The hypermotility (spastic) disorders are characterized by high-amplitude, prolonged, or repetitive contractions. They include achalasia and several other conditions, particularly the diffuse esophageal spasm (Table 9.1).

Achalasia results from the degeneration of the inhibitory myenteric neurons in the body and the LES region. This leads to a hypertensive LES which relaxes poorly and also causes aperistalsis in the body of the esophagus. Patients usually present with dysphagia to liquids and solids.

Several other spastic disorders have been characterized in patients with noncardiac chest pain (Table 9.1). They all share a similar clinical presentation. Diffuse esophageal spasm (DES) is the most severe form. It is less common than achalasia. Some patients with DES progress to achalasia.

A number of systemic conditions are associated with esophageal hypomotility including scleroderma, diabetes mellitus, and amyloidosis. These disorders are characterized by low or absent contractions. The most clinically relevant condition is scleroderma.

Scleroderma (progressive systemic sclerosis) is a multisystem connective tissue disorder that affects the skin and internal organs, especially the vascular system, gastrointestinal tract, lungs, heart, and kidneys. It is more common in women than in men and appears at any age under 50 years. Esophageal involvement occurs in 70–80 % of patients. Histopathological findings include smooth muscle atrophy and fibrosis. The end result is impaired muscle contractions in the distal esophagus and incompetence of the LES. Therefore, 50 % of patients with scleroderma-associated dysmotility complain of heartburn and/or dysphagia due to gastroesophageal reflux.

Protein-losing enteropathy is a condition in which excess protein loss into the gastrointestinal lumen is severe enough to produce hypoproteinemia. It occurs with many of the previously listed conditions causing malabsorption. Furthermore, diseases such as constrictive pericarditis, congestive heart failure, intestinal lymphangiectasia, nephrotic syndrome, and systemic lupus erythematosus may also cause protein loss from the gastrointestinal tract without any observable mucosal lesions in the bowel. The mechanism of the loss of plasma protein into the gastrointestinal tract in these diseases is not fully understood [20].

Vitamin B₁₂ deficiency due to pure dietary inadequacy of this vitamin is very rare and occurs mainly in strict vegetarians. More often gastrointestinal disorders, atrophic gastritis, pernicious anemia, congenital lack or abnormality of gastric IF, and total or partial gastrectomy cause malabsorption and consequent deficiency of this vitamin. Diseases involving the distal ileum such as Crohn’s disease, intestinal stagnant loop syndrome, and rarely congenital selective ileal malabsorption with proteinuria (Imerslund-Grasbeck syndrome) may also result in malabsorption of vitamin B₁₂.

Inflammatory bowel disease (IBD) refers to two disorders: Crohn’s disease (CD) and ulcerative colitis (UC). Both conditions are characterized by chronic relapsing intestinal inflammation. UC affects the colon only, and the inflammation is limited to the mucosa and submucosa in most cases. CD can affect the entire gastrointestinal tract from mouth to anus. The inflammation in CD is granulomatous and transmural. Besides inflammation of the gut, IBD is associated with a number of systemic manifestations including anterior uveitis, axial and peripheral arthropathy, primary sclerosing cholangitis, erythema nodosum, and pyoderma gangrenosum.

The etiology of IBD is unknown. However, many of the immunological and molecular mechanisms that mediate inflammation have been elucidated in recent years. Genetic predisposition, mucosal immune dysregulation, and environmental agents seem to play a role (Table 9.6). In genetically predisposed individuals, environmental factors can participate in the disease by inducing a broad immunological response characterized by an imbalance between anti-inflammatory mediators.

CD consists of segmental involvement by a nonspecific granulomatous inflammatory process involving all layers of the bowel with skip areas. The disease involves the small bowel in addition to the colon, and rectal sparing is typical. Less commonly it involves the mouth, tongue, esophagus, stomach, and duodenum.

The primary pathophysiological change of UC is inflammation of the mucosa and the submucosa and formation of crypt abscesses and mucosal ulceration with skip areas. The small intestine is essentially not involved [21, 22].

