Ch. 15- Diseases of Lower GI Tract

Surgical Options for Treatment of Ulcerative Colitis

(a) Proctocolectomy (removing the entire large intestine); (b) Brooke ileostomy; (c) Koch pouch ileostomy (bag/pouch located inside of body and made of person's intestine; collects in pouch and can drain using a catheter); (d) restorative proctocolectomy (J pouch- small intestine is brought down to rectum so person can use restroom like normal).

Nutrition Therapy for IBD

-A significant portion of individuals diagnosed with active Crohn's disease experience weight loss, muscle wasting, and malnutrition as well as specific nutritional deficiencies. Nutrition support is routinely required during periods of exacerbation and recovery from surgery. IBD affects normal digestion and absorption; may increase caloric, protein, and micronutrient requirements; can result in protein-energy malnutrition; and additionally may require nutrition therapy to minimize symptoms. Medications that are used to treat IBD, especially corticosteroids, may impact nutritional status by either increasing nutrient requirements or exacerbating nutrient losses. The use of bowel rest with parenteral nutrition and the use of enteral nutrition as a therapeutic component of the medical care for IBD have been debated. The exact mechanism for the role of enteral nutrition therapy in Crohn's pathophysiology is not clearly established but is assumed to be related to improvement in intestinal permeability -Nutrition assessment: Due to the significant nutritional complications and problems associated with IBD, a comprehen- sive nutrition assessment is required. This population will benefit from an integrated approach to substantiate the presence of malnutrition. The symptoms of IBS can result in changes in oral intake such as avoidance of certain foods and food groups, which may lead to poor nutrition quality of life. The severe limitations of foods seen in more extreme cases can likewise cause nutrient deficiencies, potential underweight, and malnutrition. Since IBS may present with either diarrhea, constipation, or both, the specific assessment data needed to provide appropriate nutrition care will vary. Comprehensive assessment required. -Nutrition diagnosis: May include malnutrition; inadequate energy intake; inadequate oral intake; increased nutrient needs; inadequate vitamin/mineral intake; impaired nutrient utilization; food-medication interaction; and altered nutrition-related laboratory values. -Nutrition therapy is a crucial component of treatment for active disease. Nutritional needs and deficits are signifi- cantly different during periods of remission. Acute symptoms of both UC and Crohn's involve diarrhea and abdominal pain. Because increased motility decreases the success of digestion and absorption, severe diarrhea can result in malabsorption of all nutrients. These symptoms can also result in reduced oral intake. Many patients electively restrict eating in order to minimize symptoms during acute exacerbations of the disease. Pain can cause generalized anorexia, which further decreases dietary intake. When infection and inflammation are present or when the patient is febrile, energy needs are higher than normal. Protein needs are increased, in some cases up to 150% of normal requirements. A negative nitrogen balance has been demonstrated to occur in approximately 50% of individuals with Crohn's. This is due, in part, to increased protein losses in inflammatory exudate. Crohn's patients are at risk for deficiency of micronutrients, especially calcium, vitamin D, vitamin B12, iron, zinc, and magnesium, due to malabsorp- tion and losses in blood and diarrhea. Because IBD com- monly presents in children and young adults, meeting the nutritional needs of the growing child or adolescent poses its own unique challenge. It is crucial for nutrition therapy to be designed to ensure adequate nutrients to support growth and development. Since the mainstay of treatment for IBD involves multiple medications and often surgery, these nutritional risks compound those of the disease process. For example, use of corticosteroids can result in hyperglycemia, nitro- gen wasting, and increased risk of osteoporosis. Another example is the use of sulfasalazine, which interferes with folate metabolism. Surgery increases calorie and protein requirements and additional nutrients are needed to sup- port wound healing. Depending on the extent and type of surgery, normal absorption and digestive pathways may be interrupted. Specific nutrition therapy may be required if the patient has either an ileostomy or colostomy.

Large Intestine Digestion and Absorption

-No enzymatic digestion occurs in the large intestine. In nor- mal, healthy individuals, digestion has already been accom- plished by the time chyme exits the small intestine. The primary function of the large intestine is to provide a site for reabsorption of water, electrolytes, and some vitamins. The colon's role in absorption is even more important when dis- ease affects the small intestine. The colon can increase its absorption significantly—as much as three to five times more than normal.10,11 In conditions where digestion and absorption have not occurred in the small intestine, nutrients from the small intestine are lost in the feces unless the substrate (such as fiber or resistant starch) can be fermented to short-chain fatty acids.12 The second major function of the large intestine is to serve as the site for formation and storage of feces. When chyme enters the large intestine from the ileum, it is primarily liquid. As the chyme moves along the colon, water is reabsorbed, resulting in a drier mass of fecal matter. Sodium, potassium, and other electrolytes are absorbed along with water. Feces contain undigested foodstuffs—primarily insoluble fiber—bilirubin, and bacteria. This entire process may take anywhere from 12 to 72 hours.13 As many as 400 different species of bacteria—including bifidobacteria, coliforms, bacteroides, peptococci, clostridia, lactobacteria, and methanogens—live within the colon. They provide fermentation of fiber, resistant starch, and sugar alco- hols. As these substrates undergo fermentation, short-chain fatty acids (SCFA) (acetate, propionate, butyrate) and lactate are produced. Some of the energy produced during fermenta- tion is used directly by bacteria for their own support, but the SCFA they release can provide 500-1200 kcal per day for the human host.12,14-16 These SCFA are either utilized by the colon for support of its own tissue growth or absorbed for utilization by the body elsewhere. When there is excessive substrate in the colon— such as undigested carbohydrates—gas and flatulence may result.Many factors affect not only the amount but also the types of bacteria in the colon. These factors include age and health status, composition of the diet, transit time, stress, and alcohol intake. Maintaining an optimal balance of intestinal flora is of significant inter- est in human health and nutrition. The use of resistant starch, prebiotics, probiotics, and synbiotics is currently being studied in an effort to determine their role in the promotion of the health of the colon and in the prevention and treatment of disease.Resistant starch is defined as starch components that enter the large intestine undigested. Examples of resistant starch sources include potatoes, bananas, and some legumes. Prebiotics are substances in food (such as inulin and oligosaccharides) that stimulate the beneficial flora of samll intestine. Probiotics are products containing live microorganisms that are sold as foods/supplements. Synbiotics are products that contain both prebiotics and probiotics. -Intestinal flora use undigested carbohydrate and small amounts of protein to support their own growth. Resistant starch and soluble fiber, for example, benefit the large intes- tine not only by their physical presence but through their fermentation by colonic flora.22 Lactate and short-chain fatty acids released during fermentation can then be absorbed from the colon and utilized elsewhere in the body. Probiotics, by altering the microbiota of the large intestine, may improve the microbial balance, normalize transit time, and enhance the immune defenses provided in the gut mucosa.19 Other by-products from bacterial metabolism include gas and ammonia. As described in Chapter 16, medications to induce diarrhea, which decreases the ability of the colon to reabsorb this ammonia, are used to help control abnormal ammonia levels in persons with end-stage liver disease. -Vitamin K and biotin are two endogenously produced vitamins. Biotin is produced by normal intestinal flora in the colon and is absorbed via passive diffusion.23 E. coli and Bacteroides fragilis in the colon synthesize vitamin K. The absorptive route for this endogenous vitamin K is not clear at this time. Truly, for both of these vitamins, it is difficult to estimate the contribution of endogenous synthesis. Diseases of the lower GI tract, the use of antibiotics, and the presence of prebiotics and probiotics may all potentially interfere with and/or promote endogenous synthesis. -No enzymatic digestion occurs in large intestine (everything should already be broken down and absorbed in small intestine; now we are just getting water, bile, and electrolytes that need to be reabsorbed and fiber as what we defecate) -Reabsorption of water, electrolytes (K and biotin = producing in large intestine), some vitamins. If parts of small intestine stop functioning, other parts will compensate. Similar, large intestine increases its absorption capacity 3-5x which is a form of compensation. -Formation and storage of feces (we should end up with stool that is not extremely soft or extremely hard): Takes 12-72 hrs. (takes time to move food through GI): -Insoluble fiber and bilirubin (bilirubin is what is leftover after red blood cells breakdown- gives stool darker brown color) = composition of stool. If you have an issue with gallbladder (where bilirubin is), you can have white stool or a really light colored stool. -400 species of bacteria in large intestine. It is good bacteria that ferments fibers. Fermenting fiber produces energy, which makes sure there's enough energy for large intestine. -Fermentation of fiber and sugar alcohols

Irritable Bowel Syndrome- Clinical Manifestations

-Abdominal pain, alteration in bowel habits or motility, gas, and flatulence as well as some upper GI symptoms (reflux and non-cardiac chest pain) are major symptoms for IBS. Abdominal pain can be acute and relieved by defecation, but some patients with IBS experience constant, chronic abdominal pain. Alterations in bowel habits are seen in both major types of IBS—constipation (IBS-C) and diarrhea (IBS-D). In some patients, both constipation and diarrhea are experienced (IBS-M). Increased levels of gas and flatulence are also experi- enced. Gas is produced when food passes into the large intes- tine and is only partially digested. Intestinal bacteria act on these foodstuffs, and by-products of the fermentation result in gas production. The registered dietitian can assist by providing nutrition therapy that may alter the signs and symptoms that occur as a result of specific food ingestion. -Abdominal pain, alterations in bowel habits, gas, flatulence: -Gas and flatulence because things are entering large intestine that are not fully digested. Can be painful.

Inflammatory Bowel Disease- UC and Crohn's

-Approximately 40%-50% of patients with UC have dis- ease only involving the rectum. Damage to intestinal mucosa in UC usually only involves the first two layers of tissue (mucosa and superficial submucosa) within the colon and rectum. But with chronic disease, the intestinal wall can become so thin that the mucosa is ulcerated. This is referred to as toxic megacolon. UC disease usually affects one section of the gastrointestinal tract at a time, whereas Crohn's disease often presents with a "skipping" pattern affecting multiple portions of the gastrointestinal tract. Crohn's disease can affect any portion of the gastro- intestinal tract from mouth to anus and approximately 75% of patients have some form of small intestine involvement. Crohn's disease can damage all layers of gastrointestinal mucosa. This inflammatory process is characterized by the development of fistulas that when healed are replaced by fibrotic tissue. The fibrosis can result in recurrent strictures and bowel obstructions. -UC: ulcerations lead to toxic megacolon; thin ulcerated colon -Crohn's: can lead to strictures, obstruction because wall of intestine is becoming bigger (making passageway through smaller, so things get stuck) -May have to remove part of small intestine or large intestine if UC or Crohn's occur

Celiac Disease- Clinical Manifestations

-Classic clinical symptoms of CD include diarrhea, abdominal pain and cramping, bloating, and gas production. Other symptoms that can occur in the absence of GI problems (sometimes referred to as extraintes- tinal) include bone and joint pain, muscle cramping, fatigue, peripheral neuropathy, seizures, skin rash, and mouth ulcer- ations. However, many individuals are diagnosed without these classic signs and symptoms. Some may present with iron-deficiency anemia or are found to have CD after screening for other conditions such as thyroid disease, chronic fatigue, constipation, and irritable bowel syndrome. Catassi et al. used the following as criteria for screening for CD: positive family history, chronic fatigue, unexplained anemia, abnor- mal liver function, autoimmune disorders, Down syndrome, Turner syndrome, infertility, and epilepsy/ataxia. Using these criteria, the authors achieved a 43-fold increase in the rate of diagnosis. -Diarrhea, abdominal pain, cramping, bloating, gas -Bone and joint pain: decreasing absorption of calcium and decreasing vitamin D, which can lead to bone and joint pain -Muscle cramping, fatigue: decreased calcium and potassium absorption -Peripheral neuropathy, seizures: controversial, but does occur in some individuals -Skin rash: herpetiformis (skin rash that occurs in people with celiac disease and causes blisters to appear on skin) -Mouth ulcerations: decreased absorption of B complex -Higher risk for lymphoma (has to do with t cells) and osteoporosis (calcium and vit D)

Constipation- Clinical Manifestations and Medical Diagnosis

-Clinical manifestations: -Often hard, pellet-like -Abdominal pain, bloating, gas -Medical diagnosis: -Rome Consensus III Criteria -Complete history & physical, CBC (complete blood count), TSH (constipation is a common symptom of hypothyroidism), serum glucose (if person diabetic, blood sugar is high, causes decreased blood flow to certain areas and decreased movement of GI), flexible sigmoidoscopy or colonoscopy if further evaluated needed

Bacterial Overgrowth- Clinical Manifestations and Treatment

-Clinical manifestations: Signs and symptoms are similar to all conditions of malabsorption. Diarrhea, steatorrhea, anemia, and weight loss all may be present in this condition. -Treatment: Bacterial overgrowth syndrome is treated by both correcting the underlying cause and administering broad-spectrum antibiotics such as ciprofloxacin, metronidazole, neomycin, and doxycycline to assist with modifying the microbiome. Fecal transplant, as discussed earlier in this chapter, may serve as an additional mode of therapy. -Clinical manifestations: Maldigestion, malabsorption, and weight loss -Treatment: Broad spectrum antibiotics (want to kill bacteria that is in small intestine)

Large Intestine Secretions

-Compared to the small intestine, the large intestine produces relatively few secretions. As mentioned earlier, goblet cells produce mucus that serves to protect the epithelium and assists in formation of feces. Potassium and bicarbonate are both released in the large intestine, and they play a role in the electrolyte and fluid absorption that occurs there. -Goblet cells produce mucus (protect cells of large intestine) -Potassium and bicarbonate (purpose of K+ and bicarb is to assist in fluid and electrolyte absorption)

Constipation- Etiology

-Constipation can result from any of several dif- ferent distinct causes.23,52 Slowed colonic transit can result in constipation. Constipation can be due to rectal outlet obstruction or other sources of obstruction such as fecal impaction, adhesions, or even the presence of a tumor. Pelvic floor dysfunction can cause not only slowed colonic transit but also storage of fecal contents in the rectum for long peri- ods of time. Constipation can be a major component of irrita- ble bowel syndrome, which is discussed later in this chapter. Constipation can be secondary to other medical conditions, including scleroderma, amyloidosis, and neurological dis- eases such as multiple sclerosis or Parkinson's disease. Finally, constipation can be a side effect of many different classes of medications. These include very common prescription drugs such as calcium channel blockers, antidepressants such as amitriptyline, pain medications such as morphine, diuretics, and antihistamines. Over-the-counter medications that often cause constipation include iron, calcium, and other nutrient supplements; for some individuals, even non-steroidal anti- inflammatory drugs can result in constipation. -Slowed colonic transit time -Rectal outlet obstruction (something is in the way), fecal impaction, adhesions (two parts of GI come together), tumor -Pelvic floor dysfunction: muscles and ligaments (that support vagina, uterus, bladder) -Irritable bowel syndrome -Other medical conditions; i.e., MS, Parkinson's -Side effect of medications (antidepressants, pain medications, diuretics), supplements (too much iron and calcium)

Disease Pathogenesis of IBD

-Crohn's: walls get thicker; thickening of the lumen (opening of the GI); buildup of fat; walls are thickening and cobblestoning (looks like cobbelestones on the inside of intestine) and fissures (cracks- very painful). Crohn's can happen anywhere in GI (anus to mouth). Ulcerative colitis: walls get thinner; losing mucosal lining inside of intestine which causes ulcers to form. Very dark (ulcerated). Loss of haustra. Happens in lower part of GI (in the large intestine) and even more so in the rectum and anus.

Diverticulosis/Diverticulitis

-Defined as the abnormal pres- ence of outpockets, pouches, or sacs on the surface of the small intestine or colon. Diverticulosis is most common in the adult but one form, Meckel's diverticulum, is present at birth. Meck- el's diverticula are usually found near the ileocecal valve and may cause gastrointestinal bleeding or obstruction for the newborn. -Definition: -Abnormal presence of outpockets or pouches on surface of SI (small intestine) or colon, causes inflammation. -Diverticulosis: little pockets form in large intestine, and these pockets will become inflamed. Person can have this condition and not have any signs/symptoms. When things become stuck in pockets, inflammation occurs, which becomes diverticulitis. -Diverticulitis: inflammation of the pockets -Epidemiology: -Most common in Western and industrialized countries (Because our diets are low in fiber) -5-10% of population will have diverticulitus by age of 50- 50% by age of 65.

