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© 2007 Thomson - Wadsworth Lower Gastrointestinal Tract Chapter 17
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© 2007 Thomson - Wadsworth Lower GI Tract – A&P Small Intestine Anatomy Duodenum, jejunum, ileum Maximum surface area for digestion and absorption(600 X) Folds of Kerckring Villi Microvilli – ”brush border” Specialized enterocytes from stem cells of crypts – high turnover = high nutrient need
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© 2007 Thomson - Wadsworth
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Lower GI Tract – A&P Small Intestine Motility Hormonal stimulation - gastrin Peristaltic reflex – segmental contractions Mixing of chyme MMC – motility when SI empty Motilin Other hormones: CKK, orexin, leptin
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Lower GI Tract – A&P Small Intestine Secretions Own secretions + digestive enzymes, bicarbonate, bile CCK, gastrin, secretin stimulate release of pancreatic and gallbladder secretions - see Table 17.1 Bicarbonate – neutralizes gastric HCL Bile – emulsifies fat 1.5 L intestinal juices – water & mucus
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Lower GI Tract – A&P Small Intestine Digestion Protein digestion Trypsinogen, chymotrypsinogen, procarboxypeptidases, elastase Enterokinase from brush border Peptidases Starch digestion Pancreatic amylase Lactase, maltase, sucrase, etc. from brush border Lipid digestion Pancreatic lipase, colipase Bile
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Lower GI Tract – A&P Small Intestine Absorption Active transport utilizing Na/K pump at brush border Glucose, galactose, amino acids Facilitated diffusion Fructose Lipids enter lymph via passive diffusion First converted to micelles and packaged as chlylomicrons
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Lower GI Tract – A&P Small Intestine Absorption Steatorrhea – if lipid not absorbed Most nutrients absorbed in duodenum and jejunum Ileum B 12 Reabsorption of bile – “enterohepatic circulation”
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Lower GI Tract – A&P Large Intestine Anatomy Ascending, transverse, descending, sigmoid colon No villi or microvilli Crypts produce specialized epithelial cells
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© 2007 Thomson - Wadsworth
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Lower GI Tract – A&P Large Intestine Motility Haustration – segmentation; circular muscles forms small sacs (haustra) Propulsion Mass movement Defecation
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© 2007 Thomson - Wadsworth Lower GI Tract – A&P Large Intestine Secretions Goblet cells produce mucus Potassium and bicarbonate
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© 2007 Thomson - Wadsworth Lower GI Tract – A&P Large Intestine Digestion & Absorption No enzymatic digestion occurs Reabsorption of water, electrolytes, some vitamins Formation and storage of feces Insoluble fiber, bilirubin 400 species of bacteria Fermentation of fiber and sugar alcohols
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© 2007 Thomson - Wadsworth Lower GI Tract – A&P Large Intestine Digestion & Absorption Fermentation produces SCFA and lactate Energy produced used by bacteria, for tissue growth in colon or utilization in body Excess substrate = gas, flatulence
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© 2007 Thomson - Wadsworth Lower GI Tract – A&P Large Intestine Digestion & Absorption Maintaining balance of intestinal flora Resistant starches Prebiotics Probiotics Synbiotics Vitamin K and biotin – endogenously produced
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diarrhea – increase in frequency of bowel movements or increase in water content of stools Affects consistency or volume >200 g/day adults, >20 g/kg for children Dehydration secondary to diarrhea – major global health issue
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diarrhea Acute or chronic Osmotic - increased water efflux due to an increase in osmolality Maldigestion, excessive sorbitol or fructose, enteral feeding, laxative use Resolves when NPO
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diarrhea Secretory - underlying disease causes secretions Does not resolve when NPO Bacteria, protozoa, viruses Traveler’s diarrhea Medications, prostaglandins, excess bile acids or unabsorbed fatty acids Antibiotic related GI diseases: Crohn’s, UC, celiac AIDS enteropathy, thyroid dysfunction
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diarrhea - Clinical Manifestations Watery stool; increased frequency Foul-smelling, frothy stools Presence of blood Abdominal pain & cramping Dehydration, weight loss Electrolyte and acid-base imbalances
