, and rings), cancer, or functional disorders (e.g., achalasia and paralysis).

image Odynophagia: Pain on swallowing. It is a sign of esophageal lesions, such as gastroesophageal reflux disease (GERD) and infectious esophagitis caused by viruses or fungi.

image Heartburn: A burning sensation behind the sternum. It is usually caused by GERD.

image Acid regurgitation: Reflux of gastric contents into the mouth is a sign of GERD.


5 What is the most common developmental abnormality of the esophagus?


Esophageal atresia with tracheoesophageal fistula is the most common developmental abnormality. Several anatomic variants are recognized. Food cannot pass into the stomach because the lumen of the esophagus ends in a blind pouch. Food passing through the fistula enters the trachea, causing choking and coughing. Symptoms appear soon after birth, requiring immediate surgical correction.



6 What are esophageal diverticula?


Diverticula are outpouchings of the wall of the esophagus. These outpouchings are classified on the basis of the following (Fig. 12.1):


image Stricture
image True diverticula (composed of all four layers of the normal esophageal wall)

image False diverticula (representing outpouchings of the mucosa and submucosa only)

image Pathogenesis
image Traction diverticula (pull from outside; e.g., fibrous adhesions)

image Pulsion diverticula (push from inside; e.g., increased intraluminal pressure)

image Location
image Upper esophageal diverticula (also known as Zenker pulsion diverticula)

image Diverticula of the midportion of esophagus (traction diverticula due to mediastinal and bronchial lesions; e.g., scarring of lymph nodes in tuberculosis)

image Epiphrenic (lower esophageal) diverticula (pulsion diverticula associated with diaphragmatic hernia and GERD)

image

Figure 12-1 Esophageal diverticula.


(From Stimac GK: Introduction to Diagnostic Imaging. Philadelphia, Saunders, 1992, p. 213.)



7 Define achalasia


Achalasia is a functional disorder characterized by a loss of normal esophageal peristalsis and incomplete or abnormal relaxation of the lower esophageal sphincter (LES). The LES must relax during swallowing, but if it does not and remains contracted, it will act as a barrier to the food destined to enter the stomach. Secondary dilatation of the aperistaltic esophagus proximal to the constriction occurs.


The cause of primary achalasia, a rare disease (1:100,000), is not known. Histologic studies show, however, that the spasm of the LES is associated with a loss of ganglion cells from the lower esophagus. Secondary achalasia may occur in Chagas disease because of the destruction of ganglion cells infected with Trypanosoma cruzi.



8 What are esophageal webs and rings?


Webs are mucosal folds causing narrowing of the lumen. Dysphagia caused by webs in the upper esophagus may be associated with glossitis and iron deficiency anemia (Plummer–Vinson syndrome). The disease is common in Scandinavian countries but rare in the United States.


Schatzki ring is a subepithelial semicircular fibrous strand in the wall of the esophagus. It narrows the lumen at the gastroesophageal junction. It may cause dysphagia and is best demonstrated by esophagoscopy.



9 What is hiatal hernia?


Hiatal hernia is a protrusion of the stomach above the diaphragm through a widened diaphragmatic hiatus. Hiatal hernias are quite common. Two forms are recognized (Fig. 12-2):


image Sliding hernia (90%): The gastroesophageal junction is pulled into the thorax and is found above the diaphragm. In most instances, it is asymptomatic and diagnosed accidentally during the workup of the patient for some other disease. It may be associated with GERD, heartburn, and dysphagia.

image Paraesophageal hernia (10%): The gastroesophageal junction is in the normal location, but a portion of the stomach rolls up beside it into the thorax. In most instances, it is asymptomatic, but the invaginated gastric mucosa may become strangulated by the diaphragm.

image

Figure 12-2 Hiatal hernias of the esophagus. A, Normal esophagus. B, Sliding hernia. C, Paraesophageal hernia.



10 What is congenital diaphragmatic hernia?


Congenital diaphragmatic hernia is a severe developmental defect in which the diaphragm is defective or incompletely developed. Abdominal organs dislocate through the defect into the thoracic cavity, compressing the lung and the heart. The condition is often associated with other developmental abnormalities and is usually lethal. Minor diaphragmatic defects may be repaired surgically.