Irritable Bowel Syndrome (IBS)

-Definition: -Abdominal pain or discomfort that occurs in association with altered bowel habits over a period of at least three months -Three subtypes: IBS-D (diarrhea), IBS-C (constipation), IBS-M (mixed- diarrhea and constipation) -Epidemiology:Irritable bowel syndrome is the most com- mon gastrointestinal complaint in the United States and Canada. Worldwide prevalence ranges from 1% to 20%, and in North America is estimated to be approximately 10%. This condition affects women more than men and frequently develops before age 50. This diagnosis accounts for 1.6 million health care visits resulting in more than 5 million prescriptions. -North American prevalence ~ 10% (women more likely than men; develops before the age of 15)

Constipation

-Definition: -Subjective: decrease in frequency of bowel movements -Rome III Consensus Criteria provide framework for definition constipation as a condition where at least two of the following symptoms have occurred in the previous year for at least 12 non-consecutive weeks:48-50 • Must include two or more of the following: • Straining during at least 25% of defecations • Lumpy or hard stools in at least 25% of defecations • Sensation of incomplete evacuation for at least 25% of defecations • Sensation of anorectal obstruction/blockage for at least 25% of defecations • Manual maneuvers to facilitate at least 25% of defecations (e.g., digital evacuation, support of the pelvic floor) • Fewer than three defecations per week • Loose stools are rarely present without the use of laxatives • There are insufficient criteria for diagnosis of irritable bowel syndrome -Epidemiology: Affects 63 million in U.S.

Inflammatory Bowel Disease- IBD

-Definition: Inflammatory bowel disease (IBD) is charac- terized as an autoimmune, chronic inflammatory condition of the gastrointestinal tract. IBD is actually the general term for either of two diagnoses: ulcerative colitis (UC) and Crohn's disease. These diagnoses are similar but have very distinct differences ( -Autoimmune, chronic inflammatory condition of GI tract -General term for ulcerative colitis (UC) and Crohn's disease -Epidemiology:Historically, the prevalence of IBD has been higher in countries within the Northern Hemisphere—North America and Northern European countries—and much lower in the Southern Hemisphere—in countries of Southern Europe, Asia, and Australia.92,93 But more recent examination of epidemiological data has demonstrated that incidence and prevalence are increasing worldwide even in areas with previ- ously low rates.94 Incidence of IBD in the United States ranges from 5 to 15 per 100,000 persons. Prevalence is estimated to be approximately 388-444 per 100,000. Prevalence is fairly equal in both males and females, but it is higher in those pop- ulations with Caucasian and Ashkenazi Jewish ancestry. The estimated cost of medical care for these patients is approxi- mately $1.6 billion per year in the United States. -Historically higher in Northern Hemisphere but increasing worldwide -Same in men and women

Short Bowel Syndrome

-Definition: Short bowel syndrome (SBS) results from a large resection of the small intestine. Each patient presents with a unique situation where the underlying diagnosis, the condition of the ileocecal valve, and the amount of colon that is preserved are important factors affecting the long-term prog- nosis. O'Keefe et al. have proposed the following definition: "Short bowel syndrome intestinal failure results from sur- gical resection, congenital defect or disease-associated loss of absorption and is characterized by the inability to main- tain protein, energy, fluid, electrolyte, or micronutrient balances when on a conventionally accepted, normal diet" (pp. 9-10).127 It is understood that approximately 50% of the duodenum and jejunum can be resected without significant nutrition deficits. If less than 100 cm of the small intestine is left, malabsorption is inevitable. The signs, symptoms, and severity of metabolic consequences of SBS are also dependent on the presence of the ileocecal valve and of the colon. Results from large resection of small intestine. Crohn's: skipping through GI tract. -Epidemiology: Two to three cases per million -Etiology: -Surgical resections of the small intestine and colon due to disease and trauma can result in extensive loss of sur- face area of the small intestine and colon. Without normal anatomy and physiology, malabsorption of nutrients, fluids, and electrolytes will result. Extensive loss of surface area with malabsorption of nutrients, fluids, electrolytes -Reasons for resectioning: Malignancy (cancer), any damage caused by chemotherapy (cancer), Crohn's disease, if person has had multiple resectioning, any type of trauma, volvulus (twisting of small intestine) -We can remove 50% of small intestine and not see issues regarding digestion/absorption, but once you hit 70%, there's issue (can't break down/use nutrients properly)

Pathophysiology of Malabsorption

-Nutrient digestion and absorption are dependent on normal anatomy; normal physiology with ade- quate production of enzymes, hormones, and other secretions such as bile; and appropriate motility. Malabsorption is dis- cussed here in the context of each of the main macronutrients: lipid, carbohydrate, and protein. -Fat malabsorption: The digestion and absorption process for lipid or fat is the most complex, and therefore the easiest to disrupt. Fat malabsorption is called steatorrhea—literally meaning fat in the stool. Digestion and absorption of fat require adequate colipase and pancreatic lipase, adequate emulsifier—bile—from the liver and gallbladder, and ade- quate secretion through the common bile duct and pancreatic ducts. Normal motility is necessary due to the lengthy process lipid has to undergo from micelle to chylomicron for absorp- tion. When any of these processes is disrupted, fat remains in the stool and travels undigested and unabsorbed to the large intestine. Fat-soluble vitamins are malabsorbed as well. An additional concern for fat malabsorption is the potential presence of excess oxalate. Under normal conditions, calcium within the GI tract binds with oxalate and allows for its excre- tion or metabolism. In fat malabsorption, calcium often binds with the malabsorbed fat. This allows oxalate to be absorbed and then excreted through the kidneys. Excessive amounts of oxalate have been linked to development of urothiasis or kid- ney stones. Hyperoxaluria (excessive oxalate in the urine) is responsible for about 30% of kidney stones and is considered to be their most common cause. Individuals with fat malabsorption will experience abdominal pain, cramping, and diarrhea. Stools produced will be frothy, foul-smelling, and greasy in appearance. Specific laboratory tests can diagnose steatorrhea and then assist in determination of the etiology of the malabsorp- tion. Diagnostic tests include the 72-hour quantitative fecal fat test that involves collection of stool output for 3 days after ingesting 100 g fat/day. If more than 6 g of fat are present in the stool, the diagnosis of steatorrhea can be made. This establishes malabsorption but does not determine the spe- cific cause. This test is costly and unpleasant for the patient. It often takes up to 10 days to receive results.4 These factors have led to the infrequent use of this test. The D-xylose absorption test assists in distinguishing between pancreatic dysfunction and small bowel malabsorp- tion. D-xylose is easily absorbed in the small intestine and is not metabolized. Its absorption does not require pancreatic or biliary function. In this test, after the patient drinks 25 g of D-xylose, urine is collected for 5 hours. An abnormal test result is ,4.5 g excretion, which would be consistent with small bowel abnormality such as duodenal or jejunal disease. Normal values point to malabsorption originating from pan- creatic or biliary dysfunction. Historically, the Schilling test has been used to deter- mine vitamin B12 absorption and can also be used to evalu- ate the state of absorption in the intestine. B12 absorption requires not only intrinsic factor produced in the stomach but also adequate ileal receptors. The test can be performed in two phases—one with intrinsic factor and one with- out. The patient ingests radioactive B12 and then urinary amounts of B12 are measured. With normal absorption, B12 is absorbed and the excess is excreted in the urine. Without absorption, no urinary B12 will be measured. Unfortunately, the Schilling test has not been available in the United States for several years. A small bowel X-ray with barium contrast can indicate delays of motility such as an obstruction or ileus. A faster motility can also support the diagnosis of malabsorption. Biopsy of the small bowel via endoscopy is recommended for the patient with suspected fat malabsorption. Laboratory testing for fat-soluble vitamins may also assist in corroborating the presence of fat malabsorption. -Steatorrhea: fat travels undigested and unabsorbed to large intestine (pulls water in and causes diarrhea) -Fat soluble vitamins malabsorbed (need to be attached to fat) -Potential for excess oxalate (calcium and oxalate are usually absorbed together, which is why too much milk not a bad thing; calcium attaches to malabsorbed fat (going to excrete fat and calcium), which causes increased oxalate absorption, which increases kidney stones; too much oxalate = kidney stones) -Abdominal pain, cramping, diarrhea -Dg; fecal fat test (eat 100 g of fat and test fat by collecting stool for next 72 hrs.; if over 6 g. of fat then you are diagnosed with steatorrhea) or D-xylose absorption test (distinguishing between pancreatic dysfunction and small intestine dysfunction), or small bowel x-ray.

Nutrition Therapy for Malabsorption

-Nutrition Therapy for Fat Malabsorption Restriction of fat to 25-50 g per day is a standard first step in reducing the symp- toms of fat malabsorption. Table 15.9 outlines the dietary inter- ventions for a fat-restricted diet. Additionally, medium-chain triglyceride (MCT) supplements can be used to increase caloric intake. MCT are triglycerides that contain fatty acids considered medium chain (i.e., those with 6-12 carbons). Most MCT oil products contain primarily caprylic (C8) and capric (C10) fatty acids. One-half ounce (15 mL) provides 115 kcal or 8.3 kcal/g. MCT is absorbed directly into the circulatory sys- tem from the small intestine and does not require the normal lipid digestion and absorption processes that long-chain fatty acids require. This supplement can be added to soups and other hot foods. It has a neutral flavor but, because it is an oil, cannot be mixed adequately into cold foods. Practically speaking, the use of MCT oil is difficult due to its expense, and excessive use can actually exacerbate diarrhea. If the etiology for steatorrhea originates from pancreatic dysfunction, use of pancreatic enzymes is a primary mode of treatment. An example is the product Creon , which con- sists of pancreatic lipase, amylase, and proteases. Dosages are individualized and taken with each meal or snack to ensure adequate digestion. -Nutrition Therapy for Lactose Malabsorption Lactose is the simple carbohydrate found in milk and dairy products. Lactose is also found as an ingredient in many other food products because it is often used as a filler or browning agent. Milk provides approximately 11 g of lactose per cup. Other dairy products have varying amounts, with ice cream having approximately 9 g per cup and cheese having 1-2 g per ounce. Restriction of all milk and dairy products is the major step to treat lactose malabsorption, though individuals do vary in the amounts of lactose they can tolerate. If the lactose intoler- ance is secondary to another condition or due to acute illness, lactose exclusion is recommended for approximately 4 weeks. Then small amounts of lactose can be reintroduced, which is important to ensure adequacy of the diet for nutrients such as calcium and vitamin D. Dairy products such as cheese and yogurt have smaller amounts of lactose and may be adequately tolerated. Up to 1 cup of milk can be introduced in small incre- ments throughout a 24-hour period.58 Careful monitoring will guide the practitioner and patient on the amoun®ts of lactose lactase enzyme and can be used when milk and dairy foods are ingested. See Table 15.10 for an overview of nutrition therapy for lactose malabsorption/intolerance. -Nutrition assessment:Conditions of malabsorption can result in weight loss, vitamin and mineral deficiencies, and chronic protein-calorie malnutrition. Anthropometric data, especially weight change; dietary intake of macro- and micronutrients; and biochemical data reflective of fluid status and malnutrition are especially relevant. -Accurately assess weight loss, vitamin/mineral deficiencies, chronic PEM (protein energy malnutrition) -Look at anthropometric data, weight changes, dietary intake (24 hr. recall), look for edema, focus on fluid loss -Nutrition diagnosis: -May include malnutrition; altered GI function; impaired nutrient utilization (we aren't able to absorb the nutrient); underweight; involuntary weight loss

Celiac Disease

-Definition: an autoimmune disease in genetically susceptible individuals caused by the immunological reaction to gluten. It is a unique autoimmune disease in that the environmental trigger is known, genetic profiles are established, and there is typically a resolution of symptoms when that trigger (gluten) is eliminated from the diet and environment. -Damage to intestinal mucosa from gluten exposure (look at alpha gliadin, a specific protein, what causes immune response) -Genetic and autoimmune (if person has one autoimmune disorder, likely they have another one- type 1 diabetic with celiac disease) -When you remove gluten from diet, symptoms go away. -Epidemiology: -1% worldwide -Epidemiological studies indicate CD is much more common than previously thought, at approximately 1% prevalence worldwide. In 2012, prevalence of CD was estimated using the NHANES database to be 0.71%, or 1 in 141 invididuals.60 More recently, CD was diagnosed in 30 out of a group of 976 at-risk patients (see "Etiology" section). Other countries, including Argentina, Italy, Germany, Denmark, and Finland, have published similar studies indicating a much higher prevalence in these countries. -Etiology: -It is well understood that the damage to the intes- tinal mucosa observed in CD occurs when the small intes- tine is exposed to the prolamin fraction—a-gliadin and other protein components of gluten. Gluten is found in wheat, rye, malt, and barley. In this disease, exposure to the gliadin component of gluten results in a T cell mediated inflammatory response that damages the intestinal mucosa and is accompanied by an infiltration of white blood cells into the mucosa. This inflamma- tory response is also re- flected in production of IgA antitissue transglu- taminase (anti-tTG) and antiendomysial (EMA) and antigliadin (AGA) antibodies. These anti- bodies, which serve as diagnostic indicators for CD, reflect the auto- immune nature of this disease. The major genes for CD that have been isolated include HLA-DQ2 and HLA-DQ8, which are present in 95% of all patients with CD. Over 40 genes have been identified with CD and associations with other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis have been established.62 Influential environmental factors that may be involved with the disease process include a younger age when gluten is introduced, a shorter length or absence of breast- feeding, and the presence of viral infections during infancy, all of which appear to increase the autoimmune risk. -Alpha-gliadin from wheat, rye, malt, barley: causes immune response -Infiltration of WBC; production of IgA antibodies (IgA antibodies: released from GI tract). -BROW-M (Barley, rice, oats (issue is with cross-contamination), wheat, malt).

Bacterial Overgrowth

-Definition:Bacterial overgrowth syndrome results from cross-contamination of bacteria from the colon to the small intestine. This may be a result of surgery, disease, or trauma to the GI tract. The most common definition is 105 or more colony-forming units per milliliter (CFU/mL) of bacteria grown from a small intestinal aspirate.131 Diagnosis involves quantifying the presence of bacteria from the small intestine, the use of hydrogen breath tests (see tests in "Pathophysiology" section under "Malabsorption"), and the subjective response to antibiotic treatment. Resulting from cross contamination of bacteria from colon to small intestine (bacteria from large intestine enters small intestine) -Pathophysiology:In this condition, motility of the gastro- intestinal tract is delayed due to disease, surgery, or trauma, and stasis develops. There is a high risk for development of small bowel bacterial overgrowth for those individuals with short bowel syndrome. Bacteria multiply and begin to com- pete with the host for nutrients. Malabsorption, maldigestion, and malnutrition can result. -Motility of GI tract delayed (if a food is not entering small intestine, allows for bacteria to move from large intestine to small intestine) -Bacteria competes with host for nutrients (maldigestion/malabsorption/malnutrition)

Malabsorption- Treatment

-Depends on nutrient and underlying disease

Diarrhea- Medical Diagnosis

-Diagnosis of the underlying etiology is the most important step in determining treatment of diar- rhea. Considerations that will direct diagnostic procedures are the age of the patient, hydration status, the presence of blood in the stool, and whether the patient is immunocom- promised. Important symptoms to note are any recurring characteristics of diarrheal episodes, including time of day or any relationship to food intake. Typical diagnostic work-up will begin with stool cultures that will be examined for microorganisms (viral, bacterial), ova and parasites, leukocytes, lactoferrin, and the presence of blood. Further invasive procedures such as upper endos- copy, flexible sigmoidoscopy, or colonoscopy may assist in diagnoses not determined with initial stool cultures. Osmolality and electrolyte content of the stool can also be determined and will assist in differentiation between osmotic and secretory diarrhea, but these measures are used less often in clinical practice.4 Other clinical tests will measure complete blood count, electrolytes, albumin, and thyroid-stimulating hormone. Specific diagnostic tests for C. difficile include stool sample culture and tests using the cytotoxicity assay or the enzyme immunoassay for toxins A and B. -Diagnose underlying etiology (Is it a bacteria? Food? Virus? Fat malabsorption?) -All of these will impact diagnosis: Age, hydration status, presence of blood in stool, and immunocompetency -Recurrence of episodes (every time they have a sandwich, have diarrhea. Bread = Celiac) related to time of day and food intake -Stool cultures (bacteria, viruses, parasites in blood) -Procedures such as endoscopy -Osmolality and electrolyte content (can help us differentiate between osmotic and secretory diarrhea)

