In achalasia, the LES doesn’t open properly to allow food to pass into the stomach and, in at least half of the patients with achalasia, the lower sphincter resting pressure also is abnormally high. The muscle of the lower half of the esophagus doesn’t contract normally, and peristaltic waves don’t occur. This results in food and saliva not being propelled down the esophagus and into the stomach.

Some patients with achalasia have high-pressure waves in the lower esophageal body following swallowing, but the waves aren’t effective in pushing food into the stomach. This type of achalasia is called vigorous achalasia. These abnormalities of the lower sphincter and esophageal body are responsible for food sticking in the esophagus.

Early in achalasia, inflammation occurs in the muscle of the lower esophagus, especially around the nerves. As the disease progresses, the nerves (particularly the nerves that cause the LES to relax) begin to degenerate and ultimately disappear. This damage to the nerves may cause muscle cells to begin to degenerate as well. These changes result in a lower sphincter that can’t relax and muscle in the lower esophageal body that can’t support peristaltic waves. With time, the body of the esophagus stretches and becomes dilated.

Mucosal ulceration triggers inflammation, which temporarily obstructs the appendix. The obstruction blocks mucus outflow. Pressure in the now distended appendix increases, and the appendix contracts. Bacteria multiply, and inflammation and pressure continue to increase, restricting blood flow to the organ and causing severe abdominal pain.

Inflammation may lead to infection, clotting, and tissue decay.

In acute cholecystitis, inflammation of the gallbladder wall usually develops after a gallstone lodges in the cystic duct. Gallstones typically develop when metabolism of cholesterol and bile salts is abnormal. The liver usually makes bile continuously, and the gallbladder stores it until it’s needed to help digest fat. Changes in the composition of bile may cause gallstones to form.

When gallstones block bile flow, the gallbladder becomes inflamed and distended. Growth of bacteria, usually Escherichia coli, may contribute to the inflammation and abscess formation or empyema.

Edema of the gallbladder (and sometimes the cystic duct) obstructs flow of bile, which chemically irritates the gallbladder. Cells in the gallbladder wall may become oxygen starved and die as the distended organ presses on vessels and impairs blood flow. The dead cells slough off, and an exudate covers ulcerated areas, causing the gallbladder to adhere to surrounding structures.

The initial event in cirrhosis is hepatic scarring or fibrosis. The scar begins as an increase in extracellular matrix components — fibrin-forming collagens, proteoglycans, fibronectin, and hyaluronic acid. Hepatocyte function is eventually impaired as the matrix changes. Fat-storing cells are believed to be the source of the extracellular changes. Contraction of these cells may also contribute to disruption of the lobular architecture and obstruction of the flow of blood or bile. Cellular changes producing bands of scar tissue also disrupt the lobular structure.

Colonic polyps are masses of tissue resulting from unrestrained cell growth in the upper epithelium that rise above the mucosal membrane and protrude into the GI tract.

Polyps may be described by their appearance: pedunculated (attached by a stalk to the intestinal wall) or sessile (attached to the wall with a broad base and no stalk).

Most lesions of the large bowel are moderately differentiated adenocarcinomas. These tumors tend to grow slowly and remain asymptomatic for long periods. Tumors in the sigmoid and descending colon grow circumferentially and constrict the intestinal lumen. At diagnosis, tumors in the ascending colon are usually large and are palpable on physical examination.

Whatever the cause of Crohn’s disease, inflammation spreads slowly and progressively. Enlarged lymph nodes block lymph flow in the submucosa. Lymphatic obstruction leads to edema, mucosal ulceration and fissures, abscesses, and sometimes granulomas. Mucosal ulcerations are called skipping lesions because they aren’t continuous, as in ulcerative colitis.

Oval, elevated patches of closely packed lymph follicles — called Peyer’s patches — develop in the lining of the small intestine. Subsequent fibrosis thickens the bowel wall and causes stenosis, or narrowing of the lumen. The serous membrane becomes inflamed (serositis), inflamed bowel loops adhere to other diseased or normal loops, and diseased bowel segments become interspersed with healthy ones. Finally, diseased parts of the bowel become thicker, narrower, and shorter.

Diverticula probably result from high intraluminal pressure on an area of weakness in the GI wall where blood vessels enter. Diet may be a contributing factor, because insufficient fiber reduces fecal residue, narrows the bowel lumen, and leads to high intra-abdominal pressure during defecation.

In diverticulitis, undigested food and bacteria accumulate in the diverticular sac. This hard mass cuts off the blood supply to the thin walls of the sac, making them more susceptible to attack by colonic bacteria.

Esophageal cancer includes two types of malignant tumors: squamous cell carcinoma and adenocarcinoma. Most esophageal cancers are poorly differentiated squamous cell carcinomas. Adenocarcinomas are less frequent and are contained to the lower third of the esophagus. Esophageal tumors are usually fungating and infiltrating, and they partially constrict the lumen of the esophagus.

Regional metastasis occurs early by way of submucosal lymphatics, often fatally invading adjacent vital primary organs.

According to gross appearance, gastric carcinoma can be classified as polypoid, ulcerating, ulcerating and infiltrating, or diffuse. The parts of the stomach affected by gastric carcinoma, listed in order of decreasing frequency, are the pylorus and antrum, the lesser curvature, the cardia, the body of the stomach, and the greater curvature. Gastric carcinoma infiltrates rapidly to regional lymph nodes, omentum, liver, lungs, and bone.