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diarrhea - Diagnosis Diagnose underlying etiology Age, hydration status, presence of blood in stool, immunocompetency Recurrence of episodes related to time of day and food intake Stool cultures Procedures such as endoscopy Osmolality and electrolyte content
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diarrhea - Treatment Treat underlying disease Antibiotics Restore fluid, electrolyte, acid-base balance IV therapy, rehydration solutions Medications to treat symptoms See Table 17.12 - possible side effects Suggest prevention strategies
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diarrhea - Nutrition Implications Fluid losses – dehydration, hyponatremia, hypokalemia Metabolic acidosis Malnutrition Infants and elderly at greatest risk
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diarrhea - Nutrition Interventions NPO or clear liquids – old recommendation Feed patient – stimulates recovery Oral rehydration solutions WHO – see Table 17.4 E.g. Pedialyte, Rehydralyte etc. Low-residue diet, use of pectin Pro- and prebiotics
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Pathophysiology: Lower GI Tract Constipation – decrease in frequency of bowel movements See Rome Consensus Criteria p. 474 Often hard, pellet-like Abdominal pain, bloating, gas
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Constipation – Etiology Slowed colonic transit time Rectal outlet obstruction, fecal impactation, adhesions, tumor Pelvic floor dysfunction IBS Other medical conditions; i.e. MS, Parkinson’s Side effect of medications, supplements
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Constipation – Diagnosis/ Treatment Complete hx & physical, CBC, TSH, serum glucose Colonoscopy, flexible sigmoidoscopy Treat underlying etiology Bowel retraining Enemas, cathartic, laxatives Bulking agents, stool softeners
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Constipation – Nutrition Increase whole grains, fruits, vegetables Fiber 20-35 grams/day Slowly increase fiber intake 3:1 ratio insoluble to soluble fiber See Box 17.4 Bulking agents Fluid – at least 2000 mL/day Pro- and prebiotics
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Malabsorption - maldigestion of fat, CHO, pro. Decreased villious height, enzyme production; or dysfunction of accessory organs d/t disease Decreased transit time – surgery See Table 17.5 – potential causes
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Malabsorption - fat Steatorrhea - fat travels undigested and unabsorbed to large intestine Fat-soluble vitamins malabsorbed Potential for excess oxalate Kidney stones, urothiasis, hyperoxaluria Abdominal pain, cramping, diarrhea Dg; fecal fat test or D-xylose absorption test, or small bowel x-ray
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Malabsorption - Fat - Nutrition Restrict fat 25-50 g/day Use of MCT supplements Pancreatic enzymes
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Malabsorption - CHO Lactose malabsorption Increased gas, abdominal cramping, diarrhea Dg: lactose tolerance test, lactose breath hydrogen test Restrict milk and dairy products Products such as Lactaid can be rec.
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Malabsorption - protein Protein-losing enteropathy – excessive protein loss Reduced serum protein Peripheral edema d/t oncotic pressure
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Malabsorption - Nutrition Therapy Results in weight loss, vitamin/mineral deficiencies, chronic PEM - See Table 17.6 Treat underlying disease/ nutrient being malabsorbed
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Celiac disease - damage to intestinal mucosa d/t exposure to gluten Genetic and autoimmune Occurs when alpha-gliadin from wheat, rye, malt, barley are eaten Infiltration of WBC, production of IgA antibodies
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Celiac disease - pathophysiology Damage to villi; reduced height, flattened Decreased enzyme function and surface area Maldigestion and malabsorption Occurs with other autoimmune disorders Dermatitis herpetaformis, TIDM, rheumatoid arthritis…
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Pathophysiology: Lower GI Tract Celiac disease - clinical manifestations Diarrhea, abdominal pain, cramping, bloating, gas Bone and joint pain Muscle cramping, fatigue Peripheral neuropathy, seizures Skin rash Mouth ulcerations Higher risk for lymphoma and osteoporosis
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Celiac Disease - Diagnosis/Treatment/Prognosis Biopsy of small intestinal mucosa Reversal of symptoms following gluten-free diet Identification of antibodies Refractory CD; d/t coexisting disease
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Celiac Disease - Nutrition Intervention Low-residue, low-fat, lactose-free, gluten-free diet Low-residue to minimize diarrhea Fat 45-50 g Gluten restriction for LIFE Oats controversial – limit to ½ c/day Identify hidden sources of gluten See Table 17.7 Specialty products
