BASIC SCIENCE QUESTIONS
1. Calcium is primarily absorbed in the
Calcium is absorbed through both transcellular transport and paracellular diffusion. The duodenum is the major site for transcellular transport; paracellular transport occurs throughout the small intestine. A key step in transcellular calcium transport is mediated by calbindin, a calcium-binding protein located in the cytoplasm of enterocytes. Regulation of calbindin synthesis is the principal mechanism by which vitamin D regulates intestinal calcium absorption. (See Schwartz 9th ed., p 985.)
2. Which of the following distinguishes jejunum from ileum?
A. Less prominent plica circularis
B. Smaller diameter
C. Thinner wall
D. Longer vasa recta
No distinct anatomic landmark demarcates the jejunum from the ileum; the proximal 40% of the jejunoileal segment is arbitrarily defined as the jejunum and the distal 60% as the ileum. The ileum is demarcated from the cecum by the ileocecal valve. The small intestine contains mucosal folds known as plicae circulares or valvulae conniventes that are visible upon gross inspection. These folds are also visible radiographically and help in the distinction between small intestine and colon, which does not contain them, on abdominal radiographs. These folds are more prominent in the proximal intestine than in the distal small intestine. Other features evident on gross inspection that are more characteristic of the proximal than distal small intestine include a larger circumference, thicker wall, less fatty mesentery, and longer vasa recta (Fig. 28-1). (See Schwartz 9th ed., p 980.)
FIG. 28-1. Gross features of jejunum contrasted with those of ileum. Relative to the ileum, the jejunum has a larger diameter, thicker wall, more prominent plicae circulares, a less fatty mesentery, and longer vasa recta.
3. There are four cell types which originate in the crypts of the small bowel mucosa. Which one of these cell types completes differentiation in the crypt instead of during migration to the villus?
B. Goblet cell
C. Enteroendocrine cell
D. Paneth cell
Intestinal, epithelial cellular proliferation is confined to the crypts, each of which carries an average census of 250 to 300 cells. All epithelial cells in each crypt are derived from an unknown number of the yet uncharacterized multipotent stem cells located at or near the crypt’s base. Their immediate descendants are amplified by undergoing several cycles of rapid division. These descendants then make a commitment to differentiate along one of four pathways that ultimately yield enterocytes and goblet, enteroendocrine, and Paneth cells. With the exception of Paneth cells, these lineages complete their terminal differentiation during an upward migration from each crypt to adjacent villi.
Paneth cells are located at the base of the crypt and contain secretory granules containing growth factors, digestive enzymes, and antimicrobial peptides. (See Schwartz 9th ed., p 981.)
4. The first hormone discovered in the human body was
C. Vasoactive intestinal peptide
Endocrinology as a discipline was born with the discovery of secretin, an intestinal regulatory peptide that was the first hormone to be identified. The small intestine is now recognized to be the largest hormone-producing organ in the body, both with respect to the number of hormone-producing cells and the number of individual hormones produced. Over 30 peptide hormone genes have been identified as being expressed in the GI tract. (See Schwartz 9th ed., p 987.)
5. Somatostatin causes
A. Stimulation of intestinal secretion
B. Stimulation of intestinal motility
C. Inhibition of splanchnic perfusion
D. Stimulation of intestinal mucosal growth
(See Schwartz 9th ed., p 987, and Table 28-1.)
TABLE 28-1 Representative regulatory peptides produced in the small intestine
6. The total volume of fluid secreted daily by the salivary glands, stomach, liver, and pancreas in a normal adult is approximately
A. 2 liters
B. 4 liters
C. 6 liters
D. 8 liters
(See Schwartz 9th ed., p 983, and Fig. 28-2.)
FIG. 28-2. Small intestinal fluid fluxes. Typical quantities (in volume per day) of fluid entering and leaving the small intestinal lumen in a healthy adult are shown.
7. Mutation in the NOD2 gene is associated with an increased risk of
A. Crohn’s disease
C. Adenocarcinoma of the small bowel
Specific genetic defects associated with Crohn’s disease in human patients are beginning to be defined. For example, the presence of a locus on chromosome 16 (the so-called IBD1 locus) has been linked to Crohn’s disease. The IBD1 locus has been identified as the NOD2 gene. Persons with allelic variants on both chromosomes have a 40-fold relative risk of Crohn’s disease compared to those without variant NOD2 genes. The relevance of this gene to the pathogenesis of Crohn’s disease is biologically plausible, as the protein product of the NOD2 gene mediates the innate immune response to microbial pathogens. Other putative IBD loci have been identified on other chromosomes (IBD2 on chromosome 12q, and IBD3 on chromosome 6), and are under investigation. (See Schwartz 9th ed., p 994.)