Diarrhea- Etiology

-Diarrhea can be described as either acute, persis- tent, or chronic in origin; it can also be classified as either osmotic or secretory. The etiology of the diarrhea can serve as a framework for discussion and understanding of diar- rhea-related conditions. Acute diarrhea is short term (less than 2 weeks), persistent diarrhea lasts 2-4 weeks, and diar- rhea that lasts longer than 4 weeks is considered chronic.23 Diarrhea can be associated with a number of health concerns, such as electrolyte imbalances, malabsorption, dehydration, and malnutrition. Osmolality is a measurement of the concentration of particles in solution. Normal osmolality of the gastrointes- tinal tract is approximately 300 mOsm/L. When the number of osmotically active particles in the intestine increases, the body responds by pulling water into the lumen in an attempt to normalize osmolality. When this occurs, increased water efflux results in what we refer to as osmotic diarrhea. Osmotic diarrhea can be caused by maldigestion of nutrients, exces- sive sorbitol or fructose intake, enteral feeding, and some laxatives. In general, when the causative agent is removed, osmotic diarrhea will cease. An example would be a patient whose diarrhea resolves when he is made NPO. This is one of the major differentiations between osmotic and secretory diarrhea. Secretory diarrhea also results from excessive fluid and electrolyte secretions into the intestine. The difference here is that the underlying disease is what causes excessive secre- tions, not the hyperosmolality. Thus, secretory diarrhea does not resolve when the patient is made NPO. Bacterial infec- tions often produce enterotoxins that result in this type of diarrhea. Protozoa, viruses, and other infections can also cause secretory diarrhea. Traveler's diarrhea is a common health problem affecting those who travel to other coun- tries. The major infectious agents resulting in traveler's diar- rhea are enterotoxigenic Escherichia coli, enteroaggregative E. coli, and Shigella, Salmonella, Campylobacter, Yersinia, Aeromonas, and Plesiomonas spp.27 Other potential causes of secretory diarrhea include medications, hormone-producing tumors, prostaglandins, and excessive amounts of bile acids or unabsorbed fatty acids in the colon.23,28 Diarrhea may occur as a side effect of antibiotics and other medications. These medications generally cause diar- rhea either by increasing GI motility or by altering the normal flora of the colon.29 See Table 15.3 for a list of frequently used antibiotics and other medications that can cause diarrhea. Clostridium difficile, a Gram-positive anaerobic bac- terium, is now one of the most common health care- acquired infections. The American Academy of Pediatrics has described increasing admissions in children's hospitals for C. difficile.30 When antibiotics are prescribed, their use can disturb the balance of normal flora of the colon and C. difficile has the potential to proliferate. Its endotoxins result in injury and inflammation within the colon. The most common antibiotics associated with C. difficile infection are ampicillin, amoxicillin, cephalosporins, and clindamy- cin. Symptoms can range from mild diarrhea to severe coli- tis. In mild cases, stopping the prescribed antibiotic will be enough to stop the infection. In more severe cases, antibi- otics such as metronidazole or vancomycin are generally administered.30,31 Chronic C. difficile infection may require more aggressive interventions such as a fecal transplant, dis- cussed later in this section.32 Enteral feedings are often implicated as a cause of diar- rhea. Even though changing types of formulas or reducing the rate of feeding is often proposed, the evidence for the effectiveness of this strategy is limited.33 Antibiotics and other prescribed medications are much more likely to be the cause.34 As is discussed later in this section, the use of fiber- enriched formulas provides an additional route of treatment. Traditional sources of fiber added to enteral formulas are soy polysaccharides (primarily insoluble), guar, and pectin (primarily soluble). Newer sources include fructooligosac- charides (FOS) and galactooligosaccharides (GOS). Most fiber-enriched enteral formulas contain a blend of FOS, GOS, and insoluble fiber sources.35 Delegge and Berry state that for the patient with diarrhea, it is appropriate to continue to feed enterally unless there is abdominal pain, fever, or distention, or fluid output is greater than input.33 If the stool output visu- ally looks the same as the feeding, this indicates rapid transit and malabsorption. Diarrhea is a common symptom of many gastrointesti- nal diseases. If the underlying disease disrupts normal diges- tion and absorptive capabilities, diarrhea will most often result. Examples of these conditions that are covered in this chapter include Crohn's disease, ulcerative colitis, and celiac disease. These diagnoses can also result in malabsorption of of lipids and other nutrients, which further contributes to the diarrhea. Other conditions that may present as diarrhea include pseudodiarrhea, fecal incontinence, and overflow diarrhea. The he medical provider will rule out these conditions as the eti- ology of diarrhea is examined.23 Other diseases that do not originate in the gastrointestinal tract can also present with symptoms of diarrhea. These may include, but are not lim- ited to, graft versus host disease, AIDS enteropathy with HIV infection, thyroid dysfunction, and some malignancies. -Acute or chronic: -Acute diarrhea: Have it for less than 2 weeks. -Chronic: Have it for more than 4 weeks. -If it falls between 2 to 4 weeks = persistent diarrhea. -Osmotic: increased water efflux due to an increase in osmolality (we have a lot of substances in GI tract; because there's so many substances in GI, water is pulled in). Causes: undigested nutrients, sorbitol (sugar alcohol), fructose, enteral feeds (feeding someone through tube), some laxatives can cause osmotic diarrhea. Osmotic diarrhea will subside if person stops eating (make person NPO). -Secretory: underlying disease causes secretions. If you make a person NPO with secretory, diarrhea will not go away. Causes: bacterial and viral infections, some medications that individuals are put on. Any type of GI disaese. -Side effect of medications or enteral feedings -Other illnesses may present as diarrhea and must be ruled out (chrone's disease, celiac disease)

Diarrhea- Clinical Manifestations

-Diarrhea presents as a change from the normal bowel function. This is generally a watery stool that is increased in frequency. Other characteristics of stool output will vary depending on the etiology of the diarrhea. For example, foul-smelling, frothy stools are associ- ated with steatorrhea. Composition and volume of stool are also consistent with the etiology of the diarrhea. Blood may be present in the stool, and is characterized as hematochezia, occult blood, or melena. Hematochezia is bright red blood on the surface of the stool, and represents contamination with blood from the rectum or anus. Occult blood is detected by testing the stool and usually results from bleeding in the lower gastro- intestinal tract. Melena is a dark stool caused by contamina- tion with blood from the upper GI tract. Hemoglobin from blood contributes to its dark color. Mucus in the stool may also be indicative of secretory diarrhea and may be infectious in origin. High levels of electrolytes are also consistent with secretory diarrhea.23 The presence of leukocytes in the stool indicates an inflammatory process such as inflammatory bowel disease, which is discussed later in this chapter. Other clinical manifestations that may occur with diar- rhea are abdominal pain and cramping. When defecation relieves cramping, diarrhea is generally from the distal colon. If abdominal pain and cramping continue after defecation, the origin is generally from the small bowel. Other symp- toms such as dehydration, weight loss, and electrolyte and acid-base imbalances are dependent on volumes of stool lost and represent one of the most serious consequences of diarrhea -Watery stool; increased frequency -Foul-smelling, frothy stools (for frothy stools: could be sign of accessory organ dysfunction): caused from steatorrhea (substances moving through GI tract so fast, we don't have time to digest fat, so it is excreted in stool) -Presence of blood: 1. Hematochezia (going to be bright red and usually coming from rectum- at the end of the GI) 2. Occult blood (usually coming from lower part of GI but it needs to be tested to figure out where it's coming from and it's darker in color) 3. Melena (from upper GI and dark blood) -Abdominal pain & cramping -Dehydration (a lot of fluid is leaving body, can lead to weight loss), weight loss -Electrolyte and acid-base imbalances (because so much is being lost in stool - ex: K+, bicarb)

Pathophysiology of Lower GI Tract

-Diarrhea: -Increase in frequency of bowel movements or increase in water content of stools. Affects consistency or volume. Abnormality in stool production as >200 g/day adults, >20 g/kg for children.

Diverticulosis/Diverticulitis- Pathophysiology

-Diverticula do occur in the small intestine but are most common in the colon. Factors that affect integrity of the mucosa of the colon appear to contribute to development of the diverticula. It is thought that within the colon, two or more of the muscular bands (taeniae coli) contract at the same time. This hinders motility of the colon and thus its ability to move waste products. Fecal matter becomes trapped and exerts excessive pressure against the wall of the colon. This pressure causes development of small pouches on the wall of the colon, which are referred to as diverticula. Diverticulitis is acute inflammation of the diverticula. Foodstuffs and bacteria can collect in diverticula and the mucosa can become infected. Further complications can include development of bleeding, abscess, obstruction, fistula, or perforation. -Fecal matter trapped, excessive pressure against walls of colon. -Development of pouches -Diverticulitis: pouches become inflamed -Bleeding abscess (pocket of pus), obstruction (blocks the exit), fistula (opening in GI that shouldn't be there), perforation (tear)

Diverticulosis/Diverticulitis- Clinical Manifestations

-Diverticulosis is asymptom- atic for most individuals. Diverticula are usually only diag- nosed when other tests such as a colonoscopy identify them. In approximately 20% of individuals, complications from diverticula, including diverticulitis, may develop. Signs and symptoms of diverticulitis can include fever, abdominal pain, gastrointestinal bleeding, and elevated white blood cell count. Radiology testing (ultrasound and CT scan) may be used to diagnose diverticulitis. Test results can demonstrate thick- ened walls of the colon, abscess, or inflammation. -Diverticulosis typically asymptomatic (may not know you have it) -Diverticulitis: fever, abdominal pain, GI bleeding, elevated WBC -Diagnosed by radiology testing: -Thickened walls, abscess, inflammation -Diverticulosis can be diagnosed with colonoscopy

Nutrition Intervention- Nutrition Therapy During Exacerbation of Disease- IBD

-During acute exacerbations of both UC and Crohn's disease, the extent of intestinal involvement, previous surgeries, diarrheal output, and bleeding direct the route for nutrition intervention. The literature supports a crucial role for enteral nutrition in treat- ment of active Crohn's in children. In children, enteral nutrition is preferred over the use of corticosteroids in treatment, as it allows for support of growth and development without the side effects associated with medications.104-106 For adults, enteral nutrition is recommended when use of medica- tions is not feasible and when additional nutrition is needed to improve or maintain nutritional status. Most research indicates parenteral nutrition (PN) with bowel rest is not necessary and the limited clinical trials indicate outcomes of remission are not improved. For those individuals with exten- sive intestinal involvement or short bowel syndrome, PN may be required immediately post-operatively or until there is adequate intestinal adaptation (see the section "Short Bowel Syndrome"). The type of enteral formula (chemically defined or polymeric) depends on the individual patient's medical and nutritional status. Enteral nutrition research has dem- onstrated that supplementation may play a role in modify- ing inflammatory response in the disease process. The use of enteral nutrition has been associated with improvement in clinical markers of inflammation (such as C-reactive protein), but has not consistently shown a positive effect on remission state or other clinical outcomes in adults.Energy needs for adults can be estimated using standard nutrition assessment guidelines (see Chapter 3). The amount of prior weight loss and the presence of infection will support the need for a higher energy provision. To meet growth needs of infants, children, and adolescents, specific attention to their unique requirements is important. As much as 120 kcal/kg for infants and 80 kcal/kg for adolescents may be required (see Chapter 3). If available, indirect calorimetry provides the most reliable indicator of energy needs in the hospitalized patient. Estimation of protein requirements will be based on the presence of any lean body mass wasting and biochemical parameters. ASPEN guidelines recommend 1-1.5 g protein/kg for adults. Infants, children, and adolescents may require 2.0-2.5 g/kg. If oral intake can be initiated, a low-residue, lactose-free diet with small, frequent meals is best tolerated initially. If ste- atorrhea is present, then fat should be reduced. As the patient responds to medical therapy, adding small amounts of fiber and then lactose as the patient can tolerate will advance the diet. Restricting fiber is generally only necessary during the acute exacerbation or if a stricture is present. Foods that may need to be initially restricted may be gas-producing foods, spicy or fried foods, caffeinated beverages, or any other food the individual patient identifies as problematic. The addition and advance- ment of an oral diet will need to be highly individualized. All patients should be assessed for micronutrient defi- ciencies. As noted earlier in this section, patients with IBD are at higher risk for deficiencies of calcium, vitamins D and B12, iron, zinc, and magnesium. In a normal small intes- tine, the ileum has specific receptor sites that allow for B12 absorption. Therefore, disease affecting the ileum specifically can potentially result in B12 deficiency. B12 deficiency can be treated with synthetic oral B12 as it does not require intrinsic factor and can be absorbed all along the small intestine, but note that this form must be administered in a higher dosage of 1000-2000 mcg daily. Vitamin D deficiency is treated with an oral dose of 50,000 IU once per week for 8 weeks. Maintenance can be achieved by assessing serum levels and supplementing monthly after the initial treatment. Calcium supplementation with cal- cium citrate in divided doses to provide 1200-1500 mg daily is recommended.107 It is recommended that additional supple- mentation should include zinc (12-15 mg/liter of stool output), magnesium (15-30 mEq/day), and copper (0.5-1.5 mg/day).107 Research has shown that patients with Crohn's disease have lower serum levels of antioxidants (vitamin E, vitamin C, and beta-carotene).108,109 It is thought that this might contribute to higher levels of oxidative stress in this disease. Higher levels of antioxidants may be warranted, but specific levels have not been established at this time; nor is it clear that supplement sources produce the same effect as foods. The most convincing evidence for the relationship between antioxidants and disease prevention has been in epidemiologic studies where strong associations have been demonstrated between dietary sources of fruits and vegetables and disease risk.109 Patients with IBD may avoid fruits and vegetables due to their disease symptoms and perceived intolerance to these foods. -Enteral nutrition preferred over parenteral: -If individual is using nutrition support, we want to use the gut if we can. If we don't use the gut, the gut cells die. If someone is on parental nutrition, we can also do enteral to use gut. -Assess energy needs (especially if there's weight loss or muscle wasting- use Mifflin St. Jeor) + stress factor (1.3-1.5 - can use this in place of activity factor): -30-50% more of their actual needs -May need to increase protein needs (depends on any muscle wasting- protein can be 1.0-1.5 g/kg) -Low-residue (low fiber), lactose-free diet -Small, frequent meals -Assess for micronutrient deficiencies. There's a chance we will be supplementing vitamins and minerals. Can give a multivitamin with these patients. May need to limit fat intake if steatorrhea is present, which leads to a decrease in fat soluble vitamin absorption.

Digestion and Absorption- Fermentation

-Fermentation produces SCFA (short chain fatty acids) and lactate (can be converted to glucose): SCFA (500-1200 calories per day used by large intestine, used by bacteria and for tissue growth). If substrate enters large intestine not completely digested = substances will start to be fermented by bacteria, which causes gas (these substances tend to be large and pull water into large intestine, which causes loose stool) -Energy produced used by bacteria, for tissue growth in colon or utilization in body (but used by large intestine first) -Excess substrate results in gas, flatulence (beans have a lot of fiber; as well as resistant starches such as some legumes, potatoes, unripened bananas; fiber; sugar alcohols; not able to fully digest and enter large intestine, which causes bacteria to ferment and gas and bloating; can also cause diarrhea)

Irritable Bowel Syndrome- Medical Treatment

-For those patients with IBS-D, anti- diarrheal agents can be used. These medications assist by decreasing motility and increasing consistency of the stool. (See previous discussion regarding diarrhea.) Antidiarrheal agents include diphenoxylate (Lomotil®), loperamide, atro- pine, and cholestyramine. Loperamide is the only medica- tion that has been used in controlled studies of IBS, and its effectiveness appears limited to treatment of diarrhea with- out affecting any other IBS symptoms. Antispasmodics using anticholinergic medications (dicyclomine and hyoscyamine) may be prescribed and often have better results when taken 30 minutes prior to eating. Peppermint oil has been noted to improve abdominal pain and cramping. Specific medications for IBS include those that work as either agonists or antagonists for the serotonin receptors. The class of medications that work as 5-HT4 agonists include renzapride, cisapride, and tegaserod. These medications are available in the United States only for compassionate use request. Alosetron (Lotronex®), a 5-HT3 receptor antagonist, is used for treatment of IBS-D. This medication is prescribed in the United States only under a strict, limited marketing program. Severe constipation and ischemic colitis have been reported as potential side effects of this drug. Another class of medications developed for use in IBS is the selective C-2 chloride channel activators. These medications affect chloride transport, which in turn increases fluid in the intestine and improves GI motility. Lubiprostone (Amitiza) is the medica- tion in this class that is currently available. New drugs in all of these classes are in various phases of development and testing. Tricyclic antidepressants and selective serotonin reup- take inhibitors (SSRIs) are also used to treat IBS. These medications include amitriptyline, desipramine, doxepin, or trazodone and fluoxetine, paroxetine, or sertraline, respec- tively. A summary of the research indicates that these medi- cations can be used effectively in treating the pain of IBS. Other medications used to treat IBS-C include bulking agents and osmotic laxatives. Bulking agents are supplements or medications that add psyllium, bran, or other sources of fiber to the diet. Osmotic laxatives such as Milk of Magnesia®, polyethylene glycol, and sorbitol have increased stool fre- quency of IBS-C patients but do not treat the other symptoms of IBS. Non-pharmacological treatments for IBS include cog- nitive-behavioral therapies (hypnosis, relaxation techniques, guided imagery), probiotics, and nutrition therapy. -Guided by symptoms -Antidiarrheal agents -Tricyclic antidepressants, SSRIs (SSRIs = selective serotonin reuptake inhibitors) -Bulking agents, laxatives: for patients with IBS-C. -Agonist (put something in place where serotonin would normally go- chemical that takes place of serotonin- increase gut motility. Chemical that binds to place where serotonin usually binds) or antagonists (not allowing anything to attach- decrease gut motility) or 5-HT4 receptors (receptors that allow serotonin to attach to cells) -Cognitive-behavioral therapies (hypnosis techniques)