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Pathophysiology: Lower GI Tract Irritable Bowel Syndrome (IBS) - abdominal pain with 2 of the following: Pain relieved with defecation Onset associated with change in frequency of stool Onset associated with change in form of stool Eliminate “red flag” symptoms
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBS Most common GI complaint, women more than men Aggravated by stress, anxiety, depression, emotional trauma Etiology unknown Increased serotonin, inflammatory response, abnormal motility, pain
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBS - pathophysiology Increased sensitivity to stimulation of GI tract Resulting in abdominal pain, urgency, diarrhea, constipation Infectious and inflammatory components Stress
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBS - clinical manifestations Abdominal pain, alterations in bowel habits, gas, flatulence Increased sensitivity to certain foods: lactose, wheat, high-fiber Concurrent dg; fibromyalgia, chronic fatigue syndrome, TMJ syndrome, food allergies
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBS - Treatment Guided by symptoms Antidiarrheal agents Tricyclic antidepressants, SSRIs Bulking agents, laxatives Agonists or antagonists for 5-HT4 receptors Behavioral therapies
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBS - Nutrition Therapy Can lead to nutrient deficiency, underweight, malnutrition Decrease anxiety, normalize dietary patterns
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBS - Nutrition Therapy Assess diet hx; offending foods Assess nutritional adequacy Focus on increasing fiber intake to 25 g/day Adequate fluid Pre- and probiotics Avoid foods that produce gas and swallowed air
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Pathophysiology: Lower GI Tract Inflammatory Bowel Disease (IBD) - autoimmune, chronic inflammatory condition of GI tract Ulcerative colitis (UC) Crohn’s disease See Box 17.8 for comparison
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBD - Etiology Unknown Environmental factors – smoking, infectious agents, intestinal flora, physiological changes in SI trigger abnormal inflammatory response Strong genetic association
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBD - Pathophysiology Exposure to certain triggers for those genetically susceptible Abnormal immune response Release of cytokines Destruction of mucosa UC – primarily in colon; continuous Crohn’s presents with “skipping” pattern throughout GI
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Pathophysiology: Lower GI Tract IBD - pathophysiology UC - ulcerations lead to toxic megacolon; thin, ulcerated colon Crohn’s – fistulas, strictures, obstruction
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBD - clinical manifestations Abdominal pain, bloody diarrhea, tenesmus Febrile, tachycardic CRP and ESR elevated WBC elevated Weight loss See Box 17.9, Table 17.11 – Crohn’s
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Pathophysiology: Lower GI Tract IBD - Clinical manifestation/diagnosis Radiology testing Laboratory measures Antibody testing Observation of extraintestinal disease Osteopenia Osteoporosis Dermatitis Rheumatological conditions Ocular and hepatobiliary complications
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBD - Treatment Antibiotics Immunosupressants Immunomodulators Biologic therapies Surgery
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBD - Nutrition Therapy Malnutrition; may require nutrition support May need to increase kcal, protein, micronutrients Iron, zinc, magnesium, electrolytes
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBD - Nutrition Interventions During exacerbation – enteral nutrition preferred over parenteral Supplement glutamine, arginine Assess energy needs + stress factor May need to increase protein needs 1.5-1.75 g/kg Low-residue, lactose-free diet Small, frequent meals
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBD - Nutrition Interventions May use MCT oil if steatorrhea present Restrict gas-producing foods Increase fiber and lactose as tolerated Advancement of oral diet – individualized! Multivitamin – B 12, iron, zinc, calcium, magnesium, copper, antioxidants
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract IBD - Nutrition Interventions During remission/rehabilitation Maximize energy & protein Weight gain and physical activity Normalize dietary patterns Food sources of antioxidants, Omega-3s Limit foods high in oxalate Pro- and prebiotics
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diverticulosis/diverticulitis – abnormal presence of outpockets or pouches on surface of SI or colon/ inflammation of these Low fiber intake, hx of constipation, increased colonic pressure Increases inflammatory response Other risks: obesity, sedentary, steroids, alcohol and caffeine intake, cigarette smoking
