Digestive system pathology

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Achalasia Is a functional (motor disorder) obstruction of the distal section of the esophagus with proximal dilation caused by incomplete relaxation of the lower esophageal sphincter (little or no peristalsis occurs). It occurs equally in men and women and most commonly affects individuals between the ages of 20 and 40. Clinically, these patients present with a slowly progressive dysphagia in swallowing both solids and liquids. Patients may also experience regurgitation, chest pain, and moderate weight loss. It is related to insufficient or absence of ganglion cells in the muscular coat of the distal esophageal wall. The radiographic appearance of achalasia, seen on barium studies, is a gradually tapered, smooth, conical, 1- to 3-cm narrowing of the distal esophageal segment (“rat-tail” or “beak” appearance). On sequential radiographs, especially with the patient upright, only small spurts of barium pass through the narrowed distal segment to enter the stomach. Because the esophageal contents act as a water seal, the normal gastric gas bubble may be absent.

Carcinoma of Stomach Is rarely noted until the disease is far advanced because pain is infrequently an early symptom and thus has a dismal prognosis (survival rate, 10%). There is an increased risk of gastric cancer in patients with pernicious anemia, and in persons who have had a partial gastrectomy for peptic ulcer disease 10 to 20 years post surgery. Most carcinomas occur in the distal stomach. Carcinoma of the stomach may appear as thickening of the gastric wall or as an intraluminal mass. CT is of major value in the staging of gastric carcinoma, in planning its treatment, in assessing the response to therapy, and in detecting tumor recurrence. CT can demonstrate direct tumor extension to intra-abdominal organs, and distant metastases, especially to the liver. In most cases, treatment consists of surgical resection of all or part of the stomach.

Cholelithiasis Also known as gallstones. Gallstones consist of two major types: cholesterol stones and pigment stones. Genetic predispositions associated with higher incidence include family history of the disorder; age over 40 years, and female sex. Their occurrence is also greater in people with diabetes, the obese, the elderly, and individuals who eat primarily a diet high in saturated fat, sugar, and sodium and low in fiber and nutrient density (Western diet).

Gallstones can develop whenever bile contains insufficient bile salts and lecithin in proportion to cholesterol to maintain the cholesterol in solution. Oral cholecystography (OCG) was the traditional technique for the diagnosis of gallstones. Today it has been replaced in most institutions by ultrasound Because cholesterol is not radiopaque, most gallstones are radiolucent and visible only on contrast examinations or ultrasound. In up to 20% of patients, however, gallstones contain sufficient calcium to be detectable on plain abdominal radiographs. Gallstones appear as freely movable filling defects in the opacified gallbladder. Solitary gallstones are usually rounded; multiple stones are generally faceted. Large numbers of stones can have a sandlike or gravel-like consistency and be visible only when they layer out on radiographs obtained using a horizontal beam and with the patient in an erect or lateral decubitus position. Treatment may include an ERCP or a laparoscopic cholecystectomy. If additional stones are suspected but not visualized, a T-tube may be inserted to allow for a later follow up contrast study.

Clostridium Difficile Also known C difficile or C diff. Is a bacterium that causes diarrhea and more serious intestinal conditions such as colitis. It is a nosocomial infection that is very common in the hospital environment. It is especially difficult to control because it is a spore-forming bacterium that is not eliminated by the usual routine methods of asepsis. Patients receiving antibiotic therapy are particularly susceptible to developing this infection because antibiotics tend to upset the normal balance of intestinal flora. About 20% of hospital patients receiving antibiotics develop C. difficile infections. Treatment is usually quite successful, but about 20% of treated patients relapse, sometimes developing a chronically recurring disease. C Difficile is transmitted via direct contact (enteric isolation precautions – gown, glove).

 

Crohn’s Disease Also known as Regional Enteritis, it is a chronic disease characterized by periods of exacerbation interspersed with periods of inactivity. It is an inflammatory disease of unknown cause. This disease typically affects young adults of both sexes between the ages of 14 and 24 years, with symptoms suggestive of appendicitis or acute bowel obstruction. Crohn’s disease typically occurs in the lower ileum (terminal ileum) but may be seen anywhere throughout the bowel. Most cases involve both the ileum and cecum (45%); however, it may be present in the ileum only (35%) or in the colon only (20%), and in rare cases it may affect the entire small bowel. Affected individuals have a genetic predisposition toward an unregulated intestinal immune response to various agents such as food or environmental factors that result in inflammation and abscesses, leading to the development of small ulcers. It eventually affects all layers of the bowel wall. The bowel wall thickens in response to the inflammation and may form fistulas to adjacent loops of bowel, skin, or other abdominal viscera. Subsequent fibrotic scarring may give rise to mechanical obstruction of the bowel. The combination of mucosal edema and crisscrossing fine ulcerations gives the bowel a “cobblestone” radiographic appearance. The “string sign” is demonstrated where the terminal ileum is so diseased and stenotic that the barium mixture can only trickle through a small opening that looks like a string. Presentation of the disease in two or more areas with normal intervening bowel between is identified as “skip areas”, thus the designation “regional” enteritis. These patients tend to have an increased chance of developing carcinoma of the bowel with a very poor prognosis. The progression of the disease can be demonstrated radiographically by performing a small-bowel series or enteroclysis (small bowel enema).