Diverticulosis/Diverticulotis Etiology

-Historically it has been thought that the develop- ment of diverticulosis was related to low fiber intake, history of constipation, and the resulting long-term increased colonic pressure. But more recent investigations have examined diver- ticular disease within the context of inflammation, visceral hypersensitivity, microbiome changes, and abnormal motility. Factors associated with increased risk of diverticulosis include obesity, decreased physical activity, steroids, alcohol and caffeine intakes, and cigarette smoking. -Historically associated with low fiber intake, history of constipation, increased colonic pressure (allows for pockets to form): -May be taking in too much fiber and not enough fluid -More recently focused on increases inflammatory response -Other risk factors: obesity, sedentary, steroids, alcohol and caffeine intake, cigarette smoking

Nutrition Therapy for Constipation

-Historically, nutritional treatment of constipation has con- centrated on the role of adequate fiber and fluid intake. This is despite the overall lack of outcomes research for the role of fiber in gastrointestinal disease.52,53 Survey data have indi- cated most Americans consume an average of 15 grams of fiber each day. Americans aged 1 year and older are esti- mated to consume approximately 4.9 g resistant starch per day (range 2.8-7.9 g/day).21 Adequate intake of whole grains, fruits, and vegetables has been one of the primary focuses of both the Dietary Guidelines for Americans and the Nutrition Recommendations for Canadians. -Nutrition assessment: Relevant nutrition assessment data in cases of constipation would include fluid and beverage intake, dietary fiber intake, bioactive substance intake, beliefs and attitudes, and misuse of medication, especially laxative -Fluid and beverage intake -Dietary fiber intake (but American's typically take in ~15 g of fiber a day, which isn't too much) -Bioactive substance intake (vitamins, minerals) -Beliefs and attitudes -Misuse of meds; esp. laxatives -Nutrition diagnosis: -May include inadequate fluid or fiber intake, altered GI function, or undesirable food choices

Irritable Bowel Syndrome- Etiology

-IBS historically has been designated as a "functional" disorder. This means a diagnosis is made after ruling out all other possible organic causes of the patient's symp- toms. A variety of criteria have been used to expedite the diagnosis of IBS, including the Manning and the Rome III Criteria discussed earlier in this chapter. The specific cause of IBS is unknown, but current research is focused on mul- tiple factors including genetic predisposition; altered immune response stimulated by food sensitivity and an altered micro- bial environment; an elevated inflammatory response to gas- troenteritis; small intestinal bacterial overgrowth (SIBO); abnormal release, transport, or recognition of serotonin; and an increased sensitivity of the enteric nervous system that causes abnormal motility and pain.72 Figure 15.12 pres- ents an overview of the factors thought to contribute to IBS symptoms. Other conditions that are commonly associated with IBS include celiac disease and lactose maldigestion. The American College of Gastroenterology recommends that all patients be screened for celiac disease as a component of the differential diagnosis for IBS. -Historically considered functional disorder (all other potential diagnoses must be ruled out first, and if symptoms are still present, then you can diagnose IBS) -Specific cause is unknown, but may be caused by genetic predisposition, altered immune response to food, altered microbial environment of large intestine, inflammatory conditions, small intestine bacterial overgrowth (bacteria from large intestine enter the small intestine- small intestine doesn't want bacteria in it), decreased serotonin levels (serotonin is neurotransmitter)

Sphincters of GI Tract

-Ileocecal sphincter: protects small intestine from bacteria translocation from large intestine by remaining closed except during digestive process. Maintains transit time to ensure adequacy of digestion and absorption; connects small intestine to large intestine. -Internal anal: you have no control of. -External anal: you have control of sometimes

Short Bowel Syndrome- Nutrition Intervention

-Immediately post-operatively, patients will receive parenteral nutrition. The PN prescription will be based on energy, protein, and micronutri- ent requirements (see Chapters 5 and 7). As diarrhea begins to decrease (anywhere from 2 to 6 weeks post-operatively), an oral diet can begin.126,128 Many patients require combinations of parenteral, enteral, and oral nutrition support in order to accommodate degrees of malabsorption and patient require- ments for nutrition and fluids. Sugar-free, isotonic clear liquids should be the first items offered. Nutrition therapy for SBS will vary depending on the presence of the colon. In both situations (small bowel ostomy or presence of colon), diet would prog- ress slowly to a low-residue, low-fat, lactose-free, low-oxalate diet. Caffeine and alcohol should not be initially consumed. Alcohol sugars such as xylitol, mannitol, and sorbitol are usually not tolerated. Insoluble fiber is generally not toler- ated initially but may assist in maximizing nutrient efficiency by serving as a source of fermentation in patients who have colonic continuity. In patients with small bowel ostomy, sol- uble fiber may actually assist in promoting mucosal health. Soluble fiber, like other sources of prebiotics, assists in production of short-chain fatty acids that are a primary fuel for the colon. Soluble fiber may also enhance water absorp- tion in the colon and reduce the amount of diarrhea.128,130 Overall, it is crucial to remember that the diet truly needs to be designed for the individual patient and that significant differences between patients will be likely. One item at a time is added to the diet to ensure toler- ance. If GI symptoms are exacerbated, the food added should be removed from the diet. It may be added again at a later date, depending on the patient's adaptation after surgery. It may be best to retry categories of restricted foods even as long as 6 months post-operatively, since bowel adaptation can take as long as 1-2 years.129 Many patients with SBS are discharged on home par- enteral nutrition (PN) or home enteral nutrition support (EN) in addition to the limited oral diet. PN or EN is usually cycled over 10-12 hours at home, which will allow a patient to resume normal activity. -TPN postoperatively (7-10 days, may go longer, but usually cannot meet individual's full energy needs with TPN) -Oral diets introduced as diarrhea decreases -Progress slowly to low residue, low fat, lactose free, low oxalate diet. -Add foods one at a time, and if there are issues, then eliminate that food, but food can be reintroduced at a later time and may not have any issues with that food. Avoid caffeine, alcohol, sugar alcohols, and insoluble fiber.

Nutrition Therapy for Ileostomy and Colostomy

-Implications of intestinal resection may be ana- lyzed in the context of anatomy and physiology of the gastrointestinal tract. When a certain part of the intestinal tract is removed, normal physiology and function of that portion is lost to the individual. This loss of function will pro- duce changes in motility, in absorption, and in how waste products are handled—all of which potentially can impact nutritional status. Larger resections will result in the most nutritional complications. Resections of the terminal ileum and loss of the ileocecal valve tend to result in significant fluid, electrolyte, vitamin, and min- eral deficiencies. The ileal brake controls the rate of movement from the small intestine to the large; hence, when there is loss of the ileum and/ or ileocecal valve, motility is much faster, inter- rupting normal absorption. The location of the stoma on the GI tract will also determine the type of fecal matter pro- duced. As explained earlier, the function of the colon is to reabsorb water and electrolytes. Fecal matter further along the colon will produce firmer, less watery stool. Stool output with an ileostomy, then, will be much more liquid, while output with a colostomy, depending on where it is located along the colon, will be firmer and more normal. -Nutritional intervention: -The goals for nutrition therapy are to decrease risk of obstruction, maintain normal fluid and electrolyte balance, reduce excessive fecal output and/or change consistency of output, and minimize gas and flatulence (to reduce odor and inflation of the appliance).119 After sur- gery, the patient will be transitioned to an oral diet. Evidence regarding the optimal amount of time between post-operative status and initiation of oral feeding has recently been evalu- ated. A review of the literature indicates that early oral feeding (post-operative day 1-2) after lower intestinal surgery is safe and tolerated in the majority of patients.120,121 This progression typically begins with liquids and proceeds as tolerated to a low- residue diet with four to six small feedings each day. Discharge from the hospital varies by institution but the earlier post-op feeding appears to lead to shorter hospital length-of-stay.121 Foods that may not be completely digested and that can cause stoma obstruction should be avoided for the first 6-8 weeks after surgery. These include tough fibrous meats; vegetables such as spinach, corn, and peas; dried fruits such as raisins; fruit skins and seeds; and popcorn. The patient will need to be instructed to eat slowly, chew thoroughly, and drink adequate fluids. Generally, oral intake should resemble the regular diet, meeting all nutritional needs by the 8th week post-operatively. Cohen et al. examined dietary patterns and foods associated with either improvement in GI symptoms or exacerbation of symptoms in over 2000 survey respondents.122 Results indicated that foods that consistently improved symp- toms in this cohort were yogurt, rice, and bananas. Foods that aggravated ostomy output were fruit, nuts, red meat, popcorn, dairy products, and high-fat/fried foods. If the patient experiences excessive or watery fecal out- put, the amount of insoluble fiber should be reduced while the amount of soluble fiber is increased. Applesauce, bananas, tapioca, potatoes, oatmeal, oat bran, rice, and pasta may help decrease diarrhea. Foods that cause gas and flatulence should be avoided (see Table 15.13), as these same foods can cause difficulty for the patient with an ostomy. Use of yogurt, parsley, and buttermilk may decrease gas and odor. Vitamin and mineral requirements for the patient after bowel surgery will be affected by the length and location of the remaining portions. Earlier in this chapter, absorption sites for vitamins and minerals were discussed (see Figure 15.7). More common micronutrient issues will involve vitamins K and B12. Vitamin B12 absorption is of specific concern because it requires adequate ileal receptors and a normal transit time. Research focused on absorption of dietary vitamins and minerals in patients with ileostomy has determined that most vitamins, minerals, and phytochemicals appear to be adequately absorbed in this population.123,124 Livny and col- leagues did find that beta-carotene was best absorbed from cooked carrots rather than raw carrots in these patients.125 However, since most patients' intake and tolerance vary widely, a general multivitamin is recommended. Typical daily fluid output from a colostomy ranges from 200 to 600 mL after adaptation has occurred.125 Individuals with an ileostomy are at higher risk for nutrient complica- tions. Outputs average 1200 mL per day initially, though they will decrease to close to 600 mL per day. Nutrients of concern after an ileostomy include primarily fluid and electrolytes, especially if the ileocecal valve is not intact. All nutrients may be at risk if transit time is sufficiently altered. It is estimated that individuals will lose approximately 90 mmol/L sodium within fecal output if the stoma is at the duodenojejunal flex- ure and up to 140 mmol/L sodium if the stoma is at the termi- nal ileum.119,126 Immediately post-operatively and during times of increased output, fluid intake should be monitored closely to avoid the complications of dehydration. (See Chapter 8 for methods to estimate fluid requirements.) Liberal use of salt and sodium-containing rehydration solutions is encouraged. Avoiding liquids with solid foods but sipping fluids between meals is advised. -Decrease risk of obstruction -Maintain fluid and electrolyte balance -Reduce fecal output -Minimize flatulence -After surgery transition to oral diet -Ileostomy: output is liquid so monitor fluid and electrolytes carefully; colostomy: output is solid (should absorb majority of fluid), big issue with colostomy is making sure there's no obstruction (if you're not taking in enough fluid/fiber, get a hard piece of stool that blocks intestine, and has to leave body through bag, so you can't push it out). -Right after surgery: put patient on parental nutrition, but want quick progression to enteral or oral. One day post-op: want an oral diet (start with clear liquids and then moving to low residue, and then end with 4-6 small meals a day)

Diarrhea- Epidemiology

-In U.S., 99 million new cases per year, mostly foodborne, resulting in 3100 deaths -Worldwide, diarrhea is the second leading cause of death, 760,000 children under five die per year -Salmonella, Campylobacter

Short Bowel Syndrome- Treatment

-Initially, medical treatment will focus on managing fluid and electrolyte balance. This is generally achieved by parenteral nutrition and intravenous support, and then, as the patient is able, by oral rehydration solutions. Motility is controlled by medications used to treat symptoms of diarrhea. These agents work to either decrease motility or to thicken consistency of the stool, and include medications such as LoMotil® (diphenoxylate), Immodium (loperamide), paregoric, codeine, Tincture of Opium, Kaopectate, or bismuth subsalicylate. In SBS, taking these medications rou- tinely 30 minutes before meals and at bedtime assists with control of symptoms.128,129 Octreotide (LAR® Depot), which is given intravenously, is a somatostatin analog that reduces the levels of growth hormone and has been used to treat diar- rhea in short bowel syndrome.129 These medications, while decreasing motility, may also improve digestion by increasing the amount of time nutrients and enzymes are exposed within the bowel. Gastric hypersecretion, common after extensive bowel resection, is treated by use of proton pump inhibitors or H2 antagonists. In general, though, oral medications as well as nutrient supplementation are not consistently absorbed and will need to be monitored closely. The newest class of drugs for SBS is used to enhance cell proliferation in the remaining portions of the intestinal tract and includes somatropin (Zorbtive), a recombinant human growth hormone that promotes anabolism for certain cells. Teduglutide (Gattex), a GLP-2 (glucagon-like peptide) analog, received FDA approval for use in SBS in 2012.129 Surgical treatment for short bowel syndrome includes intestinal lengthening procedures and intestinal transplant. In several outcome studies in both pediatric and adult patients, successful transplants have allowed for weaning from parenteral nutrition. -Manage fluid and electrolytes -Oral rehydration solutions -Medications for motility and diarrhea and gastric hypersecretion -Don't want to damage small intestine with acid from stomach, so individuals are prescribed proton pump inhibitors. -Once part of bowel is removed, may have a small bowel transplant.

Inflammatory Bowel Disease- Pathophysiology

-It is theorized that those individuals who are genetically suscep- tible and who are exposed to certain triggers experience an abnormal immune response. This immune response results in release of cytokines that direct an excessive and abnor- mal inflammatory reaction that ultimately destroys the intestinal mucosa. UC and Crohn's are also characterized by exacerbations of the disease process interspersed with peri- ods of remission. Approximately 40%-50% of patients with UC have dis- ease only involving the rectum. Damage to intestinal mucosa in UC usually only involves the first two layers of tissue (mucosa and superficial submucosa) within the colon and rectum. But with chronic disease, the intestinal wall can become so thin that the mucosa is ulcerated. This is referred to as toxic megacolon. UC disease usually affects one section of the gastrointestinal tract at a time, whereas Crohn's disease often presents with a "skipping" pattern affecting multiple portions of the gastrointestinal tract. Crohn's disease can affect any portion of the gastro- intestinal tract from mouth to anus and approximately 75% of patients have some form of small intestine involvement. Crohn's disease can damage all layers of gastrointestinal mucosa. This inflammatory process is characterized by the development of fistulas that when healed are replaced by fibrotic tissue. The fibrosis can result in recurrent strictures and bowel obstructions -Exposure to certain triggers by those genetically susceptible: Triggers may be smoking, bacteria, virus, change in intestinal flora, certain foods may trigger, change in physiology of GI tract; causes immune response. -Abnormal immune response -Release of cytokines -Destruction of mucosa -UC (ulcerative colitis) - primarily in colon -Crohn's presents with "skipping" pattern throughout GI- majority of Crohn's seen in ileum (lower part of small intestine) and large intestine -Going to affect multiple areas (may be really severe in one spot)

Small Intestine Absorption- Lipids and Nutrients

-Lipids enter lymph via passive diffusion: -First converted to micelles and packaged as chlylomicrons -Steatorrhea (fatty stools)- if lipid not absorbed -Most nutrients absorbed in duodenum and jejunum (this is why we are able to do gastric bypass surgery. Ileum can compensate if there are issues with duodenum or jejunum, but it takes time): -B12 absorbed only at specific sites in ileum (in order for B12 to be absorbed, it needs intrinsic factor, and intrinsic factor comes from parietal cells). Elderly are not producing as much intrinsic factor. Ileum is where we reabsorb bile acid (6-8 times per day), and the 16th time it is no longer good and we excrete it (called enterop).

Digestion and Absorption- Maintaining Balance

-Maintaining balance of intestinal flora (we have over 400 types of bacteria - good bacteria - helps maintain integrity of our digestive system): -Resistant starches: legumes (beans), potatoes, bananas -Prebiotics: fiber (helps bacteria grow in large intestine). Ex: inulin (found in plant sources. Plants that are high in inulin include onion, asparagus, garlic, bananas, artichokes) -Probiotics: live bacteria (get it from yogurt, fermented foods) -Synbiotics: mixture of pre and probiotics -Vitamin K and biotin: endogenously produced (we produce them in large intestine, but we don't know exactly how much).