11 What is GERD?


Reflux of gastric contents into the esophagus is a common disorder, typically associated with incompetence of the LES. It presents with odynophagia and dysphagia and may even cause hemorrhage. The diagnosis is suspected on the basis of typical clinical presentation and is confirmed by esophagoscopy. Esophageal biopsy may be performed during endoscopy to document the extent of inflammation or ulceration and to determine whether Barrett esophagus (with or without dysplasia) has developed.



12 Discuss the causes of GERD


GERD develops because of malfunction of the LES, which in normal circumstances prevents the entry of the gastric contents into the esophagus. Reflux may be caused by:


image Temporary increase in intraabdominal pressure (e.g., after overeating or drinking carbonated drinks)

image Prolonged intraabdominal pressure in pregnancy or obesity

image Protracted LES relaxation and uncoordinated contraction due to the action of alcohol, fatty food, cigarettes, and drugs (e.g., morphine and diazepam)

image Hiatal hernia

image Scleroderma (Fibrous tissue replacing smooth muscle cells weakens the sphincter; the esophagus is involved in 70% of patients with scleroderma.)


13 List the most common complications of GERD


Complications of long-lasting GERD are:


image Esophagitis

image Barrett esophagus

image Esophageal bleeding (with melena or hematemesis)

image Peptic ulceration (ulcers may develop in gastric or intestinal metaplasia of Barrett esophagus)

image Esophageal strictures (due to healing with scarring)

image Esophageal perforation (rare; preceded by ulceration)


14 What is the etiology of esophagitis?


Three major etiologic groups are recognized:


image Infectious esophagitis

image Chemical esophagitis (the most common form of esophagitis)

image Esophagitis as a manifestation of other diseases
image Skin diseases (e.g., pemphigus and erythema multiforme)

image Crohn disease of the ileum and colon

image Graft versus host disease (after bone marrow transplantation)


15 What are the causes of infectious esophagitis?


The esophagus is covered by squamous epithelium, which is relatively resistant to infections. Most infections occur in people with poor health, systemic disease, or those with reduced immune response. A breach in the mucosal barrier (e.g., in GERD) may allow infection to take place. The most common infections are:


image Fungal infection: Candida albicans and other fungi may grow on the surface of the squamous epithelium, such as in the mouth or the vagina.

image Viral infections: Herpes simplex virus or cytomegalovirus (CMV) infection typically occurs in immunosuppressed people.

image Bacterial infections: Bacteria do not penetrate the intact squamous epithelium but may invade ulcerated mucosa damaged by GERD. Bacterial infections account for 15% to 20% of all cases of infectious esophagitis.


16 What are the most common forms of chemical esophagitis?



image Hydrochloric acid: HCl regurgitated from the stomach is the most common cause of esophagitis in GERD.

image Strong acids or lye: These chemicals cause erosive esophagitis. Children sometimes ingest these substances accidentally, and adults may drink them intentionally while trying to commit suicide.

image Cytotoxic drugs: Such drugs inhibit the proliferation of the esophageal epithelium and prevent or delay the repair of small ulcerations that develop during feeding. These ulcerations provide a route of entry for bacteria.


Key Points: Esophagus



1. The most common diseases of the esophagus are reflux esophagitis and hiatal hernia, resulting in gastroesophageal reflux disease.

2. Carcinomas of the esophagus are of two histologic types: (1) squamous cell carcinoma originating from the squamous epithelium normally covering the esophagus and (2) adenocarcinomas arising from the metaplastic glandular epithelium in Barrett esophagus.


17 What is Barrett esophagus?


Barrett esophagus is a form of metaplasia of the esophagus. Typically, it involves the lower segment of the esophagus and is thought to be most often caused by GERD. It can be recognized on endoscopy and biopsy:


image Endoscopy: Salmon-red patches replace the normal white squamous lining of the esophagus.

image Microscopy: Columnar epithelium similar to gastric or intestinal columnar epithelium is found replacing the normal squamous esophageal epithelium. The underlying connective tissue usually shows signs of chronic inflammation.


18 What is the significance of Barrett esophagus?


Barrett esophagus is associated with a variety of clinical symptoms, most often odynophagia. The esophagus may ulcerate and bleed. The most important complication of Barrett esophagus is adenocarcinoma of the esophagus, which develops in a significant number of cases (10%).