Dysphagia Means difficulty swallowing. Esophageal dysphagia is almost always caused by disease in or adjacent to the esophagus but occasionally the lesion is in the pharynx or stomach. Swallowing disorders can occur in all age groups, resulting from congenital abnormalities, structural damage, and/or medical conditions. The incidence of dysphagia is higher in the elderly, in patients who have had strokes and patients with head and neck cancer. Causes of esophageal dysphagia can be divided into mechanical and functional causes. Functional causes include achalasia, and myasthenia gravis. Common mechanical causes include peptic esophagitis, carcinoma of the esophagus or gastric cardia and causes due to external compression of the esophagus. In many of the pathological conditions causing dysphagia, the lumen becomes progressively narrowed and indistensible. Initially only fibrous solids cause difficulty but later the problem extends to all solids and later even to liquids.

Esophageal Diverticula Esophageal diverticula (outpouchings) are common lesions that either contain all layers of the wall (traction or true diverticula) or are composed of only mucosa and submucosa herniating through the muscular layer (pulsion or false diverticula). Small diverticula do not retain food or secretions and are asymptomatic. When the diverticulum fills with food or secretions, aspiration pneumonia may result. Zenker‘s diverticula arise from the posterior wall of the upper esophagus at the pharyngoesophageal junction. Occasionally, they can become so large that they almost occlude the esophageal lumen. Diverticula do not require treatment unless they interfere with swallowing. In Zenker’s diverticulum, surgery consists of excision of the diverticulum and correction of any motility issues.

Hemorrhoids Hemorrhoids are varicose veins of the lower end of the rectum that cause pain, itching, and bleeding. Hemorrhoids are caused by increased venous pressure. The most common cause of increased pressure is chronic constipation with resulting excessive muscular straining needed to empty the bowel. Increased venous pressure can also be produced by a pelvic tumor or a pregnant uterus. On barium enema examinations, hemorrhoids occasionally can produce single or multiple rectal filling defects that simulate polyps.

Hypertrophic Pyloric Stenosis Is a congenital anomaly of the stomach in which the pyloric canal is greatly narrowed because of hypertrophy of the pyloric sphincter. It is the most common indication for surgery in infants. Its exact cause is unknown, but it seems genetically related. Researchers believe the nerves within the muscular layer are not functioning properly, and studies have shown that infants exposed to erythromycin within the first few weeks of life are at a higher risk for developing this anomaly. It occurs four times more often in male children and most often in the first-born boy. Typically, the first sign of the condition is projectile vomiting at 2 to 6 weeks of age. Affected infants often become dehydrated and fail to gain weight. Abdominal ultrasound is useful in evaluating hypertrophy of the pyloric muscle. An upper GI study demonstrates delayed gastric emptying accompanied by a classic “string sign” as the barium trickles through the narrowed, elongated pyloric canal.

Imperforate Anus Is a congenital disorder in which there is no anal opening to the exterior; the rectal pouch ends blindly above the surface of the perineum. An anal fistula is present in 80% to 90% of cases. A fistula may be present between the colon and the perineum or urethra in boys or between the colon and vagina in girls. This condition can be demonstrated radiographically with a cross-table lateral rectum projection with the patient lying prone or by performing a fistulogram. It is corrected surgically shortly after birth and may require a temporary colostomy.

Megacolon Also known as Hirschsprung’s disease. It is caused by an absence of neurons in the bowel wall, typically in the sigmoid colon. The absence of neurons in the bowel wall prevents the normal relaxation of the colon and subsequent peristalsis, which results in gross dilatation to the point of narrowing and constriction. It is a congenital disorder occurring in approximately one in 5000 births, is a familial disease, primarily affecting men. This disorder becomes apparent shortly after birth, when the affected infant passes little meconium and the abdomen becomes distended. As the patient ages, the continued effects are severe constipation and recurrent fecal impactions. It is important to diagnose this disease early because, if left untreated, it can progress to toxic megacolon. Toxic megacolon develops from bacterial overgrowth leading to fluid and electrolyte imbalances in the infant that could result in death. When performing contrast studies on patients with megacolon, an aqueous iodinated contrast medium should be used instead of barium. Whenever the colon is enlarged, the increased area of the mucosal lining provides greater opportunity for rapid, excessive absorption of water from the barium suspension. This predisposes these patients to barium impactions.