Malabsorption

-Malabsorption is a general term referring to malabsorption of fat, carbohydrate, or protein as a result of maldigestion or damage to the anatomy and physiology of the small intestine. -Definition: Maldigestion of fat, carbohydrate, protein (if we can't fully digest a food, we can't fully absorb the nutrients from that food- so fat, carb, and protein will keep moving through GI, which will cause gas, bloating, diarrhea) -Etiology:Damage to the anatomy and physiology of the small intestine due to disease is the most common cause of malab- sorption. Conditions such as celiac disease, Crohn's disease, and even protein-calorie malnutrition result in decreased villous height, decreased enzyme production, and subsequent malabsorption and/or maldigestion. Dysfunction of the acces- sory organs of digestion (liver, pancreas, and gallbladder) may also serve as the origin of the maldigestion. Decreased transit time, as seen in diarrhea or following surgical changes in the anatomy, also can result in either mal- digestion or malabsorption. For example, after a gastrectomy, dumping syndrome causes a rapid transit through the small intestine, which prevents adequate exposure to enzymes and adequate time for the absorptive mechanisms. -Decreased villous height (villi being damaged: not able to absorb/digest nutrients), enzyme production, or dysfunction of accessory organs (pancreas, liver, gallbladder) due to disease -Decreased transit time: usually due to surgery (gastric resectioning, ruoff, dumping syndrome)

Diverticulosis/Diverticulitus- Nutrition Intervention

-Many Americans consume only limited amounts of fiber. Nutrition therapy to treat or prevent diverticulosis will include a high-fiber diet providing the recommended 25-35 g/day.53,115 Historically, it has been common practice to avoid nuts, seeds, and hulls with the theory that these may aggravate the condition or result in inflamma- tion. There is not adequate evidence to support this advice and the restriction is no longer recommended.118 Many patients, especially older adults, will need to use a fiber supplement if they are unable to consume adequate fiber from foods. Products that may be used to normalize GI function include Fiberall® and Metamucil®, bulk-forming agen®ts made from psyllium, a source ofinsolublefiber,andBenefiber ,solubledietaryfiberextracted from guar gum. Other sources of fiber supplementation such as methylcellulose have also been used successfully. Certainly the preferred method to increase fiber intake is through foods, but, if needed, these supplements are available. Adequate fluid intake should always accompany any increase in fiber intake. The patient with acute diverticulitis will be progressed from bowel rest to clear liquids. The patient can then move toward a low-residue diet until inflammation and bleeding are no longer a risk. -High fiber for diverticulosis (25-35 g of fiber) -Not adequate evidence to restrict nuts, seeds, hulls (if they're taking in adequate amount of fiber, we shouldn't worry about nuts/seeds/hulls because everything is moving through) -Fiber supplement if person not taking in adequate amount of fiber, but if taking in fruits, vegetables, whole grains, don't need to. -Bowel rest with progression for diverticulitis (NPO initially, then clear liquids, then low residue until inflammation is gone): -Low residue = low fiber -Once inflammation subsides, go back to high fiber diet. -Educate patient on low fiber until inflammation is gone, and then educate on high fiber once patient leaves.

Nutrition Therapy for Rehabilitation During Periods of Remission- IBD

-Maximizing energy and protein intakes to facilitate rehabilitation should be the primary goal. Weight gain within a normal healthy range combined with physical activity will ensure rebuilding of protein stores and muscle mass. Depend- ing on the extent of disease and the response to treatment, specific dietary modifications will need to be individualized. It is always a goal to normalize dietary patterns and encourage a variety of all foods as the patient is able to tolerate them. Consumption of foods high in antioxidants (e.g., carot- enoids, vitamin E, vitamin C, and selenium) and omega-3 fatty acids has been associated with protection against inflam- mation. These would include fruits, vegetables, vegetable oils, nuts, and fishes such as tuna and salmon. Glutamine, short-chain fatty acids, antioxidants, and immunonutrition with omega-3 fatty acids will likely be important therapeutic alternatives in the management of inflammatory bowel diseases, though the documented beneficial effects are still being established.Foods high in oxalate may increase risk for urolithiasis or kidney stones, which can occur in IBD. These foods include, for example, cocoa, tea, wheat germ, strawberries, nuts, spin- ach, beets, baked beans, peanut butter, tofu, and high doses of vitamin C supplements (.2 g/day). As has been previously discussed in this chapter, use of probiotics and prebiotics enhances the normal flora of the GI tract. In several recent studies, consumption of foods and sup- plements with probiotics and prebiotics has been associated with decreased symptoms for patients with IBD and a positive change in anti-inflammatory markers. -Maximize energy & protein: based on their normal needs (NOT based on exacerbation needs, so use normal activity factor because you want them to increase their physical activity) -Weight gain (if they lost during exacerbation, want them to return to normal weight) and physical activity -Normalize dietary patterns: want them to eat a proper amount of all food groups -Food sources of antioxidants, Omega-3s -Limit foods high in oxalate: Individuals with IBD are at increased risk of developing kidney stones, so we prevent kidney stones by decreasing oxalate intake. -Probiotics and prebiotics: to restore gut microflora

Small Intestine Motility

-Motility of small intestine is controlled by enteric nervous system and influenced by variety of hormones, peptides, and neurotransmitters. -As the chyme enters the duodenum from the stomach, the hormone gastrin and the intestinal pacemaker cells (the interstitial cells of Cajal) stimulate the onset of segmental contractions. This segmentation (ringlike contractions long length of small intestine- contracted segments relax and preciously relaxed areas contract. Oscillating contractions mix chyme within small intestine lumen) motility allows mixing of chyme with digestive secretions. In the duodenum, contractions occur approximately every 9 minutes, with a slower rate further down the small intestine. It may take as long as 3-5 hours to complete the process. -Additionally, when the small intestine is empty, motiliity continues with the action of the migrating motility complex (MMC). The MMC, first described in 1969, consists of much weaker contractions that occur approximately every 100-150 minutes and serves the purpose of ridding the small intestine of any leftover bacteria or waste. Motilin, a hormone secreted by the small intestine, assists in the control of the MMC. Additional hormones and neuropeptides assist in the regulation of small intestine motility and release of intestinal secretions. These include somatostatin, vasoactive inhibitory peptide, neurotensin, serotonin, cholecystokinin, orexin, leptin, and ghrelin. Motility of the small and large intestine is of much interest due to its possible role in several diseases and its importance in enteral nutrition support. -Anatomy of small intestine influences motility and rate of transpit. Ex: ileocecal valve helps control rate of movement of food from ileum to ascending colon. -Hormonal stimulation: gastrin (gastrin is produced in stomach; when gastrin enters small intestine, it initiates muscle contractions). -Peristaltic reflex: segmental contractions (muscle contractions allow for chime to mix with intestinal juices because this is where digestion is occurring, and we need digestion to get nutrients into simplest form) -Mixing of chyme -MMC (migrating motility complex): motility when SI empty. Causes muscular contractions even when chyme is not present. Ensures that small intestine is clean (every 100-150 minutes). Motilin (hormone that is responsible for MMC). -Other hormones: CCK, orexin (assists in increasing appetite), leptin (decreases appetite) -Ileocecal valve helps to control rate of food movement (from small intestine) -Small intestine motility: movement of chyme through small intestine.

Nutrition Assessment for Lower GI Tract Conditions

-Multiple disorders: -Differing etiologies and care (some are autoimmune, some are genetic, some are caused from trauma) -Share common factors in assessment

Large Intestine Motility

-Musculature of the large intestine provides the basic structure that supports its motility. The large intestine has repeating bands of longitudinal skeletal muscle (called taeniae coli) that follow the length of the colon and circular smooth muscle that covers the entire organ. -entire organ. Motility of the large intestine can be categorized into several distinct types. In the small intestine, motility includes segmentation, which allows for mixing of intestinal contents. Likewise, the large intestine also uses a type of segmentation, called haustra- tion. Haustration occurs when circular muscle forms small sacs called haustra. Haustra hold amounts of chyme as it is mixed with secretions of the colon. Haustra can form and then disappear when intestinal contents are moved through the colon. Other types of movement that accomplish motility include propulsion, mass movements, and defecation. Propulsion is accomplished by alternating waves of relaxation and contraction of smooth muscle lasting several minutes. Intestinal contents can move in both directions within the colon, allowing for adequate absorption of fluid and electrolytes. Mass movements occur when there is a significant contraction of a large portion of the colon. This generally occurs several times a day and moves a large portion of intestinal contents along the colon. Finally, defecation occurs when distention of the rectum relaxes the anal sphincter. This final movement is ultimately (usually) under voluntary control. -Haustration (mechanism for moving chyme through large intestine): -Circular muscles forms small sacs (haustra). Moves forwards and backwards to ensure we are absorbing all the water we need to absorb. -Propulsion: contraction of the haustra. Movement of chyme to absorb the fluid and electrolytes (Na, Cl, K). -Mass movement: occurs a couple times a day. Big contraction that moves everything forward. -Large intestine motility: Chyme (in liquid form) enters large intestine and absorb as much of that water as possible, which gives us a solid stool. -Need relaxation of internal and external sphincter.

Nutrition Therapy for IBS

-Nutrition assessment: The symptoms of IBS can result in changes in oral intake such as avoidance of certain foods and food groups, which may lead to poor nutrition quality of life. The severe limitations of foods seen in more extreme cases can likewise cause nutrient deficiencies, potential underweight, and malnutrition. Since IBS may present with either diarrhea, constipation, or both, the specific assessment data needed to provide appropriate nutrition care will vary. -Can lead to nutrient deficiency, underweight, malnutrition (if individual has issue with GI tract, individual stays away from certain foods, and will only eat certain foods (decrease in energy, vitamin/mineral intake)) -Nutrition diagnosis: May include inadequate oral intake; altered GI function; undesirable food choices; food- and nutrition-related knowledge deficit; disordered eating pattern

Short Bowel Syndrome- Nutrition Therapy

-Nutrition assessment:Maintenance of nutritional and hydration status is critical for individuals with SBS; therefore, assessment of fluid and beverage intake is especially impor- tant. Aggressive nutrition support and safe progression to an oral diet require careful attention by the entire health care team. Accurate assessment of surgical history with antici- pated bowel function along with an in-depth understanding of nutrient absorption are essential in the care of patients receiv- ing nutrition support and transitional feedings. Assessment of fluid and beverage intake -Nutrition diagnosis: May include inadequate energy intake; inadequate protein intake; malnutrition; inadequate vitamin/mineral intake; unintentional weight loss; altered GI function; and impaired nutrient utilization

Nutrition Therapy for Celiac Disease

-Nutrition assessment:Some individuals may present with a severely damaged small intestine and thus with severe mal- absorption, which will result in significant weight loss, vitamin and mineral deficiencies, and, ultimately, protein-energy mal- nutrition. Most patients actually do not present with extensive weight and protein deficiencies but may have micronutrient deficiencies. Nutrition interventions are lifelong and require significant education from a registered dietitian who is up to date and knowledgeable about the GFD. Nutrition assess- ment should not only evaluate the extent to which anthro- pometric changes and nutrient imbalances may be present, but also explore social networks, knowledge and beliefs, and adherence behaviors. -Assess anthropometric changes, nutrient imbalances (person could have unintentional weight loss) -Explore social networks, knowledge and beliefs and dietary adherence -Nutrition diagnosis: -May include impaired nutrient utilization (villi in small intestine = can't absorb nutrients), altered GI function -Can also use food and nutrition-related knowledge deficit

Diarrhea- Nutrition Diagnosis and Intervention

-Nutrition diagnosis: Common nutrition diagnoses associated with diarrhea and its physical impact on nutritional status include inadequate energy intake; inadequate oral intake; inadequate fluid intake; altered GI function; and involuntary weight loss. Other potential diagnoses may be a result of inadequate intake or excessive losses. A common example in diarrhea is excessive potassium losses. -Usually associated with excessive losses or inadequate intake (inadequate energy/fluid/oral intake) -Nutrition intervention: Nutrition therapy for diarrhea is designed to restore normal fluid, electrolyte, and acid-base balance; decrease gastrointestinal motility; thicken the con- sistency of the stool; repopulate the gastrointestinal tract with normal flora; and gradually introduce foods that allow the patient to return to a normal diet without aggravation of symptoms.37-40 Historically, nutrition therapy for diarrhea has included making the patient NPO or prescribing clear liquids. Current practice recognizes the importance of stimulating the gastrointestinal tract by feeding the patient. This speeds recovery of damaged cells. In addition, clear liquids are typi- cally high in simple carbohydrates, which increase osmolality of the gastrointestinal tract. This actually can make diarrhea worse due to hyperosmolality. Oral rehydration solutions are designed to both restore fluid and electrolyte balance and enhance absorption in the intesti- nal tract. There are several commercially prepared rehydra- tion solutions such as Pedialyte® and Rehydralyte®. The World Health Organization has a standard recipe for an oral rehydra- tion solution: 13 to 23 tsp table salt, 3⁄4 tsp sodium bicarbonate, 1 3 tsp potassium chloride (salt substitute), 1 1 3 tbsp sugar or rice powder, and 1 L bottled or sterile water (see Table 15.5). The use of rice powder yields a solution with reduced osmolality that appears to be just as effective as those with sucrose as a carbo- hydrate source.40,41 Nutrition therapy to decrease motility should focus on avoiding high-sugar beverages and foods high in simple carbohydrates (lactose, sucrose, or fructose); sugar alcohols (sorbitol, xylitol, mannitol); caffeine; and alcoholic beverages. Gas-producing foods (Table 15.13) should be avoided. As mentioned previously, adding sources of soluble fiber and resistant starch has been the most typical route to thicken the consistency of the stool. For infants this may include the use of banana flakes, apple powder, or other pectin sources, which can be added to infant formula and to other foods for children and adults. If the infant has begun solid foods, strained bananas, applesauce, and rice cereal are the best ini- tial food choices; historically, the BRAT (bananas, rice, apple- sauce, and toast) eating pattern has been used to guide the initial food choices for acute diarrhea, but it does not provide a sufficient variety of nutrients for long periods of use.38 Another step in treating diarrhea is the use of probiot- ics and prebiotics.29,42 These foods and supplements support growth of healthy flora and/or repopulate the intestinal tract with healthy bacteria (see Box 15.1 for suggestions of food sources of probiotics). As mentioned previously, undigested substrates are fermented to SCFA. Probiotics and prebiot- ics will increase the amount of SCFA produced. Research indicates SCFA promote water and electrolyte absorption in the colon, which reduces the incidence of diarrhea.43 Other research has suggested that probiotics and prebiotics may improve the mucosal defense in the GI tract and may also reduce the growth of harmful bacteria. This may play a signifi- cant role in reducing diarrhea associated with enteral feeding. Other research has studied the effect of using probiotics and prebiotics as part of the treatment for radiation-induced diar- rhea, diarrhea secondary to rotavirus, and traveler's diarrhea. Dosages for probiotics and prebiotics are still being established because current research has not provided con- sistent enough data to make dosage recommendations or to consistently recommend supplementation.44,45 Another chal- lenge in using probiotics as nutrition therapy is the difficulty in maintaining the viability of the organisms. Heat, light, and aging are just some of the issues that can affect the actual dosage provided by a food product or supplement. Currently the Food and Drug Administration (FDA) does not allow any health claims regarding probiotics, but has established manufacturing and safety guidelines. Government regula- tion varies depending on the product's intended use: It may be regulated as a dietary supplement, a food ingredient, or a drug.46 If it is sold as a dietary supplement, it does not require FDA approval. Dietary supplement labels may make claims about how the product affects the structure or func- tion of the body without prior FDA approval, but they cannot make health claims (claims that the product reduces the risk of a disease) without the FDA's consent. Box 15.1 and 15.2 provide guidance to the practitioner on probiotic/prebiotic recommendations to clients. In adults and older children, introduction of solid foods should begin with a low-residue diet. Even though the term low residue is used in practice, there can be confusion as to what it means. The typical scenario for a low-residue diet begins with adding refined starches (e.g., rice) and then slowly adding other foods to the diet. -Historically we would put people on NPO or clear liquids (clear liquids are usually high in simple sugars) - we want to feed the person as soon as we can because it stimulate the GI tract and increases healing time so they are able to heal -Now recognize importance of stimulating GI tract -May use oral rehydration solutions - Pedialyte or oral rehydration solution (WHO- 1/3 tsp salt, ¾ tsp of sodium bicarb (baking soda), 1/3 tsp salt substitute that contains sodium and potassium, 1 1/3 tsp sugar, 1 L of bottled water) -Focus on decreasing motility by increasing soluble fiber (BRAT diet bananas, applesauce, rice, white toast). Avoid drinks that are high in sugar, sugar alcohols, caffeine, alcohol. -FIVE MAJOR GOALS OF NUTRITION INTERVENTION: 1. Restore fluid and electrolyte balance 2. Decrease GI motility 3. Thicken stools 4. Replace microflora (we lose a lot of bacteria) 5. Increase oral intake -Use of prebiotics and probiotics

Malabsorption- Nutrition Intervention

-Nutrition intervention for malabsorption: The purpose of nutrition therapy is to provide structure for elimination of the malabsorbed nutrient from the diet, but at the same time provide appropri- ate substitutions in order to ensure maintenance of nutritional status. -Nutrition intervention for fat malabsorption: (restrict fat to 25-50 g./day). Medication: Creon (Contains lipase, amylase, protease. Taken with meal. Breaks down CHO, pro, fats. Can be given for any macronutrient malabsorption issue) and MCT oil (Medium chain triglyceride- usually added to soups. Can be absorbed directly into blood stream. ½ oz. = 115 calories). -Nutrition intervention for lactose malabsorption