8. Which of the following statements about gut-associated lymphoid tissue (GALT) is NOT true?
A. GALT contains approximately 20% of the body’s immune cells
B. Peyer’s patches are part of the GALT and function as an inductive site (to process foreign antigens)
C. IgA is produced by plasma cells in the lamina propria of the small bowel
D. IgA dimmers bound to secretory components are resistant to degradation in the lumen of the gut by proteolytic enzymes
The intestinal component of the immune system, known as the gut-associated lymphoid tissue (GALT), contains over 70% of the body’s immune cells. The GALT is conceptually divided into inductive and effector sites. Inductive sites include Peyer’s patches, mesenteric lymph nodes, and smaller isolated lymphoid follicles scattered throughout the small intestine (Fig. 28-3).
Effector lymphocytes are distributed into distinct compartments. IgA-producing plasma cells are derived from B cells and are located in the lamina propria. CD4+ T cells are also located in the lamina propria. CD8+ T cells migrate preferentially to the epithelium, but are also found in the lamina propria. These T cells are central to immune regulation; in addition the CD8+ T cells have potent cytotoxic T lymphocyte activity. IgA is transported through the intestinal epithelial cells into the lumen, where it exists in the form of a dimer complexed with a secretory component. This configuration renders IgA resistant to proteolysis by digestive enzymes. IgA is believed to both help prevent the entry of microbes through the epithelium and to promote excretion of antigens or microbes that have already penetrated into the lamina propria. (See Schwartz 9th ed., pp 985, 986.)
FIG. 28-3. Gut-associated lymphoid tissue. Select components of the gut-associated lymphoid tissue are schematically represented. Peyer’s patches consist of a specialized follicle-associated epithelium (FAE) containing M cells, a subepithelial dome (SED) rich in dendritic cells (DC), and B-cell follicle containing germinal centers (GC). Plasma cells in the lamina propria produce immunoglobulin A (IgA), which is transported to the intestinal lumen where it serves as the first line of defense against pathogens. Other components of the gut-associated lymphoid tissue include isolated lymphoid follicles, mesenteric lymph nodes, and regulatory and effector lymphocytes. B = B cell; T = T cell.
9. The digestion of proteins in healthy individuals is initiated by
Protein digestion begins in the stomach with action of pepsins. This is not, however, an essential step, because surgical patients who are achlorhydric, or have lost part or all of their stomach, are still able to successfully digest proteins. Digestion continues in the duodenum with the actions of a variety of pancreatic peptidases. These enzymes are secreted as inactive proenzymes. This is in contrast to pancreatic amylase and lipase, which are secreted in their active forms. In response to the presence of bile acids, enter-okinase is liberated from the intestinal brush border membrane to catalyze the conversion of trypsinogen to active trypsin. (See Schwartz 9th ed., p 984, and Fig. 28-4.)
FIG. 28-4. Protein digestion. Dietary proteins must undergo hydrolysis into constituent single amino acids and di- and tripeptides before being absorbed by the intestinal epithelium. These hydrolytic reactions are catalyzed by pancreatic peptidases (e.g., trypsin) and by enterocyte brush border peptidases.
10. Contraction of the inner circular layer of the bowel wall
A. Shortens the bowel
B. Narrows the bowel lumen
C. Promotes villus motility but doesn’t affect peristalsis
D. Promotes mixing of the luminal contents but doesn’t affect peristalsis
Contraction of the outer longitudinal muscle layer results in bowel shortening; contraction of the inner circular layer results in luminal narrowing. Contractions of the muscularis mucosa contribute to mucosal or villus motility, but not to peristalsis. (See Schwartz 9th ed., p 986.)
11. Which of the following is an excitatory transmitter for small bowel motility?
A. Nitric oxide
B. Vasoactive intestinal peptide
C. Adenosine triphosphate
This intrinsic contractile mechanism is subject to neural and hormonal regulation. The enteric motor system (ENS) provides both inhibitory and excitatory stimuli. The predominant excitatory transmitters are acetylcholine and substance P, and the inhibitory transmitters include nitric oxide, vasoactive intestinal peptide, and adenosine triphosphate. In general, the sympathetic motor supply is inhibitory to the ENS; therefore, increased sympathetic input into the intestine leads to decreased intestinal smooth muscle activity. The parasympathetic motor supply is more complex, with projections to both inhibitory and excitatory ENS motor neurons. Correspondingly, the effects of parasympathetic inputs into intestinal motility are more difficult to predict. (See Schwartz 9th ed., pp 986, 987.)
12. Which cells are responsible for generating the basic rhythm of peristalsis in the bowel?
A. Paneth cells
B. Cells of Cajal
C. Ganglion cells in Auerbach’s plexus
D. Ganglion cells in Meissner’s plexus
The interstitial cells of Cajal are pleomorphic mesenchymal cells located within the muscularis propria of the intestine that generate the electrical slow wave (basic electrical rhythm or pacesetter potential) that plays a pacemaker role in setting the fundamental rhythmicity of small intestinal contractions. (See Schwartz 9th ed., p 986.)
13. Which of the following is the most prevalent fat consumed in a Western diet?
A. Long-chain triglycerides
B. Medium-chain triglycerides
C. Short-chain triglycerides
Approximately 40% of the average Western diet consists of fat. Over 95% of dietary fat is in the form of long-chain triglycerides; the remainder includes phospholipids such as lecithin, fatty acids, cholesterol, and fat-soluble vitamins. Over 94% of the ingested fats are absorbed in the proximal jejunum. (See Schwartz 9th ed., p 985.)