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Pathophysiology: Lower GI Tract Diverticulosis/diverticulitis – pathophysiology Fecal matter trapped, excessive pressure against walls of colon Development of pouches Diverticulitis - when these pouches become inflamed Food stuff and bacteria can collect and result in infection Bleeding abscess, obstruction, fistula, perforation
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diverticulosis/-itis – clinical manifestations -osis – asymptomatic -itis - fever, abdominal pain, GI bleeding, elevated WBC Diagnosed by radiology testing Thickened walls, abscess, inflammation
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diverticulosis/-itis – Treatment/ Nutrition Therapy Specific focus on fiber Pro- and prebiotic supplementation Acute – NPO with bowel rest Antibiotics Surgical resection
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© 2007 Thomson - Wadsworth Pathophysiology: Lower GI Tract Diverticulosis/-itis – Nutrition Therapy -osis - high-fiber diet + 6-10 grams Avoid nuts, seeds, hulls Fiber supplement -itis – low-fiber diet Bowel rest, clear liquids Avoid nuts, seeds, fibrous vegetables
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© 2007 Thomson - Wadsworth Surgical Interventions: Lower GI Tract Ileostomy and Colostomy Creation of a stoma Ileostomy – colon and rectum are removed Colostomy - rectum removed Pouch appliance used too collect waste See Fig. 17.12
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Surgical Interventions: Lower GI Tract Ileostomy and Colostomy – Nutrition Decrease risk of obstruction Maintain fluid and electrolyte balance Reduce fecal output Minimize flatulence After surgery transition to oral diet Clear liquids progress to low-residue with 4-6 small meals/day
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© 2007 Thomson - Wadsworth Surgical Interventions: Lower GI Tract Ileostomy and Colostomy – Nutrition Reduce risk for stoma obstruction Tough, fibrous meats, vegetables, dried fruits, fruit skins, seeds, popcorn Eat slowly, chew thoroughly Drink adequate fluids
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© 2007 Thomson - Wadsworth Surgical Interventions: Lower GI Tract Ileostomy and Colostomy – Nutrition Excessive, watery fecal output Reduce insoluble fiber and increase soluble fiber Avoid foods that cause gas and flatulence Use of yogurt, parsley, buttermilk to decrease gas and odor Multivitamin and B 12 supplementation
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© 2007 Thomson - Wadsworth Short Bowel Syndrome Short bowel syndrome - large resection of small intestine Less than 200 cm of functional SI Extensive loss of surface area in SI and colon Malabsorption: nutrients, fluids, electrolytes
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© 2007 Thomson - Wadsworth Short Bowel Syndrome Short bowel syndrome Prognosis depends on length of remaining small bowel, health of remaining GI, any co-morbid conditions Major vitamin and mineral losses Fat malabsorption – Vit. A, D, E, K Sodium, Mg, iron, zinc, selenium, calcium loss
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© 2007 Thomson - Wadsworth Short Bowel Syndrome Short bowel syndrome Postoperative period - 3 distinct phases 7-10 days: Extensive fluid and electrolyte losses, large volume of diarrhea, TPN Several months: Reduced diarrhea volume, adaptation of remaining bowel, enteral nutrition, transition to oral diet 1-2 years: Continued adaptation of bowel, intestinal tract increases in length, diameter, and villous height
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© 2007 Thomson - Wadsworth Short Bowel Syndrome Short bowel syndrome - treatment Manage fluid and electrolytes Oral rehydration solutions Medications for motility, diarrhea and gastric hypersecretion
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© 2007 Thomson - Wadsworth Short Bowel Syndrome Short bowel syndrome – nutrition TPN postoperatively Oral diets introduced as diarrhea decreases May require combination of TPN and enteral nutrition Sugar-free, isotonic clear liquids introduced first Progress slowly to low-residue, low-fat, lactose-free, low-oxalate diet Avoid caffeine and alcohol Avoid sugar alcohols and insoluble fiber See Table 17.15
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© 2007 Thomson - Wadsworth Bacterial Overgrowth Bacterial overgrowth resulting from cross contamination of bacteria from colon to SI Motility of GI tract delayed Bacteria competes with host for nutrients Maldigestion, malabsorption, weight loss
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© 2007 Thomson - Wadsworth Bacterial Overgrowth Clinical manifestations/treatment Diarrhea, steatorrhea, anemia, weight loss Dg with hydrogen breath test Antibiotics Fat and lactose eliminated initially Identify and treat nutrient of malabsorption
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