Celiac Disease- Nutrition Intervention

-Nutrition therapy and education will center on the GFD. Patients will need to learn identification of gluten-containing foods, label reading, steps to prevent cross-contamination, identification of gluten in non-food items, and selection of an overall healthy diet with avoidance of gluten.68,69 Initially, some patients following the GFD may need to address secondary malabsorption (such as lactose) until the intestine has healed. Secondary lactase deficiency is common in this disorder due to damaged villi and enzyme secretion. As villi are regenerated and absorp- tive capability returns, lactose can be added back to the diet slowly and usually does not require a lifelong restriction. On the other hand, gluten does require a lifelong restric- tion. The patient will need to avoid all foods and other products that contain wheat, rye, barley, and malt. Certi- fied gluten-free oats in quantities of #50 g (about 1⁄2 cup dry rolled oats) are currently considered to be safe.68 Specific interventions for gluten-free nutrition therapy are outlined in Table 15.11. In 2012, the FDA published final rules that defined the term "gluten-free" to mean that the food item so labeled must contain ,20 ppm of prolamin.70 This regulation does not apply to foods regulated by the U.S. Department of Agriculture (meats and poultry) or the Tobacco Tax and Trade Bureau (such as distilled beverages), where this label- ing is voluntary. The labeling definition does apply to any food imported into the United States. National organizations such as the Celiac Disease Foundation, Canadian Celiac Associa- tion, and Gluten Intolerance Group of North America provide excellent resources for persons diagnosed with CD. -Low residue (which is low fiber), low-fat, lactose free, gluten-free diet = do these until the villi are repaired, and then they can go back to eating normal about of fiber, fat, lactose, but keep gluten out of diet: -#1 nutrition intervention: gluten-free diet (educate patient on foods that contain gluten, what foods to stay away from; do thorough education on reading food labels for things that are hidden in ingredient list; talk about cross contamination; talk about gluten in nonfood products) -Identify hidden sources of gluten -Specialty products (gluten free products) -If something is labeled as gluten free, it has to have <20 ppm prolamin (group of proteins found in plants- ex: alpha gliadin)

Nutrition Therapy for Diverticulosis/Diverticulitis

-Nutrition therapy for diverticulosis/diverticulitis: Research indicates that dietary habits may be strongly linked to the etiology of diverticulosis. Nutrition therapy should then focus on those nutrition interventions that could impact disease course. Recent publications have called into question the use of high-fiber diets for treatment and/or preven- tion of diverticulosis.116 As the complex pathophysiology of diverticulosis is better understood, more effective nutrition therapy interventions will follow. At present, there does not appear to be adequate evidence to eliminate the high-fiber diet recommendation.117 The patient with diverticulosis is not at any more risk for malnutrition than any other individual. The presence of diverticulitis with infection and inflamma- tion does impact nutritional requirements if this condition is prolonged or if other complications, such as sepsis, occur -Nutrition assessment: Evaluate dietary fiber intake -Nutrition diagnosis: Altered GI function; inadequate fiber intake

Nutrition Therapy for Bacterial Overgrowth

-Nutrition therapy will be consistent with the level of malab- sorption that is present. Nutrients most commonly malab- sorbed (fat and lactose) should be eliminated from the diet initially until the underlying condition is treated. Methods to increase nutrient density will accompany any restrictions, and steps should be made to maximize caloric and protein intakes to replenish nutrient stores -Consistent with level of malabsorption (if we have issue breaking down lactose, want to limit lactose intake; if issue breaking down fat, limit fat intake) -Malabsorbed nutrients eliminated -Increase nutrient density -Maximize calorie and protein intake

Diarrhea- Nutrition Therapy

-Nutritional consequences of diarrhea are initially depen- dent on the volume of gastrointestinal losses and then on the length of the disease course. Large-volume losses can quickly lead to dehydration and electrolyte and acid-base imbalances. Hyponatremia and hypokalemia are both common with diar- rhea. Metabolic acidosis may develop due to excessive loss of bicarbonate ions in stool output (see Chapters 8 and 9). Infants and older adults are at particular risk because their bodies are much more sensitive to rapid shifts in both fluids and electrolytes. Maintaining homeostasis is more difficult for both of these populations, in part due to the inability of their renal systems to act quickly enough for adequate com- pensation. Chronic diarrhea can also cause fluid and electro- lyte complications and can result in malnutrition and specific symptoms.37-40 Historically, nutrition therapy for diarrhea has included making the patient NPO or prescribing clear liquids. Current practice recognizes the importance of stimulating the gastrointestinal tract by feeding the patient. This speeds recovery of damaged cells. In addition, clear liquids are typi- cally high in simple carbohydrates, which increase osmolality of the gastrointestinal tract. This actually can make diarrhea worse due to hyperosmolality. Oral rehydration solutions are designed to both restore fluid and electrolyte balance and enhance absorption in the intesti- nal tract. There are several commercially prepared rehydra- tion solutions such as Pedialyte® and Rehydralyte®. The World Health Organization has a standard recipe for an oral rehydra- tion solution: 13 to 23 tsp table salt, 3⁄4 tsp sodium bicarbonate, 1 3 tsp potassium chloride (salt substitute), 1 1 3 tbsp sugar or rice powder, and 1 L bottled or sterile water (see Table 15.5). The use of rice powder yields a solution with reduced osmolality that appears to be just as effective as those with sucrose as a carbo- hydrate source.40,41 Nutrition therapy to decrease motility should focus on avoiding high-sugar beverages and foods high in simple carbohydrates (lactose, sucrose, or fructose); sugar alcohols (sorbitol, xylitol, mannitol); caffeine; and alcoholic beverages. Gas-producing foods (Table 15.13) should be avoided. As mentioned previously, adding sources of soluble fiber and resistant starch has been the most typical route to thicken the consistency of the stool. For infants this may include the use of banana flakes, apple powder, or other pectin sources, which can be added to infant formula and to other foods for children and adults. If the infant has begun solid foods, strained bananas, applesauce, and rice cereal are the best ini- tial food choices; historically, the BRAT (bananas, rice, apple- sauce, and toast) eating pattern has been used to guide the initial food choices for acute diarrhea, but it does not provide a sufficient variety of nutrients for long periods of use.38 Another step in treating diarrhea is the use of probiot- ics and prebiotics.29,42 These foods and supplements support growth of healthy flora and/or repopulate the intestinal tract with healthy bacteria (see Box 15.1 for suggestions of food sources of probiotics). As mentioned previously, undigested substrates are fermented to SCFA. Probiotics and prebiot- ics will increase the amount of SCFA produced. Research indicates SCFA promote water and electrolyte absorption in the colon, which reduces the incidence of diarrhea.43 Other research has suggested that probiotics and prebiotics may improve the mucosal defense in the GI tract and may also reduce the growth of harmful bacteria. This may play a signifi- cant role in reducing diarrhea associated with enteral feeding. Other research has studied the effect of using probiotics and prebiotics as part of the treatment for radiation-induced diar- rhea, diarrhea secondary to rotavirus, and traveler's diarrhea. Dosages for probiotics and prebiotics are still being established because current research has not provided con- sistent enough data to make dosage recommendations or to consistently recommend supplementation.44,45 Another chal- lenge in using probiotics as nutrition therapy is the difficulty in maintaining the viability of the organisms. Heat, light, and aging are just some of the issues that can affect the actual dosage provided by a food product or supplement. Currently the Food and Drug Administration (FDA) does not allow any health claims regarding probiotics, but has established manufacturing and safety guidelines. Government regula- tion varies depending on the product's intended use: It may be regulated as a dietary supplement, a food ingredient, or a drug.46 If it is sold as a dietary supplement, it does not require FDA approval. Dietary supplement labels may make claims about how the product affects the structure or func- tion of the body without prior FDA approval, but they cannot make health claims (claims that the product reduces the risk of a disease) without the FDA's consent. Box 15.1 and 15.2 provide guidance to the practitioner on probiotic/prebiotic recommendations to clients. -In adults and older children, introduction of solid foods should begin with a low-residue diet. Even though the term low residue is used in practice, there can be confusion as to what it means. The typical scenario for a low-residue diet begins with adding refined starches (e.g., rice) and then slowly adding other foods to the diet. -Fluid losses: -Dehydration (take this into consideration when looking at their lab values), hyponatremia (low sodium levels), and hypokalemia (low potassium levels). -Metabolic acidosis (bicarb is leaving through stool) -Malnutrition (we aren't absorbing anything because it is leaving so quick through the GI; every time you eat, you flush it out, so you don't want to eat very often) -Infants and elderly at greatest risk (decreased ability for the body to compensate, particularly, the renal system (acid base balance related to kidney))

Small Intestine Digestion

-Pancreatic juices provide the primary digestive enzymes in the small intestine. The protein-digesting enzymes include trypsinogen, chymotrypsinogen, procarboxypeptidases, and elastase. Pancreatic amylase is the primary enzyme involved in starch digestion. Pancreatic lipase and colipase accomplish the largest proportion of lipid digestion. Brush border enzymes in the small intestine include lactase, alpha-dextrinase, sucrase, maltase, and glucosi- dase, which provide final digestion of all carbohydrates (see Figure 15.4). Other brush border enzymes include entero- kinase, which activates the pancreatic enzyme trypsinogen to form trypsin. Trypsin then activates other trypsinogen mol- ecules and pancreatic proenzymes. Together, these enzymes degrade protein into smaller units (oligopeptides of two to six amino acids and free amino acids). Peptidases, located in the brush border, are responsible for digestion of oligopeptides into free amino acids, dipeptides, and tripeptides that can then be absorbed . -Starch digestion: -Pancreatic amylase (released from pancreas; break down amylose) -Lactase, alpha-dextrinase, sucrase, maltase, and glucosidase from brush border (these all help get everything to their simplest form) -Protein digestion: -Trypsinogen, chymotrypsinogen, procarboxypeptidases, and elastase: these all come from pancreas -Enterokinase (major role is active enzyme trypsinogen, which allows for proteins to be broken down and to its simples form free amino acids and di/tripeptides) from brush border

Lipid Digestion

-Pancreatic lipase (enzyme responsible for breakdown of fat; is ready to break down fat), and colipase (excreted from pancreas, and assists in breaking down fat; has to be activated by trypsin) -Bile (needed to emulsify fat- produced in liver, stored in gallbladder)

Inflammatory Bowel Disease- Clinical Manifestations

-Patients with UC present with signs and symptoms including abdominal pain, bloody diar- rhea, and tenesmus (urgency for defecation). Patients with severe disease often are febrile, are tachycardic, and have diar- rhea that contains pus and mucus. The Montreal classification system is a clinical tool that is used describe the clinical and endoscopic presentation of both Crohn's and UC.96 The True- love and Witts Criteria are a method to classify the severity of UC.97 Radiological testing in UC will often show severe inflammation of the large bowel with thickened walls and superficial ulcerations, and, over time, the haustra become edematous and thickened. In Crohn's, radiographic images will demonstrate small bowel and terminal ileum abnormali- ties with frequent evidence of strictures. Serological testing for markers of IBD includes serum levels of cytokines (IL-1, IL-6, and tumor necrosis factors as measures of inflamma- tion) and antiglycan antibodies (ASCA and ANCA). The use of these markers has increased, and is proposed not only for diagnosis but for evaluating response to treatment. Other acute-phase reactants such as C-reactive protein and the erythrocyte sedimentation rate (ESR) are elevated but are not necessarily specific to intestinal inflammation. Most recently, elevated calprotectin (Cal), lactoferrin (Lf ), and polymorpho- nuclear neutrophil elastase (PMN-e) levels in stool have been found to be indicative of exacerbations for IBD. White blood cell (WBC) count can also be elevated, and leukocytes in stool confirm the inflammatory process. Biochemical indi- ces for anemia are generally depressed, and in severe disease often confirm significant anemia. Patients with Crohn's disease experience abdominal pain, diarrhea, and tenesmus. They are much less likely to have blood in their stool but usually experience more abdominal pain and cramping than patients with UC. Disease involv- ing the small intestine places the individual at higher nutri- tional risk than disease involving only the colon. Weight loss, muscle wasting, and malnutrition can be common in Crohn's due to both increased requirements and decreased oral intake. Crohn's disease can also be insidious, presenting with only mild symptoms or only those that are extraintestinal in nature. As discussed previously, Cal, Lf, and PMN-e levels in stool have been found to be indicative of exacerbations of Crohn's disease.98,99 In severe exacerbations, low albumin levels and elevated WBC are common. Imaging tests may demonstrate deep ulcerations that often skip over portions of the GI tract. Fistulas and tracts between ulcerations can be observed in severe disease -Abdominal pain, bloody diarrhea (most likely going to see this in UC rather than Crohn's because UC affects part of large intestine), tenesmus (tenesmus is urgency to defecate- may see this in UC and Crohn's) -Febrile, tachycardic -CRP and ESR elevated: any time there is inflammation, these are elevated. -Cal, Lf, and PMN-e levels in stool, but they shouldn't be. -ASCA more specific for Crohn's; pANCA more specific for UC: measure to see which one is more elevated (helps with diagnosis). Antiglucan antibodies -WBC elevated -Weight loss (not uncommon because if there'd destruction to small or large intestine, you are decreasing its absorptive capabilities)

Short Bowel Syndrome- After Surgery

-Phase 1: 7-10 days after surgery: extensive fluid and electrolyte losses, large volume of diarrhea, TPN (total parental nutrition: feeding through the vein and giving bowel a rest. Getting macronutrients, fluid, vitamins/minerals, however, it is difficult to give individuals nutrients with parenteral). -Phase 2: Months after surgery: reduced diarrhea volume, adaptation of remaining bowel, enteral nutrition transition to oral diet. People may not tolerate foods orally, so try it later. -Phase 3: One to two years after surgery: continued adaptation of bowel, intestinal tract increases in length and diameter, and villous height

Protein Malabsorption

-Protein-losing enteropathy: muscle wasting; don't usually see this on its own, usually in relation to another disease (this is a symptom of 65 other diseases) -Reduced serum protein -Peripheral edema (reduced serum protein, which leads to peripheral edema - oncotic pressure- if we don't have adequate amount of protein, fluid will just sit in legs).

Short Bowel Syndrome- Pathophysiology

-Several factors will determine the prog- nosis of this condition: extent of remaining small intestine, presence of the colon, presence of the ileocecal valve, health of the remaining gastrointestinal tract, and any comorbid condi- tions the individual may have. The distal ileum is also impor- tant to consider as it assists in regulation of transit time and without it, symptoms of malabsorption and dumping will most likely be present. Though each case is highly individualized, most research agrees that a resection of more than 70% of the GI tract or that leaves ,100 cm of small intestine will result in severe nutritional and metabolic complications.126,128,129 The post-operative period for SBS generally follows three distinct phases. The first period ranges anywhere from 7 to 10 days and is characterized by extensive fluid and electrolyte losses within large volumes of diarrhea. During this phase, patients are dependent on parenteral nutrition, which not only provides required nutrients but manages fluid and elec- trolyte balance. The second post-operative phase may last for several months and is characterized by reduction in diarrhea vol- umes with the initial stages of adaptation of the remaining bowel. It is during this phase that enteral nutrition can be introduced with a gradual transition to an oral diet.126 During the third phase, there is continued adapta- tion of the remaining bowel. This includes increased blood flow, secretions, and mucosal cell growth. The inner lumen of the remaining small intestine increases in diameter and this, along with an increase in villous height, allows for increased absorptive surface area. This time frame varies, but may range from 1 to 2 years.128,129 Enteral feeding, espe- cially early exposure to enteral nutrition, supports successful adaptation. As mentioned earlier, the amount of remaining bowel determines the extent of this condition. Loss of the ileum pre- vents B12 absorption and reabsorption of bile salts. Reduction in bile salts further contributes to fat malabsorption. No other part of the intestinal tract can compensate for these losses. The ileocecal valve not only controls intestinal motility but also prevents translocation of bacteria from the colon to the small intestine. When this control is lost, nutritional and met- abolic complications are much more prominent. Because one of the primary functions of the colon is reabsorption of both fluid and electrolytes, electrolyte and fluid balance are much more likely to be regulated if the colon remains in continuity. Vitamin and mineral losses are major issues in SBS. When fat is malabsorbed, the intestine is unable to absorb adequate amounts of vitamins A, D, E, and K. These will need to be supplemented appropriately, and levels within the body will need to be evaluated. Other nutrients often deficient include sodium, magnesium, iron, zinc, selenium, and calcium because they are often lost in the large volumes of diarrhea. -Prognosis depends on length of remaining small bowel, health of remaining GI, any co-morbid conditions: very individualized: 70% start to see issues. -Major vitamin and mineral losses -Fat malabsorption affecting vitamins A, D, E, K. Bile reabsorbed at end of small intestine, pieces are missing, which causes bile reabsorption. Bile helps emulsify fat so we can break it down and reabsorb it. -Sodium, magnesium, iron, zinc, selenium, calcium loss. Diarrhea: can't digest/absorb.