14. Which of the following is the origin of the epithelium of the small bowel?
D. Neural crest
The first recognizable precursor of the small intestine is the embryonic gut tube, formed from the endoderm during the fourth week of gestation. The gut tube is divided into foregut, midgut, and hindgut. Other than duodenum, which is a foregut structure, the rest of the small intestine is derived from the midgut. The gut tube initially communicates with the yolk sac; however, the communication between these two structures narrows by the sixth week to form the vitelline duct. The yolk sac and vitelline duct usually undergo obliteration by the end of gestation. Incomplete obliteration of the vitelline duct results in the spectrum of defects associated with Meckel’s diverticula. (See Schwartz 9th ed., p 981.)
15. Digestion of dietary starches is initiated by
D. Brush border hydrolases
Pancreatic amylase is the major enzyme of starch digestion, although salivary amylase initiates the process. The terminal products of amylase-mediated starch digestion are oligosaccharides, maltotriose, maltose, and alpha-limit dextrins (Fig. 28-5). (See Schwartz 9th ed., p 983.)
FIG. 28-5. Carbohydrate digestion. Dietary carbohydrates, including starch and the disaccharides sucrose and lactose, must undergo hydrolysis into constituent monosaccharides glucose, galactose, and fructose before being absorbed by the intestinal epithelium. These hydrolytic reactions are catalyzed by salivary and pancreatic amylase and by enterocyte brush border hydrolases.
16. Meissner’s plexus is located in which layer of the bowel wall?
The submucosa consists of dense connective tissue and a heterogeneous population of cells, including leukocytes and fibroblasts. The submucosa also contains an extensive network of vascular and lymphatic vessels, nerve fibers, and ganglion cells of the submucosal (Meissner’s) plexus. The muscularis propria consists of an outer, longitudinally oriented layer and an inner, circularly oriented layer of smooth muscle fibers. Located at the interface between these two layers are ganglion cells of the myenteric (Auerbach’s) plexus. (See Schwartz 9th ed., p 981.)
1. Which of the following decreases absorption of intraluminal water in the small bowel?
Dopamine, somatostatin, and glucosteroids all increase the absorption of water from the small bowel. Vasopressin decreases absorption of water. (See Schwartz 9th ed., p 983, and Table 28-2.)
TABLE 28-2 Regulation of intestinal absorption and secretion
Agents that stimulate absorption or inhibit secretion of water
Agents that simulate secretion or inhibit absorption of water
Atrial natriuretic factor
Vasoactive intestinal peptide
2. What is the approximate clinical recurrence rate (return of symptoms) 5 years after surgery for Crohn’s disease?
Most patients whose disease is resected eventually develop recurrence. If recurrence is defined endoscopically, 70% recur within 1 year of a bowel resection and 85% by 3 years. Clinical recurrence, defined as the return of symptoms confirmed as being due to Crohn’s disease, affects 60% of patients by 5 years and 94% by 15 years after intestinal resection. Reoperation becomes necessary in approximately one third of patients by 5 years after the initial operation, with a median time to reoperation of 7 to 10 years. (See Schwartz 9th ed., p 997.)
3. Which of the following is NOT a known cause of chronic intestinal pseudo-obstruction?
B. Parkinson’s disease
D. Familial visceral myopathy (type I)
Chronic intestinal pseudo-obstruction can be caused by a large number of specific abnormalities affecting intestinal smooth muscle, the myenteric plexus, or the extraintestinal nervous system (Table 28-3). Visceral myopathies constitute a group of diseases characterized by degeneration and fibrosis of the intestinal muscularis propria. Visceral neuropathies encompass a variety of degenerative disorders of the myenteric and submucosal plexuses. Both sporadic and familial forms of visceral myopathies and neuropathies exist. Systemic disorders involving the smooth muscle, such as progressive systemic sclerosis and progressive muscular dystrophy, and neurologic diseases such as Parkinson’s disease also can be complicated by chronic intestinal pseudo-obstruction. In addition, viral infections such as those associated with cytomegalovirus (CMV) and Epstein-Barr virus can cause intestinal pseudo-obstruction. (See Schwartz 9th ed., p 992.)
TABLE 28-3 Chronic intestinal pseudo-obstruction: Etiologies
Familial visceral myopathies (types I, II, and III)
Familial visceral neuropathies (types I and II)
Childhood visceral myopathies (types I and II)
Smooth muscle disorders
Collagen vascular diseases (e.g., scleroderma)
Muscular dystrophies (e.g., myotonic dystrophy)
Chagas’ disease, Parkinson’s disease, spinal cord injury
Diabetes, hypothyroidism, hypoparathyroidism
(e.g., phenothiazines and tricyclic antidepressants)
4. B12 deficiency can occur after
B. Gastric bypass
C. Ileal resection
D. All of the above
Vitamin B12 (cobalamin) malabsorption can result from a variety of surgical manipulations. The vitamin is initially bound by saliva-derived R protein. In the duodenum, R protein is hydrolyzed by pancreatic enzymes, allowing free cobalamin to bind to gastric parietal cell-derived intrinsic factor. The cobalamin-intrinsic factor complex is able to escape hydrolysis by pancreatic enzymes, allowing it to reach the terminal ileum, which expresses specific receptors for intrinsic factor. Subsequent events in cobalamin absorption are poorly characterized, but the intact complex probably enters enterocytes through translocation. Because each of these steps is necessary for cobalamin assimilation, gastric resection, gastric bypass, and ileal resection can each result in vitamin B12 insufficiency. (See Schwartz 9th ed., p 985.)