The appendix is a diverticulum of an average of 10 cm in adults arising from the posteromedial wall of the cecum. This fact accounts for its variable positions (retrocecal, subcecal, retroileal, pre-ileal, or pelvic) and behind much of the diversity in clinical presentations among patients with acute appendicitis [23].

The pathophysiology of appendicitis begins with obstruction of the narrow appendiceal lumen by causes, including fecaliths, lymphoid hyperplasia (related to viral illnesses such as upper respiratory infections, mononucleosis, or gastroenteritis), gastrointestinal parasites, foreign bodies, and Crohn’s disease. Continued secretion of mucus results in elevated intraluminal pressure, leading to tissue ischemia, overgrowth of bacteria, transmural inflammation, appendiceal infarction, and possible perforation. Inflammation may subsequently extend into the parietal peritoneum and adjacent structures causing abdominal abscesses.

Acute appendicitis is the most common reason for emergency abdominal surgery and must be differentiated from other causes of abdominal pain. The overall diagnostic accuracy achieved by medical history, physical examination, and laboratory tests has been approximately 80 % as the presentation may be atypical. In atypical cases, ultrasonography and computed tomography (CT) may help lower the rate of unnecessary surgeries. The accuracy rates for ultrasonography range from 71 to 97 % and the modality is highly operator dependent and difficult in patients with a large body habitus. The accuracy rate of CT scanning is between 93 and 98 %. However, there is controversy regarding the use of contrast media [23].

Incidence of colorectal cancer is highest in developed countries such as the United States and Japan and lowest in developing countries in Africa and Asia. It is the third most common type of cancer in both men and women in the United States. Pathologically most (over 95 %) of colorectal cancers are adenocarcinomas. Surgery, chemotherapy, radiation therapy, and immunotherapy are the lines of treatment. Nuclear medicine has an important role in the follow-up to detect recurrence. FDG PET has an important role as it is more sensitive than computed tomography for the detection of metastatic or recurrent disease and may improve clinical management in more than 25 % of cases [24]. It is of particular importance to differentiate post-therapy fibrosis and inflammation from viable tumor in presacral region.

The localization of the specific bleeding site in patients presenting with acute GI bleeding remains a serious clinical problem. Acute gastrointestinal bleeding (GIB) can be divided into bleeding in the upper (proximal to the ligament of Treitz) or lower tract. If acute upper GIB is a possibility, lavage with a nasogastric tube should identify acute or subacute bleeding. Endoscopy will localize 80–97 % cases of acute upper bleeding; of these 75 % will resolve spontaneously or with conservative medical therapy and 10 % will require surgery. Because of the length and tortuosity of the colon and contamination of fecal matter and blood, endoscopy is not that successful in lower GIB cases. Peptic ulcers are the most common cause of upper GIB; other causes include gastritis, esophageal varices, Mallory-Weiss tear, esophagitis with or without hiatal hernia, and carcinoma [25]. The three leading causes of lower GIB are diverticular disease, angiodysplasia, and colorectal cancer. Other causes include inflammatory bowel disease, ischemic colitis, infectious colitis, and anorectal disease. This bleeding usually resolves spontaneously in 80 % of cases and rebleeds in 25 %. Angiodysplasias account for 20 % of significant lower GIB and tend to rebleed.

Meckel’s diverticulum is a vestige of the omphalomesenteric duct that is present in about 2 % of the population with two thirds younger than 2 years. It is an outpouch usually found on the antimesenteric border of the ileum, 50–80 cm proximal to the ileocecal valve. Ectopic gastric mucosa is present in about 30 % of cases. Nearly all diverticula responsible for rectal bleeding contain ectopic gastric mucosa. Bleeding, which is usually massive and painless, may result from ileal mucosal ulceration due to acid secretion.

Patients with lower GIB should be stabilized and supported while diagnostic studies are performed. Scintigraphy has emerged as the imaging modality of first choice for localizing bleeding sites in the lower gastrointestinal tract. It is more sensitive for slow or intermittent bleeding, which is a common occurrence. If the scan is positive, arteriography can be employed to deliver vasopressin or embolic agents selectively into the bleeding artery.