Chapter 39. The Intestines: I. Structure & Function; Malabsorption Syndrome; Intestinal Obstruction

The intestine begins at the pylorus and ends at the anorectal junction. It is divided into the small and large intestine, which are separated by the ileocecal valve. The small intestine is composed of the duodenum, jejunum, and ileum and is about 6 meters long in adults; the large intestine is composed of the cecum, ascending, transverse, descending, and sigmoid colon and the rectum, totaling about 1.5 meters in length in adults.

The intestinal wall has four layers:

1.  Mucosa, which is lined by glandular epithelium. The small intestine is characterized by the presence of villi and crypts (Figure 39-1). The villi increase the surface area for absorption. The colonic mucosa has no villi and is composed only of crypts. The crypts contain proliferating cells that continually divide to replace lost surface epithelial cells.

2. Submucosa, which contains blood and lymphatic vessels and the submucosal nerve plexus.

3. Muscularis externa, which is composed of 2 layers in the small intestine. In the large intestine, the longitudinal muscle is attenuated to form the taenia coli. The muscle is responsible for propulsive peristalsis. The myenteric plexus of nerves is situated between the 2 muscle layers and provides the neural impetus to peristalsis.

4. Serosa, which is the peritoneal lining in those parts of the intestine that lie in the peritoneal cavity.

The intestine digests and absorbs essential components from ingested food, eliminating the waste at defecation. Digestion is effected in the upper small intestine by enzymes contained in the secretions of intestinal juice, pancreatic juice, and bile. The small molecules resulting from digestion—monosaccharides, amino acids, and fatty acids—are absorbed in the small intestine. The colon absorbs water from the liquid ileal effluent to form solid feces.

Malabsorption

See Malabsorption Syndrome.

Intestinal Obstruction

Mechanical obstruction may result from (1) lesions outside the intestine that compress or constrict the intestine, eg, fibrous adhesions in the peritoneal cavity and hernial sacs; (2) intramural lesions such as fibrous strictures and neoplasms; (3) volvulus of the intestine (see Volvulus); (4) intussusception (see Intussusception; and (5) intraluminal foreign bodies.

Failure of peristalsis may be the result of paralysis of the intestinal smooth muscle (paralytic ileus) or abnormalities of the myenteric plexus, eg, congenital megacolon (Hirschsprung's disease), or smooth muscle diseases, eg, familial visceral myopathy. Paralysis occurs after abdominal surgery, in patients with peritoneal inflammation, and in severe acute intestinal inflammation (eg, toxic megacolon).

Intestinal obstruction has the following physiologic consequences:

1. Failure of propulsive movement of intestinal contents, leading to constipation and absence of flatus.

2. Accumulation of food and fluid secretions in the intestine proximal ...