IBS- Nutrition Intervention

-Since IBS etiology and patho- physiology are complex and differ among individuals, nutri- tion therapy goals for IBS will focus on interventions for the patient's specific symptoms and his or her response to specific food triggers. These may include exclusion of individual foods that are not tolerated or that are suspected to cause an aller- gic reaction. Nutrition education should focus on normalizing overall dietary patterns, ensuring adequate nutritional intake, eliminating those foods that trigger symptoms, and taking the necessary steps to reduce gas production and abnormal motility. One intervention for treating IBS is the use of a traditional exclusion diet. This approach eliminates all possible foods related to the patient's symptoms. Then each food is added back within a specific time period. If the patient does not experience any symptoms when the food is added back to the diet, that food is considered to be tolerated and allowed to be included in the regular diet. The American College of Gastroentrology states that the research studies on exclusion diets have demon- strated variable success and, in general, were not randomized controlled trials.72 The methodology to identify food allergies (skin prick, IgA, IgE) is also problematic (see Chapter 9 for more information on food allergies and exclusion diets). The presence of lactose indigestion does not necessarily mean that it is a cause of IBS, but certainly the two can coexist. Breath hydrogen tests can confirm this. Additionally, taking a careful diet history relating signs and symptoms with lactose ingestion or presenting a milk challenge would be other steps to determine if lactose should be avoided. Generally, elimina- tion of lactose for 1-2 weeks is adequate to determine the success of this intervention. The most significant progress for nutrition therapy in IBS has been the development of the fermentable oligo-, di-, and monosaccharides and polyols (FODMAP) approach.86-90 The rationale for this intervention focuses on the fact that foods high in FODMAPs are not well digested and that their osmotic load contributes to luminal distention, as shown in 416 Part 4 Nutrition Therapy ym • y y mptoms hypersensitivity • Gut inflammation/ immune activity • Barrier defects? • • • Other factors Figure 15.13. These foods are also highly fermentable and lead to further distention and gas production. These are the typi- cal signs and symptoms associated with IBS. Food sources of FODMAPs are listed in Table 15.12. Though limited num- bers of studies are available, a recent, well-designed double- blind crossover study demonstrated that the FODMAP diet significantly reduced symptoms for those IBS patients in the trial.86,87 As discussed in Table 15.2, nutrition assessment includes food diaries or a diet history that should focus on dietary components that the patient has associated with any increase in gastrointestinal symptoms. This recent research is very promising and it is hoped that continued research will confirm the efficacy of nutrition therapy for IBS. Registered dietitians are encouraged to become knowledgeable about the FODMAP diet and the steps to guide the patient through the process of elimination of these foods and their reintro- duction as appropriate while ensuring optimal nutritional intake throughout the trial. Once a baseline nutritional history has been established and nutrition problems are identified, the RD and patient can begin to identify any needed changes in diet. Overall nutri- tional adequacy should be addressed first. Many patients with IBS tend to eat erratically due to their gastrointestinal symp- toms, and often eating is associated with a high level of anxi- ety and stress. Establishing a regular eating pattern that does not exacerbate symptoms is a crucial initial step. Historically, the most common nutrition intervention for IBS has been increasing fiber intake, but research does not support the effectiveness of this intervention. In fact, insoluble fiber sources may exacerbate symptoms.72 The only current recommendation for fiber supplementation in IBS patients is the use of ispaghula husk, which is more com- monly known as psyllium. For those patients with IBS-C, psyllium supplementation may assist in normalizing bowel movements. Of course, increased fluid is also necessary as fiber intake is increased. Probiotics have received attention for their potential use in IBS. Translating the research to practice poses some difficulty, though. Many of the studies have used a variety of strains with a variety of dosages. The largest studies have demonstrated improvement in the symptoms of bloating and gas production with probiotics use.44 As discussed earlier in this chapter, adding these foods and supplements may be beneficial within the overall nutrition therapy plan.44-46 Due to problems with gas and flatulence, providing recommendations to relieve these symptoms will also be beneficial. Simple carbohydrates that cause gas are raffinose, lactose, fructose, and sorbitol. Avoiding foods that produce gas and taking steps to decrease swallowed air will decrease gas production. Products such as Beano® or Bean-zyme® provide alpha-galactosidase, which potentially decreases the volume of undigested carbohydrate entering the large intestine and thus decreases the amount of gas produced. -Depends on symptoms and food triggers -Exclusion diet (What is recommended- Remove majority of gas producing foods and add them back in one by one to determine which foods are causing the issue) -Fermentable oligo-, di-, and monosaccharides and polyols (FODMAP) approach: Eliminating foods that are gas producing (remove foods that are associated with gas/flatulence) -Relieve symptoms associated with gas and flatulence -Increase insoluble fiber if individual has IBS-C (pulls water in)

Normal Anatomy and Physiology of Lower GI Tract

-Small intestine anatomy (narrow; can be up to 20 ft.): -3 parts of small intestine: duodenum, jejunum, and ileum. These are not separate components, but each differs in anatomy, motility, secretion, digestion, absorption. Anatomy is organized to provide maximum surface area and allow for complete digestion and absorption of most foods. -Maximum surface area (increased about 600x- folds, villi, and microvilli increase the surface area) for digestion and absorption. Tissue of small intestine is circularly folded into folds of Kerckring. Rising from mucosal surface are finger like projections called villi. On surface of villi are fine hair like projections called microvilli (this area is often referred to as brush border- the combined features of these anatomical features increase surface area of small intestine to 600x greater than it would be if intestine were straight flat tube. -Spaces between villi are called CRYPTS. These crypts are location of steam cells from which specialized epithelial cells (ENTEROCYTES) for small intestine develop. They migrate up villi where after serving their function, they're sloughed off and replaced with newly generated enterocytes (absorptive cells). Because of this rapid turnover, enterocytes have high nutrient needs that must be met continially to maintain integrity of intestine. Malnutrition/disease result in decreased villous height. The higher up an enterocyte goes, the more likely it is to die because the lumen in the small intestine is a harsh environment (acidic). Turnover is high, to make new cells it requires a lot of energy (you need to eat).

Common Surgical Interventions for the Lower GI Tract

-Surgical resections may be warranted for many diagnoses dis- cussed in this chapter, including IBD and diverticulitis. Specific details of each individual's disease course will determine the need for surgical intervention. These may include disease refrac- tory to current medical treatment, an abscess not responding to antibiotic therapy and bowel rest, or acute emergencies such as peritonitis or gastrointestinal bleeding. The extent of the surgical resection and procedure used again depend on the individual patient's disease course. The most common procedures are discussed here with a review of the nutritional implications. Ileostomy and Colostomy Surgical resection of the colon and rectum requires development of a new path for feces to be excreted from the body. Many of these surgeries create a stoma— a surgically created artificial opening into the abdomen—from which waste products can be excreted. An ileostomy is removal of the colon and rectum. The end of the ileum is surgically attached to the stoma. The individual then uses an appliance pouch) where feces and other waste products are collected. A colostomy exists when the rectum only is removed and the end of the colon is surgi- cally attached to the stoma. Again, the individual utilizes a pouch appliance to collect waste products. Alternatives procedures where the outside surgical appliance can be avoided are available. These procedures, which create internal pouches where waste products can collect, include ileoanal reservoir surgery, ileal pouch-anal anastomosis, and continent ileostomy. -Ileostomy and colostomy: -Creation of a stoma (opening in abdominal wall- connect part of large or small intestine so that waste can be eliminated from body) -Ileostomy: colon and rectum are removed (end of GI = ileum, everything else is gone). Waste that is collected is liquid (majority of fluid is absorbed in large intestine, but no longer have large intestine, so looking for dehydration, vitamin/mineral inadequacy) -Colostomy: rectum removed (still have the large intestine). Want to avoid any blockages. -Pouch appliance used to collect waste

Small Intestine Absorption

-The anatomy of the small intestine, as discussed earlier, is uniquely constructed to accomplish maximal digestion and absorption. Each villus contains access to the circulatory and lymphatic systems via capillaries and lymphatic vessels, and villi thus provide necessary routes for absorbed nutrients. Absorption for end products of digestion occurs primarily through active transport and may utilize a Na1/K1 pump system at the brush border. Glucose, galactose, and amino acids utilize this type of absorption mechanism. Fructose uses facilitated/carrier-mediated transport as its absorptive mechanism and is affected by the presence of glucose, amino acids, and the total amount of fructose. Fructose malabsorption has been of recent interest for its potential contribution to gastrointestinal symptoms. Additional research indicates that some nutrients, including glucose, may be absorbed in part through a paracel- lular route. This means that small amounts of nutrients may leak between epithelial cells. Other research has indicated that the amount of glucose absorbed may be directly related to motility of the duodenum. Lipid absorption is much more difficult due to its insolubility in water. For lipids to be successfully absorbed, they must undergo several steps and utilize several protein carriers. Fatty acids and other lipid components must be first incorpo- rated into micelles in the gut lumen before absorption into the enterocytes. Then, they must be incorporated into chylomicrons (a type of lipoprotein) that can then enter the lymphatic system via passive absorption. Due to this complex absorption mechanism, many diseases of the small intestine can interrupt normal fat digestion and absorption. Understanding the steps of fat digestion and absorption can assist in differentiation of diseases affecting the small intestine or ancillary organs of digestion. For example, pancreatic dis- ease may reduce the amount of pancreatic lipase available for adequate digestion. Crohn's disease may decrease transit time and reduce the ability of the small intestine to accomplish all the steps required for digestion and absorption. Steatorrhea, an abnormal amount of fat in the stool, is the condition that develops when lipid is not digested or absorbed correctly. As mentioned earlier, portions of the small intestine can adapt to absorb most nutrients. However, in a normal, healthy individual, most nutrients will be absorbed in the duodenum and jejunum. The ileum can also accommodate absorption of many nutrients if foodstuffs remain there long enough. One exception to this is the absorption of B12, which can occur only at specific receptor sites in the ileum. The ileum is also the primary site for reabsorption of bile acids, though some may also be reabsorbed in the jejunum and colon. This process is referred to as the enterohepatic circulation of bile acids. Since bile acids are exclusively pro- duced in the body, these substances need to be recirculated back to the liver in order to maintain an adequate body pool of approximately 4 g. Bile acids recirculate from the small and large intestine back to the liver approximately six to eight times per day. When disease interrupts enterohepatic circulation, fat malabsorption can occur. Furthermore, in hypercholesterolemia, the medication cholestyramine is used to bind bile acids in order to decrease the body pool and reduce serum levels of cholesterol.

Irritable Bowel Disease- Etiology

-The exact etiology for IBD is unknown but the current working hypothesis involves the interaction of both environmental and clinical factors that cause an inappro- priate immune response in geneticallly predisposed individuals.95 These factors may include environmental factors such as smoking, infectious agents, intestinal flora, diet, and physiological changes in the small intestine from which an abnormal inflammatory response is triggered. There is a strong genetic association for IBD as evidenced by posi- tive family history in approxi- mately 5%-15% of patients. In identical twins, the incidence of IBD is 44% versus only 3.8% in fraternal twins. Numerous genes associated with IBD susceptibility have been rec- ognized and many share simi- lar genetic factors with other autoimmune diseases. -Interaction of both environmental and clinical factors that cause an inappropriate immune response in genetically predisposed individuals -Cause is unknown -Strong genetic association -Positive family history in 5-15% of cases

Carbohydrate Malabsorption

-The most common example of carbohydrate malabsorption is lactose malabsorption, com- monly referred to as lactose intolerance or lactose maldiges- tion. Over the previous decade, specific polymorphisms that identify geographic and ethnic traits for lactase persistence and lactose maldigestion have been discovered.56 When there is inadequate lactase available for digestion, or if anatomy or motility does not allow adequate exposure to lactase, lactose will travel to the large intestine undigested and unabsorbed. Bacteria in the large intestine will cause the lactose to undergo fermentation, which creates increased gas and abdominal cramping. Undigested lactose also pulls additional water into the large intestine, contributing to abdominal cramping and resulting diarrhea. Lactose intolerance is commonly associ- ated with other gastrointestinal diagnoses including irritable bowel syndrome, celiac disease, and inflammatory bowel disease. Lactose malabsorption can be diagnosed using either a lac- tose tolerance test or lactose hydrogen breath test. In the latter, after the baseline breath hydrogen concentration is measured, the patient consumes 25-50 grams of lactose. Breath hydrogen concentration is remeasured in 3-8 hours. An increase .20 ppm suggests lactose malabsorption. This test is preferred over the lactose tolerance test and has approximately 90% sensitivity. -Lactose malabsorption (decreased production of lactose or decreased motility) -Increased gas, abdominal cramping, diarrhea -Diagnosis: lactose tolerance test, lactose breath hydrogen test -Restrict milk and dairy products (yogurts are tolerated better than liquid milk because yogurt contains bacteria and bacteria breaks down lactose; harder cheeses) -Products such as lactaid (add lactase which breaks down lactose) can be recommended. -PROTEIN Malabsorption: n Protein malabsorption is most commonly referred to as protein-losing enteropathy. This is not a specific disease, but it occurs, as do most all malabsorption disorders, as a result of other diseases. Excessive protein loss in the gastro- intestinal tract has been noted in over 65 different diagnoses.59 Excessive protein is lost in the stool, and the patient will experi- ence reduced serum levels of proteins and an increasing amount of peripheral edema due to the reduced oncotic pressure. Treatment Appropriate treatment for malabsorption will depend on the nutrient that is malabsorbed and the underlying disease causing malabsorption.

Celiac Disease- Prognosis and Treatment

-The only current treatment for CD is nutrition therapy consisting of a gluten-free diet (GFD). After avoidance of all gluten, villous height generally returns to normal. As the anatomy returns to normal, maldigestion and malabsorption (if present) resolve, as do the physical signs and symptoms. Unfortunately, a small percentage of patients continue to experience intestinal damage despite a GFD. Abdulkarim and colleagues found the most common reasons for continued villous damage (or refractory CD [RCD]) were unknown gluten contamination and the pres- ence of coexisting diseases such as pancreatic insufficiency, irritable bowel syndrome, and malignancy.65 A recent trial of a nutrition therapy to eliminate sources of cross- contamination has demonstrated success in correctly iden- tifying RCD patients.66 Other examinations of RCD indicate differences in immunopathology and overall prognosis in this small subset of individuals. -Gluten-free diet normalizes villous height -Maldigestion and malabsorption resolve (as the villi repair themselves) -Reduction in physical signs and symptoms -Refractory celiac disease often due to unknown gluten contamination and co-existing disease: when people are not sure what products contain gluten, they may be unknowingly consuming gluten. Co-existing disease: any type of pancreatic dysfunction, IBS, and tumor/malignancy.