19 Which pathologic changes precede adenocarcinoma in Barrett esophagus?


Adenocarcinoma developing in Barrett esophagus is typically preceded by histologically recognizable dysplasia. Pathologists classify such dysplasia as mild or severe. Severe dysplasia must be followed up clinically in every case, and partial resection of the esophagus is recommended in some instances because such dysplasia has a propensity to progress to invasive adenocarcinoma.



20 What is Mallory–Weiss syndrome?


Mallory–Weiss syndrome is characterized by bleeding from esophageal lacerations that develop because of violent retching. It is typically encountered in chronic alcoholics.



21 List key facts about esophageal varices



image Dilatation of submucosal veins of the esophagus may occur.

image Dilatated veins bulge underneath the epithelium of the esophagus and can be recognized through esophagoscopy.

image One cause is portal hypertension.

image Cirrhosis is the most common cause; thrombosis of portal vein and hepatocellular carcinoma are less common causes.

image Rupture of varices is an important cause of hematemesis.

image Hematemesis is accompanied by high mortality.


22 How common is esophageal cancer?


Esophageal cancer is not common in the United States, but it is a disproportionately high cause of cancer-related deaths. The incidence of esophageal cancer is increasing in the United States:


image Six percent of all GI cancers (incidence: 6:100,000 in the United States)

image Peak age, 50 to 60 years

image More common in men than in women (4:1)

image More common in African Americans than in others (4:1)

image More common in areas of Asia (e.g., Iran and China) and Africa than in the United States and Europe

image Poor prognosis (25% 5-year survival rate)


23 List the risk factors for esophageal cancer



image Environmental factors that could account for the higher incidence of esophageal cancer in areas of Asia and Africa (e.g., soil, tea, or food) have not been identified.

image Tobacco smoking is the major risk factor in the United States (increased risk: 10–20 times).

image Chronic alcohol abuse increases risk by 5 times.

image Barrett esophagus is a definite risk factor for adenocarcinoma (10–20 times).

image Preexisting esophageal disease increases the risk, but these diseases (e.g., achalasia) are rare.


24 Which part of the esophagus is most often affected by carcinoma?


Most esophageal carcinomas develop in the midportion or the lower third of the esophagus. The upper third of the esophagus is least commonly involved.



25 Describe the gross appearance of esophageal carcinoma


Esophageal carcinoma typically narrows the lumen of the esophagus or affects peristalsis, thus causing dysphagia. On gross examination, tumors may present as:


image Ulceration (most common)

image Polypoid outgrowth protruding into the lumen

image Induration of the wall, with concentric or excentric narrowing of the lumen

Tumor cells spread early through the lymphatics into adjacent mediastinal organs. Metastases are first found in the local lymph nodes.



26 How are esophageal carcinomas classified histologically?



image Squamous cell carcinoma: It accounts for 60% of all esophageal tumors in the United States, 90% in Africa and Asia.

image Adenocarcinoma: It accounts for 40% of all esophageal tumors in the United States. Adenocarcinomas develop in Barrett esophagus and are typically located in the lower segment of the esophagus and at the gastroesophageal junction.


STOMACH



27 What is the most important developmental disorder of the stomach?


Congenital hypertrophic pyloric stenosis affects 1 in 400 to 600 infants. The disease shows a multifactorial pattern of inheritance, but it may also be associated with chromosomal developmental disorders (e.g., Turner syndrome). Typically, it presents with projectile vomiting. It is caused by hypertrophy of the smooth muscle in the pyloric portion of the stomach, which may be palpated through the abdominal wall. Surgical incision provides relief and is routinely performed with excellent results.



28 What is gastritis?


Gastritis is an inflammation of the mucosa of the stomach. It is a common disease that may occur in an acute or a chronic form. Morphologically, acute gastritis typically presents with shallow erosions of the mucosa (erosive gastritis). Chronic gastritis may be erosive or nonerosive.