5. Which of the following is NOT true about imaging a patient with suspected bowel obstruction?
A. Imaging has poor sensitivity for detecting intestinal ischemia
B. Water-soluble enteral contrasts are preferred for CTt imaging in cases of bowel obstruction
C. Bowel greater than 3 cm on a plain film is suggestive of a small bowel obstruction
D. The specificity of plain films and CT scans in diagnosing small bowel obstruction is the same (approximately 80%)
The finding most specific for small bowel obstruction on abdominal radiographs is the triad of dilated small bowel loops (>3 cm in diameter), air-fluid levels seen on upright films, and a paucity of air in the colon. The sensitivity of abdominal radiographs in the detection of small bowel obstruction ranges from 70 to 80%. Specificity is low because ileus and colonic obstruction can be associated with findings that mimic those observed with small bowel obstruction. False-negative findings on radiographs can result when the site of obstruction is located in the proximal small bowel and when the bowel lumen is filled with fluid but no gas, thereby preventing visualization of air-fluid levels or bowel distention. The latter situation is associated with closed-loop obstruction. (See Schwartz 9th ed., p 989.)
Computed tomographic (CT) scanning is 80 to 90% sensitive and 70 to 90% specific in the detection of small bowel obstruction. The findings of small bowel obstruction include a discrete transition zone with dilation of bowel proximally, decompression of bowel distally, intraluminal contrast that does not pass beyond the transition zone, and a colon containing little gas or fluid (Fig. 28-6). CT scanning may also provide evidence for the presence of closed-loop obstruction and strangulation. Closed-loop obstruction is suggested by the presence of a U-shaped or C-shaped dilated bowel loop associated with a radial distribution of mesenteric vessels converging toward a torsion point. (See Schwartz 9th ed., p 989.)
Strangulation is suggested by thickening of the bowel wall, pneumatosis intestinalis (air in the bowel wall), portal venous gas, mesenteric haziness, and poor uptake of IV contrast into the wall of the affected bowel (Fig. 28-7). CT scanning also offers a global evaluation of the abdomen and may therefore reveal the etiology of obstruction. (See Schwartz 9th ed., p 988.)
The CT scan usually is performed after administration of oral water soluble contrast, or diluted barium. The water soluble contrast has been shown to have prognostic and therapeutic values too. Several studies and a subsequent meta-analysis have shown that appearance of the contrast in the colon within 24 hours is predictive of nonsurgical resolution of bowel obstruction. Although use of oral contrast did not alter the rate of surgical intervention, it did reduce the overall length of hospital stay in those presenting with small bowel obstruction.
FIG. 28-6. Small bowel obstruction. A computed tomographic scan of a patient presenting with signs and symptoms of bowel obstruction. Image shows grossly dilated loops of small bowel, with decompressed terminal ileum (I) and ascending colon (C), suggesting a complete distal small bowel obstruction. At laparotomy, adhesive bands from a previous surgery were identified and divided.
FIG. 28-7. Intestinal pneumatosis. This computed tomographic scan shows intestinal pneumatosis (arrow). The cause of this radiologic finding was intestinal ischemia. Patient was taken emergently to the operating room and underwent resection of an infarcted segment of small bowel.
6. Which of the following is the most common indication for surgery in a patient with Crohn’s disease?
A. Intestinal obstruction
B. Intestinal perforation
C. Gastrointestinal hemorrhage
D. Growth retardation
Fifty to 70% of patients with Crohn’s disease will ultimately require at least one surgical intervention for their disease. Surgery generally is reserved for patients whose disease is unresponsive to aggressive medical therapy or who develop complications of their disease (Table 28-4). Failure of medical management may be the indication for surgery if symptoms persist despite aggressive therapy for several months or if symptoms recur whenever aggressive therapy is tapered. Surgery should be considered if medication-induced complications arise, specifically corticosteroid-related complications, such as cushingoid features, cataracts, glaucoma, systemic hypertension, compression fractures, or aseptic necrosis of the femoral head. Growth retardation constitutes an indication for surgery in 30% of children with Crohn’s disease.
One of the most common indications for surgical intervention is intestinal obstruction. Abscesses and fistulas frequently are encountered during operations performed for intestinal obstruction in these patients, but are rarely the only indication for surgery. Most abscesses are amenable to percutaneous drainage and fistulas unless associated with symptoms or metabolic derangements do not require surgical intervention. Less common complications that require surgical intervention are acute GI hemorrhage, perforations, and development of cancer. (See Schwartz 9th ed., p 996.)