Peptic Ulcer Disease Peptic ulcer disease is a group of inflammatory processes involving the stomach and duodenum. It is caused by the action of acid and the enzyme pepsin secreted by the stomach and occurs most frequently on the lesser curvature. The range of peptic ulcer disease varies from small and shallow superficial erosions to huge ulcers that may perforate through the bowel wall. The major complications of peptic ulcer disease are hemorrhage, gastric outlet obstruction, and perforation. Peptic ulcer disease is the most common cause of acute upper gastrointestinal bleeding. Free perforation of a peptic ulcer located in the anterior wall of the stomach or duodenum is the most common cause of pneumoperitoneum with peritonitis. Narrowing of the lumen of the distal stomach or duodenal bulb caused by peptic ulcer disease is by far the most common cause of gastric outlet obstruction. Duodenal ulcer is the most common manifestation of peptic ulcer disease. More than 95% of duodenal ulcers occur in the first portion of the duodenum (the duodenal bulb). Radiographically, an active duodenal ulcer demonstrates an ulcer crater, which appears in profile as a small collection of barium projecting from the lumen. When seen face on, the ulcer hollow appears as a rounded or linear collection of contrast material surrounded by lucent folds that often radiate toward the crater . Secondary signs of duodenal ulcer disease include thickening of the mucosal folds and a deformity of the duodenal bulb. Symmetric narrowing of the duodenal bulb in its midportion may produce the typical “cloverleaf” deformity of chronic duodenal ulcer disease. Gastric ulcers usually occur on the lesser curvature of the stomach. Unlike duodenal ulcers, which are virtually always benign, up to 5% of gastric ulcers are malignant.

Tracheoesophageal Fistula There are 2 categories: congenital and acquired. Congenital tracheoesophageal (TE) fistulas result from the failure of a satisfactory esophageal lumen to develop completely separate from the trachea. Esophageal atresia and TE fistulas are often associated with other congenital malformations involving the skeleton, cardiovascular system, and gastrointestinal tract.  There are 4 types of congenital fistulas:

Type I, both the upper and lower segments of the esophagus are blind pouches (this type is 2nd most frequent)

Type II the upper esophageal segment communicates with the trachea, whereas the lower segment ends in a blind pouch. Because there is no connection between the trachea and the stomach, there is no radiographic evidence of gas within the abdomen. Oral administration of contrast material in this condition immediately outlines the tracheobronchial tree.

Type III lesion (the most common type) consists of an upper segment that ends in a blind pouch at the level of the bifurcation of the trachea or slightly above it, and a lower segment attached to the trachea by a short fistulous tract. Plain radiographs of the abdomen demonstrate the presence of air in the bowel that has freely entered the stomach through the fistulous connection between the trachea and the distal esophagus.

Type IV There are two forms of type IV TE fistula. In one, the upper and lower esophageal segments end in blind pouches, both of which are connected to the tracheobronchial tree. In this form, gas is seen in the stomach, and oral contrast material outlines both fistulas and the bronchial tree. In the other form of type IV fistula (called an H fistula), both the trachea and the esophagus are intact. These two structures are connected by a single fistulous tract that can be found at any level from the cricoid cartilage of the trachea to the tracheal bifurcation. Unlike the other forms of TE fistula, the H fistula may not be identified in infancy and, if it is small and only occasionally causes emptying of material into the lungs, can permit survival into adulthood. Immediate surgical repair will prevent the infant from dying of starvation. If a fistula exists, delayed surgical repair may result in aspiration pneumonia.

About 50% of acquired fistulas between the trachea and esophagus are caused by malignancy in the mediastinum. Almost all the rest result from infectious processes or trauma. Fistulous communications between the esophagus and the tracheobronchial tree can be the result of esophageal instrumentation and perforation. This is most common after esophagoscopy, but may also occur after or even the insertion of a nasogastric tube. Blunt or penetrating trauma to the chest, especially after crush injury, can result in esophageal perforation and fistulization. After traumatic perforation of the thoracic esophagus, chest radiographs may demonstrate air dissecting within the mediastinum and soft tissue, often with pleural effusion or hydropneumothorax. The introduction of an oral contrast agent may demonstrate the site of perforation and the extent of fistulization. Gastrograffin™ should not be administered to a patient when querying a fistula due to the possibility of it leaking into the lungs causing serious pulmonary complications.

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