Irritable Bowel Syndrome- Pathophysiology

-The pathophysiology of IBS is complex and, as previously stated, not completely understood. Pro- posed etiological factors may be examined in context of what we know about the normal physiology of the gastrointestinal tract. In IBS, abnormal motility is considered to be a major fac- tor contributing to symptoms of abdominal pain and altered bowel habits. Contraction and motility are regulated through the gastrointestinal tract's own specialized pacemaker cells called the interstitial cells of Cajal. The autonomic nervous system relays input for the smooth muscle of the GI tract through a specialized enteric ner- vous system. Two types of neurons regulate the contraction of smooth muscle, motility, and secretory functions of the GI tract. Abnormalities in brain-gut communication may contribute to the underlying pathophysiology of IBS.75 Primary neurotransmitters involved in transmission of impulses include acetylcholine, substance P, vasoactive intes- tinal polypeptide (VIP), and nitric oxide. Other neurotrans- mitters and modulators involved in neuroregulation for the GI tract include norepinephrine, serotonin, neuropeptide Y, melatonin, and gamma-aminobutyric acid (GABA). Serotonin (also known as 5-HT4 [5-hydroxytrypta- mine]) is synthesized from the amino acid tryptophan. More than 95% of serotonin is found within the GI tract, with the remaining 5% active within the brain. Serotonin can activate both excitatory and inhibitory neurons in the gastrointesti- nal tract. Serotonin stimulates both the release of acetylcho- line, causing smooth muscle contraction, and the inhibitory neurons that release nitric oxide, which results in relaxation of smooth muscle. Altered serotonin levels have been docu- mented in all types of IBS and may lead to abnormal motor and secretory function. The mechanism for these effects is not clear, even though reduced levels have been documented in IBS-C and increased levels have been measured in IBS-D. Research is focused on determining whether the abnormal levels result from altered release, altered synthesis, or altered transport.76 MMC, dis- cussed earlier, is an additional type of motility whose weak contractions serve to constantly sweep through the small intestine and remove leftover waste. Patients with IBS appear to have abnormal periods of MMC contractions when com- pared to controls.d to controls.77 Individuals with IBS have an increased sensitivity to stimulation of the gastrointestinal tract. This means that, when exposed to the same stimuli, most individuals do not develop the symptoms that IBS patients experience: abdomi- nal pain, urgency, diarrhea, or constipation. For example, when IBS patients were evaluated using balloon-distention and duodenal lipid infusion, they experienced significantly more abdominal pain and gastrointesti- nal symptoms than controls.78,79 There is also interest in the role of SIBO as a component of IBS. The contribution of SIBO to IBS has been difficult to establish because testing for SIBO is neither consis- tently sensitive nor specific. One recent study, however, determined that 33 out of 50 child subjects with IBS had abnormal lactulose breath tests, which serve as a marker for SIBO.80 Though antibiotics have resulted in a decrease of symptoms such as bloating or gas production when used in IBS treatment, they are not FDA approved as a compo- nent of the treatment protocol. Other studies have observed development of IBS after infec- tious enteritis. Specific organisms that have been documented include Blastocystis hominis, Campylobacter, Salmonella, and parasites such as Trichinella spiralis.81 At least two-thirds of IBS patients associate the signs and symptoms they experience with characteristics of the foods that they eat, including the size of the meal; the fat content; and the inclusion of lactose, fructose, sorbitol and other sugar alcohols, beans/lentils, wheat, caffeine, and carbonated drinks. The "food triggers" reported by an individual patient may become the foundation for nutrition therapy in IBS.82 These are discussed in more detail in the "Nutrition Therapy for Irritable Bowel Syndrome" section. As discussed earlier, the intestinal mucosa serves as a barrier between contents of the lumen and the rest of the body. Altered GI mucosal permeability has been documented in IBS and Camilleri et al. suggest that many of the previ- ously discussed factors are actually triggers leading to this increased permeability. The increased permeability of the mucosa then leads to inflammation and altered perception of pain. Continued research into this complex condition will guide interventions for the affected patient.83 Other concurrent diagnoses that occur with IBS include fibromyalgia, chronic fatigue syndrome, temporoman- dibular joint (TMJ) syndrome, and food allergies. Though correlations with certain psychiatric conditions have been documented frequently in patients with IBS, no specific connections have been made. Some researchers feel previ- ous physical and sexual abuse may increase sensitivity to GI stimulation and thus may contribute to symptoms. Stress is known to exacerbate symptoms of IBS in some individuals. -Complex and not well-understood -Abnormal motility plays major role in symptoms (increased/decreased motility, diarrhea, constipation) -Abnormalities in brain-gut communication -Increased sensitivity to stimulation of the gastrointestinal tract -Small intestinal bacterial overgrowth (bacteria from large intestine enters small intestine) -Increased permeability of the mucosa (things get through that shouldn't get through) -Serotonin: neurotransmitter released from enterochromaffin cells of the GI. Serotonin made from amino acid tryptophan. Serotonin is responsible for release of acetylcholine (excitatory) and nitric oxide (inhibitory). Acetylcholine (things are moving through too quickly- speeds motility) and nitric acid (things slow down) are responsible for motility. Some individuals have decrease in protein called Sert (protein responsible for carrying serotonin, so might be hanging out in GI longer than it needs to. -2/3 of patients link symptoms of IBS with foods they take in- gas producing foods. Stress exacerbates these symptoms

Small Intestine Secretions

-The small intestine produces its own secretions and also receives secretions from ancillary organs of digestion, including the pancreas and gallbladder. These secretions include hormones, digestive enzymes, bicarbonate, and bile. As chyme moves from the stomach into the duode- num, the hormones cholecystokinin, gastrin, and secretin stimulate release of pancreatic and gallbladder secretions. Bicarbonate from the pancreas neutralizes the very acidic chyme as it enters from the stomach. Neu- tralization protects the duodenum from acidity and supports a favorable environment for both digestion and absorption. Bile from the gallbladder supplies emulsification needed for adequate lipid digestion. Other secretions of the small intestine include approxi- mately 1.5 liters of intestinal "juices" or succus entericus. These secretions, which are primarily water and mucus, provide both the appropriate water-soluble environment for digestion and protection for the mucosa of the small intestine. Important digestive enzymes are secreted at the brush border of the small intestine. -Own secretions (cells of small intestine release substances) + digestive enzymes (come from other areas, such as pancreas primarily), bicarbonate, bile -CCK (present when fat enters small intestine; responsible for release of bile), gastrin, and secretin stimulate release of pancreatic and gallbladder: Bicarbonate = neutralizes gastric HCL -Bile = emulsifies fat (allows for fat and water mix, which allows enzymes to start digesting) -Other small intestine secretions include: -1.5 liters of intestinal "juices" - water and mucous (provide the right environment for enzymes to function)

Celiac Disease- Medical Diagnosis

-Traditionally, diagnosis for CD was confirmed by biopsy of the small intestine mucosa and sub- sequent documentation of villous atrophy, crypt hyperpla- sia, and lymphocytic and plasma cell infiltrate in the lamina propria. Reversal of symptoms after restriction of gluten provided the final evidence. Even though biopsy remains the gold standard for diagnosis, it is common now to ini- tially diagnose CD using serological testing. The recom- mended tests include tissue transglutaminase (tTG) and antiendomysial IgA antibody (EMA). The most commonly used marker, tTG, has a 95%-98% sensitivity with 94%-95% specificity. EMA has an 85%-98% sensitivity and 97%-100% specificity. -Gold standard: biopsy of small intestinal mucosa (take cells out of small intestine) -Reversal of symptoms following gluten free diet (remove all gluten from diet and see if symptoms go away) -Serological testing now commonly used (blood tests that test for antibodies)- tTG and EMA

Diverticulosis/Diverticulitis- Treatment

-Treatment for diverticulosis involves only nutri- tion therapy, with a specific focus on fiber intake and use of probiotic and prebiotic supplementation. Treatment for acute diverticulitis begins with making the patient NPO with com- plete bowel rest until symptoms (bleeding and/or diarrhea) subside. Antibiotics are used to treat any infection. The most common antibiotic regimens involve medications for Gram-negative rods and anaerobes such as ciprofloxacin and metronidazole.115 For those patients with complications (such as abscess or sepsis), surgical resections are likely necessary. -Specific focus on fiber recently questioned- we recommend high fiber for individuals with diverticulosis (25-35 g. = DRI for fiber; also want individuals to increase fluid intake) -Diverticulitis with inflammation and infection may affect nutrition if prolonged or complications occur (we tend to do liquid diets, which you will not get adequate amount of nutrients from liquid diet) -Only treatment is nutrition therapy- prevent constipation. If person has symptoms that are severe, then surgery is an option -Pockets will stay there for rest of life

Diarrhea- Treatment

-Treatment of the underlying disorder is the most important component of therapy. If the diarrhea is infectious in nature, antibiotics will be the first line of treatment. Restor- ing normal fluid, electrolyte, and acid-base balance is crucial. This is accomplished through either intravenous therapy or the use of oral rehydration solutions (discussed in the "Nutri- tion Therapy" section).23,36 Other medications can be used to treat the symptoms of diarrhea. These agents work either to decrease motility or to thicken the consistency of the stool. These include medi- cations such as LoMotil®, Immodium, Tincture of Opium, paregoric, Kaopectate®, or bismuth subsalicylate. It is impor- tant to note any medication side effects for these drugs. See Table 15.4 for a list of antidiarrheal medications and possible side effects/drug-nutrient interactions. Fecal microbiota transplantation, an alternative treat- ment for chronic refractory diarrhea, is a procedure used to restore normal colonic flora. In this procedure, stool is obtained from a healthy donor and is infused into the patient, usually via colonoscopy.32 Prevention of diarrhea should be a major focus of any discussion regarding this condition, especially in at-risk pop- ulations such as travelers, immunosuppressed individuals, infants and children in daycare settings, and institutional- ized populations.23,26 Recommendations for the prevention of diarrhea worldwide include strategies such as:26 • Improving access to clean water and safe sanitation • Promoting hygiene education • Exclusive breastfeeding • Improving weaning practices • Immunizing all children, especially against measles • Using latrines • Keeping food and water clean • Washing hands with soap (the baby's as well) before touching food • Sanitary disposal of stools -Treat underlying disease -Antibiotics -Restore fluid, electrolyte, and acid-base balance -IV therapy, rehydration solutions (ex: Pedialyte, rehydration formula) -Medications to treat symptoms -Suggest prevention strategies (drink clean water, promote breastfeeding, proper hygiene and make sure individuals washing hands especially if washing food, immunizations, keep food and water safe)

Constipation- Treatment

-Treatment of the underlying etiology will direct medical care for constipation. Common interventions include bowel retraining and use of enemas or cathartic and laxative medications. Other medications involve bulking agents and stool softeners. -Treat underlying etiology -Bowel retraining -Enemas, cathartic (given to patient that helps accelerate defecation), laxatives (medications that ease defecation by pulling water into GI) -Bulking agents (soluble fiber assists in pulling water into GI), stool softeners (pull water into GI)

Inflammatory Bowel Disease- Treatment

-Treatments for both UC and Crohn's disease include anti-inflammatory medications, antibiotics, immuno- suppressive medications, immunomodulators, and biologic therapies as well as surgical intervention. Medical treat- ment for ulcerative colitis historically has used combinations of both antibacterial coverage with sulfapyridine and anti-inflam- matory 5-aminosalicylic acid (5-ASA) therapy (see Table 15.4 for information about this and other medications used for diseases of the lower GI tract). The most commonly used med- ications in this category today include olsalazine, balsalazide, and mesalamine (Asacol, Claversal, and Pentasa). Immuno- modulators work to inhibit inflammatory cell proliferation by interrupting cellular RNA and by inhibiting the overall immune response. These medications include azathioprine (AZA) and 6-mercaptopurine (6-MP). Corticosteroids work to inhibit the overall inflammatory response and are commonly used to treat UC. Antibiotics are used when there is an acute infection. Treatment for Crohn's disease can utilize all categories of medical treatments listed previously. Aminosalicylate medi- cations are typically used in Crohn's disease that has ileal and colon involvement. These include mesalamine and sulfasala- zine. As in UC, the immunomodulators azathioprine (AZA) and 6-mercaptopurine (6-MP) are used. Corticosteroids, such as prednisone or budenoside, are often used in acute exacerbations, especially in severe-fulminant disease, but patients are at risk for becoming steroid dependent. Antibiotics used include metroni- dazole and ciprofloxacin. Biologic therapy for Crohn's disease includes infliximab, adalimunab, and certolizumab pegol, meth- otrexate, cyclosporine, and natalizumab. These medications work to interrupt tumor necrosis factor-alpha (TNF-alpha) and thus the cytokine-directed inflammatory activity. Other clas- sifications of biologic therapies include selective anti-adhesion molecules and anti-interleukin antibodies.95,100 Drug choices are determined by the severity of the disease and whether the goal is to induce remission or to maintain a current remission. Surgical intervention is required in both UC and Crohn's disease in over 60% of patients. The most common procedure in UC is a total colectomy, and in Crohn's disease, the ileos- tomy. Surgery is performed due to non-responsive disease and/or acute complications such as perforation, obstruction, or abscess. These surgical procedures are described in greater detail later in this chapter in the section "Common Surgical Interventions for the Lower GI Tract. -These are all for Crohn's and UC: -Antibiotics: if there's infection -Immunosuppressants: autoimmune disease -Immunomodulators -Biologic therapies: block tumor necrosis factors. -Surgery: required in about 60% of cases (majority of people will have to have surgery to remove colon or part of colon). UC patients: Total Colectomy (remove the whole colon- the end of the GI tract is the ileum). Crohn's patients: Usually, individuals have ileostomy (ileum is attached to hole in side of person's abdomen - called stoma- and bag will collect waste products). -Malnutrition may require nutrition support (if we are not absorbing enteral, may have to do parental nutrition, which is nutrition through the vein)

Constipation- Nutrition Interventions

-Twenty-five to 35 g of dietary fiber are recommended for adults each day. Based on caloric intake, this would be approximately 10-13 g of dietary fiber per 1000 kcal. For children over the age of 2 years, fiber intake is recommended to be the amount equal to their age plus 5 grams/day.53 Ensuring adequate fiber and fluid intake has been the foun- dation for nutrition therapy in constipation treatment. Fiber results in increased stool weight that assists in providing for con- sistent bowel movements and a colonic transit time of 2-4 days.53 Despite the lack of current outcome evidence, the relationship between fiber and normal laxation provides the basis for the cli- nician to make recommendations for a gradual increase in fiber to the daily goal of 25-35 g. This should begin slowly with adding one to two high-fiber foods each day. Total fiber in foods includes a mixture of dietary fiber and functional fiber—including resis- tant starch. Even though food is recommended as the optimal route for fiber sources, due to individual tolerance, some individuals—especially older adults— may not be able to achieve levels in the highest ranges without using fiber supplementation. High-fiber nutri- tion therapy to be used for treatment of constipation. Suggestions for fiber supplements that can be used in treat- ment (under "Laxatives: Bulking Agents"). At the same time that fiber intake is increased, the clinician should also emphasize adequate fluid intake. Adults should ingest a minimum of 2000 mL/day (approximately 8-10 cups/day). Probiotics and prebiotics have also been recommended for treatment of constipation. For example, consumption of fructans or fructooligosaccharides (FOS) has been shown to soften feces and to assist in relieving constipation. Fructans are defined as chains of fructose molecules with glucose on the terminal end of the chain. Common examples include inulin and levan. They naturally occur in wheat-containing grain products such as breads, cereals, and pasta. -Increase whole grains, fruits, vegetables -Fiber 25-35 grams/day (slowly increase fiber intake) -Bulking agents (retain water, increase peristalstis contractions- Metamucil) -Fluid - at least 2000 mL/day -Probiotics and prebiotics

Diarrhea- Nutrition Assessment

-When completing a nutrition assessment for a patient with diarrhea, it is especially impor- tant to review the following types of assessment data: fluid and beverage intake, energy and mineral intake, medication/ complementary alternative medicine use, safe food and water availability, weight change, biochemical data (reflective of hydration status), nutrition-focused physical findings (especially those related to the digestive system and skin), and past medical/surgical history. -Fluid and beverage intake -Energy and mineral intake: figure out what they're eating -Meds and herbal supplement use -Weight change: especially important for chronic diarrhea patients -Biochemical data: lab values skewed because there is a chance the individuals are dehydrated -Nutrition focused physical findings: not absorbing vitamins/minerals/energy/protein, look at their hair, nails, look for edema if necessary -Past medical and surgical history

Celiac Disease- Pathophysiology

-When the small intestine is exposed to specific sequences of amino acids found in the protein portion of gluten (wheat [gliadin], rye [secalin], and barley [hordein]), there is a toxic and inflammatory response. The immune response to gluten signals T lymphocytes to pro- duce various cytokines, which in turn direct the inflammatory response. The innate immune response results in activated cytoxic T cells that ultimately damage the enterocytes. Both inflammatory and innate immune responses damage the villi; villous height is reduced, and they are flattened in appearance (see Figure 15.10). The damage to the enterocytes results in a reduced absorptive surface area and loss of digestive enzymes.59 (Chapter 9 provides more detail about the immune response with in-depth coverage of both innate and adaptive immunity.) Celiac disease is often accompanied by other systemic auto- immune disorders, including type 1 diabetes mellitus; thyroid disease; systemic lupus erythematous; primary biliary cirrho- sis; rheumatoid arthritis; Sjögren's, Down, Turner, and William syndromes; and IgA deficiency. Persons with CD are consid- ered to be at higher risk for lymphoma and osteoporosis as well as the complications of nutrient deficiencies and malnutrition. -Damage to villi; reduced height; flattened (this occurs because of autoimmune response): -By laying flat: decreasing space for absorption (so there is usually a lot of diarrhea with celiac disease), can't release enzymes to break down nutrients, and also from inflammation. Once remove BROW-M from diet, villi will repair themselves. -Decreased enzyme function and surface area -Maldigestion and malabsorption -Occurs with other autoimmune disorders (type 1 diabetes, thyroid diseases, rheumatoid arthritis).

Anatomy of Large Intestine

-anatomy of the large intestine has both significant differ- ences from and important similarities to the anatomy of the small intestine. First, mucosa of the large intestine form three nearly straight portions rather than the circular folds found in the small intestine. The colon's major portions are referred to as the ascending colon, the transverse colon, and the descending colon (see Figure 15.8). The final section of the colon is referred to as the sigmoid colon due to its "S" shape. The sigmoid colon ends in the rectum where another sphinc- ter (the anal sphincter) controls voluntary release of intesti- nal contents. Second, the large intestine does not have villi or microvilli, though it contains large pits or crypts (crypts of Lieberkuhn) that are similar to the crypts between villi in the small intestine. Again, similar to the small intestine, cells are generated within these crypts and, after migration, differentiate into specialized epithelial cells such as goblet cells, which produce mucus. -Ascending, transverse, descending, sigmoid colon: -Nearly straight rather than curved like small intestine -No villi or microvilli -Crypts produce specialized epithelial cells including goblet cells (goblet cells produce mucous)