TABLE 28-4 Indications for surgical intervention in Crohn’s disease
Acute onset of severe disease
Crohn’s colitis ± toxic megacolon (rare)
Failure of medical therapy
Persistent symptoms despite long-term steroid use
Recurrence of symptoms when high-dose steroids are tapered
Drug induced complications (Cushing’s disease, hypertension)
Development of disease complications
7. The most common location for a primary adenocarcinoma of the small bowel is
D. None of the above—the distribution is roughly equal
Adenocarcinomas, as well as adenomas (from which most are believed to arise), are most commonly found in the duodenum, except in patients with Crohn’s disease, in whom most are found in the ileum. Lesions in the periampullary location can cause obstructive jaundice or pancreatitis. Adenocarcinomas located in the duodenum tend to be diagnosed earlier in their progression than those located in the jejunum or ileum, which are rarely diagnosed before the onset of locally advanced or metastatic disease. (See Schwartz 9th ed., p 1000.)
8. Following a gastric bypass, which form of calcium should be used as a supplement?
A. Calcium carbonate
B. Calcium chloride
C. Calcium gluconate
D. Calcium citrate
Abnormal calcium levels are increasingly seen in surgical patients who have undergone a gastric bypass. Although usual calcium supplementation is in the form of calcium carbonate, which is cheap, in such patients with low acid exposure, calcium citrate is a better formulation for replacement therapy. (See Schwartz 9th ed., p 985.)
Calcium chloride and calcium gluconate are used as food additives but are not used as calcium supplements.
9. The most common cause of acute mesenteric ischemia is
A. Arterial embolus
B. Arterial thrombosis
C. Vasospasm (nonocclusive mesenteric ischemia)
D. Venous thrombosis
Four distinct pathophysiologic mechanisms can lead to acute mesenteric ischemia:
1. Arterial embolus
2. Arterial thrombosis
3. Vasospasm (also known as nonocclusive mesenteric ischemia)
4. Venous thrombosis
Embolus is the most common cause of acute mesenteric ischemia, and is responsible for more than 50% of cases. The embolic source is usually in the heart; most often the left atrial or ventricular thrombi or valvular lesions. Indeed, up to 95% of patients with acute mesenteric ischemia due to emboli will have a documented history of cardiac disease. Embolism to the superior mesenteric artery accounts for 50% of cases; most of these emboli become wedged and cause occlusion at branch points in the mid- to distal superior mesenteric artery, usually distal to the origin of the middle colic artery. In contrast, acute occlusions due to thrombosis tend to occur in the proximal mesenteric arteries, near their origins. Acute thrombosis is usually superimposed on pre-existing atherosclerotic lesions at these sites. Nonocclusive mesenteric ischemia is the result of vasospasm and usually is diagnosed in critically ill patients receiving vasopressor agents. (See Schwartz 9th ed., p 1006.)
10. Which of the following factors is associated with poor spontaneous enterocutaneous fistulae closure rate?
B. Albumin level >4
C. Long (>2 cm) fistula tract
D. Anscence of epithelialization in fistula tract
Fistulas have the potential to close spontaneously. Factors inhibiting spontaneous closure, however, include malnutrition, sepsis, inflammatory bowel disease, cancer, radiation, obstruction of the intestine distal to the origin of the fistula, foreign bodies, high output, short fistulous tract (2 cm), and epithelialization of the fistula tract (Table 28-5). (See Schwartz 9th ed., p 998.)
A useful mnemonic designates factors that inhibit spontaneous closure of intestinal fistulas: ‘FRIEND’(Foreign body within the fistula tract, Radiation enteritis, Infection/Inflammation at the fistula origin, Epithelialization of the fistula tract, Neoplasm at the fistula origin, Distal obstruction of the intestine). (See Schwartz 9th ed., p 998.)
TABLE 28-5 Factors negatively impacting enteric fistula closure
Medications such as steroids
Fistula related to Crohn’s disease
Fistula in radiated fields
Persistence of local inflammation and sepsis
Presence of a foreign body (e.g., meshes or sutures)
Epithelialization of fistula tract
Fistula tract 2 cm
Distal obstruction to the fistula site
11. Which of the following has been shown to be effective in reducing the duration of postoperative ileus?
A. NG suction
B. Aggressive fluid administration
C. Early enteral feeding
D. Rectal suppository
Given the frequency of postoperative ileus and its financial impact, a large number of investigations have been conducted to define strategies to reduce its duration. Although often recommended, the use of early ambulation and routine NG intubation has not been demonstrated to be associated with earlier resolution of postoperative ileus. There is some evidence that early postoperative feeding protocols are generally well tolerated, reduce postoperative ileus, and can result in a shorter hospital stay. The administration of NSAIDs such as ketorolac and concomitant reductions in opioid dosing have been shown to reduce the duration of ileus in most studies. Similarly, the use of perioperative thoracic epidural anesthesia/analgesia with regimens containing local anesthetics combined with limitation or elimination of systemically administered opioids have been shown to reduce duration of postoperative ileus, although they have not reduced the overall length of hospital stay. Interestingly, recent data have suggested that limiting intra and postoperative fluid administration can also result in reduction of postoperative ileus, and shortened hospital stay. Table 28-6 summarizes some of the measures used to minimize postoperative ileus. (See Schwartz 9th ed., p 993.)