29 What are the most common causes of acute gastritis?


Acute erosive gastritis is a self-limited inflammation of the gastric mucosa. Clinically, it presents with epigastric burning, pain, nausea, and vomiting. Variable amounts of blood may be found in the vomitus. Pathologically it is characterized by shallow blood-suffused mucosal erosions surrounded by acute inflammatory cells. These mucosal changes may be caused by:


image Aspirin and nonsteroidal antiinflammatory drugs (NSAIDs)

image Alcohol

image Acid and alkali (e.g., suicidal ingestion)

image Stress

image Shock-related mucosal ischemia (e.g., in burns, brain trauma, and surgery)

image Sepsis (This is most often streptococcal sepsis, but other systemic infections may affect the stomach as well. Viral gastritis is found in immunosuppressed people.)

A mnemonic for the previous list is “3A + 3S”: aaacute ssstress)



30 Discuss why gastric erosions develop in acute gastritis


Erosions may develop because of the direct effects of a potentially toxic substance (e.g., alcohol), oversecretion or back-diffusion of hydrochloric acid, or a breakdown of the local mucosal defense system against the corrosive action of gastric juice. For example, hypoperfusion of the gastric mucosa in shock makes the mucosal cells more susceptible to the action of pepsin and hydrochloric acid. Aspirin and NSAIDs inhibit the local synthesis of prostaglandins and weaken the mucosal defense system.



Key Points: Stomach



1. Acute gastritis is caused by irritants and nonsteroidal antiinflammatory drugs, whereas chronic gastritis is most often caused by Helicobacter pylori.

2. Peptic ulcer, a multifactorial disease associated with H. pylori infection, is the most common cause of hematemesis.

3. Gastric carcinoma is an adenocarcinoma that occurs in several forms but always has a poor prognosis.


31 What are Cushing and Curling ulcers?


These eponyms are used for gastric stress ulcers. Such ulcers are deeper than erosions and may extend all the way to the muscularis mucosae. Cushing (who was a famous neurosurgeon) gave his name to ulcers caused by brain injury. Curling ulcers are found in burn patients. (An easy way to remember which is which is to think “things curl in fire.”)



32 Describe the main forms of chronic nonerosive gastritis


Chronic nonerosive gastritis is inflammation of the mucosa of the stomach that may be caused by immunologic mechanisms, infection, and prolonged ingestion of drugs or alcohol or cigarette smoking. Several clinicopathologic forms of chronic gastritis are recognized:


image Chronic type A gastritis (autoimmune gastritis)

image Chronic type B gastritis (Helicobacter pylori gastritis)

image Hypertrophic gastritis (Menetrier disease; in this rare form of gastritis, the gastric mucosa has giant folds.)

image Uncommon forms of gastritis (e.g., eosinophilic, lymphocytic, and granulomatous gastritis; these are rare, and diagnosis is made histologically.)


33 Is it possible to distinguish type A and type B chronic gastritis in biopsy material examined microscopically?


Type A is an autoimmune disease, whereas type B is an infectious disease caused by H. pylori. In early stages of the disease, it is possible to distinguish type A from type B gastritis histologically, but in advanced stages, such a distinction is not always possible.


In the early stages of autoimmune gastritis, the mucosa of the fundus and body is infiltrated with lymphocytes and plasma cells. Acute stages of H. pylori infection are associated with infiltrates of neutrophils in the glands and the lamina propria. H. pylori can be seen in the gastric glands, mostly in the pyloric antrum. As the diseases progress, both forms of chronic gastritis are accompanied by:


image Atrophy of gastric glands

image Intestinal metaplasia

image Lymphocytic follicles in the atrophic mucosa

In this advanced stage of the disease, it is difficult to find H. pylori, which does not survive in the metaplastic intestinal glands. Reliable histopathologic distinction of type A from type B chronic gastritis becomes impossible in the disease’s later stages.



34 Is it possible to clinically distinguish type A from type B chronic gastritis?


As stated previously, the histologic diagnosis of type B chronic gastritis depends primarily on finding H. pylori in the gastric biopsies. Because the gastroscopic findings are similar in both forms of gastritis and H. pylori cannot always be found in advanced stages of the disease, other tests (e.g., urea breath test or antibody test for H. pylori) must be performed. The most important aspects of type A and type B gastritis useful for distinguishing one form of gastritis from the other are listed in Table 12-1.