TABLE 28-6 Measures to reduce postoperative ileus
12. Which of the following is a recognized risk factor for Crohn’s disease?
A. Male gender
B. Having been breastfed as an infant
C. Low socioeconomic status
The incidence of Crohn’s disease varies among ethnic groups within the same geographic region. For example, members of the Eastern European Ashkenazi Jewish population are at two- to fourfold higher risk of developing Crohn’s disease than members of other populations living in the same location. Most studies suggest that Crohn’s disease is slightly more prevalent in females than in males.
Both genetic and environmental factors appear to influence the risk for developing Crohn’s disease. The relative risk among first-degree relatives of patients with Crohn’s disease is 14 to 15 times higher than that of the general population. Approximately one in five patients with Crohn’s disease will report having at least one affected relative. The concordance rate among monozygotic twins is as high as 67%; however, Crohn’s disease is not associated with simple mendelian inheritance patterns. Although there is a tendency within families for either ulcerative colitis or Crohn’s disease to be present exclusively, mixed kindreds also occur, suggesting the presence of some shared genetic traits as a basis for both diseases.
Higher socioeconomic status is associated with an increased risk of Crohn’s disease. Most studies have found breastfeeding to be protective against the development of Crohn’s disease. Crohn’s disease is more prevalent among smokers. Furthermore, smoking is associated with the increased risk for both the need for surgery and the risk of relapse after surgery for Crohn’s disease. (See Schwartz 9th ed., p 993.)
13. A patient with an asymptomatic 4-cm duodenal diverticulum should be treated with
A. Observation alone
B. Endoscopic ablation of the diverticular mucosa
D. Segmental duodenectomy
Asymptomatic acquired diverticula should be left alone. Bacterial overgrowth associated with acquired diverticula is treated with antibiotics. Other complications, such as bleeding and diverticulitis, are treated with segmental intestinal resection for diverticula located in the jejunum or ileum.
Bleeding and obstruction related to lateral duodenal diverticula generally are treated with diverticulectomy alone. These procedures can be technically difficult for medial duodenal diverticula that penetrate into the substance of the pancreas. Complications related to these medial duodenal diverticula should be managed nonoperatively if possible, using endoscopy. In emergent situations, bleeding related to medial duodenal diverticula can be controlled using a lateral duodenotomy and oversewing of the bleeding vessel. Similarly, perforation can be managed with wide drainage rather than complex surgery. Whether diverticulectomy should be done in patients with biliary or pancreatic symptoms is controversial and is not routinely recommended. (See Schwartz 9th ed., p 1006.)
14. The most common location for gastrointestinal stromal tumors (GIST) is
Sixty to 70% of GISTs are located in the stomach. The small intestine is the second most common site, containing 25 to 35% of GISTs. There appears to be no regional variation in the prevalence of GISTs within the small intestine. GISTs have a greater propensity to be associated with overt hemorrhage than the other small intestinal malignancies. (See Schwartz 9th ed., p 1000.)
15. Which of the following findings is virtually pathognomic for Crohn’s disease?
A. Terminal ileal inflammation
B. Thickened ileal wall
C. Fat wrapping
D. Ulceration in the ileal mucosa
A feature of Crohn’s disease that is grossly evident and helpful in identifying affected segments of intestine during surgery is the presence of fat wrapping, which represents encroachment of mesenteric fat onto the serosal surface of the bowel (Fig. 28-8). This finding is virtually pathognomonic of Crohn’s disease. The presence of fat wrapping correlates well with the presence of underlying acute and chronic inflammation. (See Schwartz 9th ed., p 993.)
The other findings listed can be found in Crohn’s disease but are not specific, as they can also be found in other causes of ileal inflammation, such as infection.
Acute ileitis caused by Campylobacter and Yersinia species can be difficult to distinguish from that caused by an acute presentation of Crohn’s disease. Typhoid enteritis caused by Salmonella typhosa can lead to overt intestinal bleeding and perforation, most often affecting the terminal ileum. The distal ileum and cecum are the most common sites of intestinal involvement by infection due toMycobacterium tuberculosis. This condition can result in intestinal inflammation, strictures, and fistula formation, similar to those seen in Crohn’s disease. CMV can cause intestinal ulcers, bleeding, and perforation. (See Schwartz 9th ed., p 995.)
FIG. 28-8. Crohn’s disease. This intraoperative photograph demonstrates encroachment of mesenteric fat onto the serosal surface of the intestine (“fat wrapping”) that is characteristic of intestinal segments affected by active Crohn’s disease.
16. Early postoperative obstruction following laparotomy
A. Occurs in approximately 8% of patients undergoing laparotomy
B. Is best treated surgically if signs of ischemia are detected
C. Is most common after extensive retroperitoneal dissection
D. Can be diagnosed with plain radiographs in >90% of patients
Obstruction presenting in the early postoperative period has been reported to occur in 0.7% patients undergoing laparotomy. Patients undergoing pelvic surgery, especially colorectal procedures, have the greatest risk for developing early postoperative small bowel obstruction. The presence of obstruction should be considered if symptoms of intestinal obstruction occur after the initial return of bowel function or if bowel function fails to return within the expected 3 to 5 days after abdominal surgery. Plain radiographs may demonstrate dilated loops of small intestine with air-fluid levels but are interpreted as normal or nonspecific in up to one third of patients with early postoperative obstruction. CT scanning or small bowel series is often required to make the diagnosis. Obstruction that occurs in the early postoperative period is usually partial and only rarely is associated with strangulation. Therefore, a period of extended nonoperative therapy (2 to 3 weeks) consisting of bowel rest, hydration, and total parenteral nutrition (TPN) administration is usually warranted. However, if complete obstruction is demonstrated or if signs suggestive of peritonitis are detected, expeditious reoperation should be undertaken without delay. (See Schwartz 9th ed., p 990.)
17. The presumed cell of origin for gastrointestinal stromal tumors (GIST) is
A. Cell of Cajal
B. Paneth cell
C. Enteroendocrine cell
A defining feature of GISTs is their gain of function mutation of protooncogene KIT, a receptor tyrosine kinase. Pathologic KIT signal transduction is believed to be a central event in GIST pathogenesis. The majority of GISTs have activating mutations in the c-kit protooncogene, which cause KIT to become constitutively activated, presumably leading to persistence of cellular growth or survival signals. Because the interstitial cells of Cajal normally express KIT, these cells have been implicated as the cell of origin for GISTs. KIT expression is assessed by staining the tissues for CD117 antigen, which is part of the KIT receptor, and present in 95% of GISTs. (See Schwartz 9th ed., p 999.)
18. Which of the following is the LAST to recover from postoperative ileus?
B. Small bowel
D. None of the above—the recovery is simultaneous
Following most abdominal operations or injuries, the motility of the GI tract is transiently impaired. Among the proposed mechanisms responsible for this dysmotility are surgical stress-induced sympathetic reflexes, inflammatory response mediator release, and anesthetic/analgesic effects; each of which can inhibit intestinal motility. The return of normal motility generally follows a characteristic temporal sequence, with small intestinal motility returning to normal within the first 24 hours after laparotomy and gastric and colonic motility returning to normal by 48 hours and 3 to 5 days, respectively. Because small bowel motility is returned before colonic and gastric motility, listening for bowel sounds is not a reliable indicator that ileus has fully resolved. Functional evidence of coordinated GI motility in the form of passing flatus or bowel movement is a more useful indicator. Resolution of ileus may be delayed in the presence of other factors capable of inciting ileus such as the presence of intra-abdominal abscesses or electrolyte abnormalities. (See Schwartz 9th ed., p 992.)
19. Which of the following is NOT a known cause of ileus?
C. Myocardial infarction
(See Schwartz 9th ed., p 992, and Table 28-7.)
TABLE 28-7 Ileus: Common etiologies
Calcium channel blockers
Spinal cord injury
20. A high output enterocutaneous fistula is defined as draining more than
A. 100 mL/day
B. 500 mL/day
C. 1000 mL/day
D. 2000 mL/day
Enterocutaneous fistulas that drain less than 200 mL of fluid per day are known as low-output fistulas, whereas those that drain more than 500 mL of fluid per day are known as high-output fistulas. (See Schwartz 9th ed., p 998.)
21. The most common complication seen in adults with a Meckel’s diverticulum is
B. Meckel’s diverticulitis
Intestinal obstruction is the most common presentation in adults with Meckel’s diverticula. Diverticulitis, present in 20% of patients with symptomatic Meckel’s diverticula, is associated with a clinical syndrome that is indistinguishable from acute appendicitis. Neoplasms, most commonly carcinoid tumors, are present in 0.5 to 3.2% of symptomatic Meckel’s diverticula that are resected.
Intestinal obstruction associated with Meckel’s diverticulum can result from several mechanisms:
1. Volvulus of the intestine around the fibrous band attaching the diverticulum to the umbilicus
2. Entrapment of intestine by a mesodiverticular band (Fig. 28-9)
3. Intussusception with the diverticulum acting as a lead point
4. Stricture secondary to chronic diverticulitis
Meckel’s diverticula can be found in inguinal or femoral hernia sacs (known as Littre’s hernia). These hernias, when incarcerated, can cause intestinal obstruction.
Bleeding is the most common presentation in children with Meckel’s diverticula, representing over 50% of Meckel’s diverticulum-related complications among patients younger than 18 years of age. Bleeding associated with Meckel’s diverticula is rare among patients older than 30 years of age. (See Schwartz 9th ed., p 1003.)
FIG. 28-9. A. Meckel’s diverticulum with mesodiverticular band. B. One mechanism by which Meckel’s diverticula can cause small bowel obstruction is entrapment of the intestine by a mesodiverticular band.