TABLE 12-1 Major Aspects of Type A And Type B Gastritis



















































Feature Type A Gastritis* Type B Gastritis
Distribution of lesions Fundus, diffuse Pyloric antrum, focal
Gastric secretion Reduced Normal, +, or −
Antibodies to parietal cells Yes No
Other autoimmune diseases Yes No
Vitamin B12 (in serum) Low Normal
Pernicious anemia + −
Gastrin (in serum) Increased Normal
Antibodies to Helicobacter pylori − +
Incidence Less common More common
Age dependence Yes Yes
Cancer risk Increased Increased

* Type A gastritis is associated with four As: autoimmune disease, antibodies to pyloric cells, anemia (pernicious), and achlorhydria (reduced hydrochloric acid secretion).



35 Which form of chronic gastritis is associated with a higher risk of cancer?


Type A gastritis is associated with a higher relative risk of gastric adenocarcinoma. However, because type B chronic gastritis is much more prevalent, it is thought to be the cause of many more cancers than type A gastritis. In this context, it is worth noting that the World Health Organization has designated H. pylori as a potential human carcinogen. Epidemiologic data link H. pylori to an increased incidence of gastric adenocarcinoma and lymphoma in many areas of the world, especially southern Europe, South America, and Asia.



36 Explain the pathogenesis of peptic ulcer


The pathogenesis of peptic ulcers is not fully understood. It is, however, generally accepted that the mucosal ulcerations are chemically mediated and develop because of the action of HCl and pepsin on a “weakened” or “susceptible” gastric or duodenal mucosa. Because the gastric acid of ulcer patients does not contain unusually high quantities of HCl or pepsin, it is postulated that the glands are damaged by a back-diffusion of hydrogen ions.



37 Which factors play a role in the development of peptic ulcers?


Peptic ulcer is a multifactorial disease, and several factors contribute to its pathogenesis:


image Infection: H. pylori is found in 90% of duodenal and 65% of gastric ulcer patients. H. pylori secretes urease, protease, and phospholipases that may cause mucosal injury and may serve as “barrier breakers,” facilitating the chemical injury of mucosal cells. Eradication of H. pylori infections contributes to the healing of peptic ulcers.

image Neuroendocrine factors: The secretion of gastric juices is under neuroendocrine control, which becomes dysregulated in peptic ulcer patients. Stress, nervous tension (type A personality), and endocrine disorders have been implicated in the pathogenesis of peptic ulcers, but the exact role of these putative insults is not known. For example, the hypersecretion of hormones such as corticosteroids and gastrin is associated with peptic ulcers in hormonal hypersecretion syndromes such as Cushing and Zollinger–Ellison syndromes, respectively. However, there is no definitive evidence that these hormones play a role in the pathogenesis of “garden variety” solitary peptic ulcers. Vagotomy (excision of the vagus nerve) is used only in the treatment of complicated persistent ulcers resistant to other treatment modalities.

image Local mucosal factors: Drugs such as NSAIDs reduce the secretion of prostaglandins and damage the mucosal barrier. Alcohol, spicy food, and substances that stimulate acid secretion may play a pathogenetic role. Antacid treatment and suppression of gastric acid with histamine-2 blockers promote healing of ulcers. There is no evidence that dietary modification is helpful in the treatment of peptic ulcer disease.


38 Where are peptic ulcers most often located?



image Ninety-eight percent of all peptic ulcers are located in the duodenum and stomach.

image Duodenal ulcers are more common than gastric ones (4:1) and are located in the proximal area just beyond the pylorus.

image Gastric ulcers are located on the lesser curvature, most often at the junction of the body and pyloric antrum.

image Most ulcers are solitary.

image In approximately 20% of cases, the ulcers are multiple, and both duodenum and stomach are involved.

image Rare locations for ulcers include the esophagus, the small intestine, and the Meckel diverticulum.

image Peptic ulcers in unusual locations, multiple ulcers, and ulcers that do not respond to the usual therapy are found in association with gastrin-secreting tumors (Zollinger–Ellison syndrome).


39 Describe the gross pathology of peptic ulcers



image On gross examination or gastroscopy, peptic ulcers present as a sharply demarcated round or oval defect of the mucosa.
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