22. Which of the following is NOT an extraintestinal manifestation of Crohn’s disease?
A. Pyoderma gangrenosum
B. Erythema nodosum
An estimated one fourth of all patients with Crohn’s disease will have an extraintestinal manifestation of their disease. One fourth of those affected will have more than one manifestation. Many of these complications are common to both Crohn’s disease and ulcerative colitis, although as a whole, they are more prevalent among patients with Crohn’s disease than those with ulcerative colitis. The most common extraintestinal manifestations are listed in Table 28-8. The clinical severity of some of these manifestations, such as erythema nodosum and peripheral arthritis, is correlated with the severity of intestinal inflammation. The severity of other manifestations, such as pyoderma gangrenosum and ankylosing spondylitis, bears no apparent relationship to the severity of intestinal inflammation. (See Schwartz 9th ed., p 995.)
TABLE 28-8 Extraintestinal manifestations of Crohn’s disease
Primary sclerosing cholangitis
Endocarditis, myocarditis, pleuropericarditis
Interstitial lung disease
23. Stricturoplasty is contraindicated in a patient with Crohn’s disease who, at the time of surgery, is found to have
A. Multiple areas of stenosis
B. Stricture(s) >12 cm in length
C. A fistula at the level of the stricture
D. A stricture proximal to severe ileocecal disease
An alternative to segmental resection for obstructing lesions is stricturoplasty (Fig. 28-10). This technique allows for preservation of intestinal surface area and is especially well suited to patients with extensive disease and fibrotic strictures who may have undergone previous resection and are at risk for developing short bowel syndrome. In this technique, the bowel is opened longitudinally to expose the lumen. Any intraluminal ulcerations should be biopsied to rule out the presence of neoplasia. Depending on the length of the stricture, the reconstruction can be fashioned in a manner similar to the Heinecke-Mikulicz pyloroplasty (for strictures less than 12 cm in length) or the Finney pyloroplasty (for longer strictures as much as 25 cm in length). For longer strictures, variations on the standard stricturoplasty, namely the side-to-side isoperistaltic enteroenterostomy, have been advocated, and used for strictures with mean lengths of 50 cm. Stricturoplasty sites should be marked with metallic clips to facilitate their identification on radiographs and during subsequent operations. Stricturoplasty is associated with recurrence rates that are no different from those associated with segmental resection. Because the affected bowel is left in situ rather than resected, there is the potential for cancer developing at the stricturoplasty site. However, as data on this complication are limited to anecdotes, this risk remains a theoretical one. Stricturoplasty is contraindicated in patients with intra-abdominal abscesses or intestinal fistulas. The presence of a solitary stricture relatively close to a segment for which resection is planned is a relative contraindication. In general, stricturoplasty is performed in cases where single or multiple strictures are identified in diffusely involved segments of bowel, or where previous resections have been performed, and maintenance of intestinal length is of great importance. (See Schwartz 9th ed., p 997.)
FIG. 28-10. Stricturoplasty. The wall of the strictured bowel is incised longitudinally. Reconstruction is performed by closing the defect transversely in a manner similar to the Heinecke-Mikulicz pyloroplasty for short strictures (A), or the Finney pyloroplasty for longer strictures (B).
24. The most common cause of small bowel obstruction is
D. Crohn’s disease
Intra-abdominal adhesions related to prior abdominal surgery account for up to 75% of the cases of small bowel obstruction. Over 300,000 patients are estimated to undergo surgery annually to treat adhesion-induced small bowel obstruction in the United States. Less prevalent etiologies for small bowel obstruction include hernias, malignant bowel obstruction, and Crohn’s disease. (See Schwartz 9thed., p 998, and Table 28-9.)
TABLE 28-9 Small bowel obstruction: Common etiologies
Primary small bowel neoplasms
Secondary small bowel cancer (e.g., melanoma-derived metastasis)
Local invasion by intra-abdominal malignancy (e.g., desmoid tumors)
External (e.g., inguinal and femoral)
Internal (e.g., following Roux-en-Y gastric bypass surgery)
Congenital abnormalities (e.g., webs, duplications, and malrotation)
25. Which of the following is NOT associated with successful weaning of TPN in patients with short bowel syndrome?
A. Length of small bowel >200 cm
B. Presence of ileocecal valve
C. Presence of colon
D. Age >30 years
See Table 28-10. Pediatric patients adapt better than adult patients. (See Schwartz 9th ed., p 1010.)
TABLE 28-10 Risk factors for development of short bowel syndrome after massive small bowel resection
Small bowel length 200 cm
Absence of ileocecal valve
Absence of colon
Diseased remaining bowel (e.g., Crohn’s disease)
26. Which of the following agents has been shown to improve closure of enterocutaneous fistulae in Crohn’s disease?
Infliximab is a chimeric monoclonal anti–tumor necrosis factor alpha antibody that has been shown to have efficacy in inducing remission and in promoting closure of enterocutaneous fistulas. It generally is used for patients resistant to standard therapy to help taper steroid dosage. Infliximab generally is well tolerated but should not be used in patients with ongoing septic processes, such as undrained intra-abdominal abscesses. (See Schwartz 9th ed., p 996.)