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Lower Gastrointestinal Tract
Chapter 17
© 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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Lower GI Tract – A&P
• Small Intestine Absorption
Steatorrhea – if lipid not absorbed
Most nutrients absorbed in duodenum
and jejunum
Ileum
• B12
• Reabsorption of bile – “enterohepatic
circulation”
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Lower GI Tract – A&P
• Large Intestine Anatomy
Ascending, transverse, descending,
sigmoid colon
No villi or microvilli
Crypts produce specialized epithelial
cells
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Lower GI Tract – A&P
• Large Intestine Motility
Haustration – segmentation; circular
muscles forms small sacs (haustra)
Propulsion
Mass movement
Defecation
© 2007 Thomson - Wadsworth
Lower GI Tract – A&P
• Large Intestine Secretions
Goblet cells produce mucus
Potassium and bicarbonate
© 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
© 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
© 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
© 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
© 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
© 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
© 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
© 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
© 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
© 2007 Thomson - Wadsworth
Pathophysiology:
Lower GI Tract
• Diarrhea - Nutrition Implications
Fluid losses – dehydration,
hyponatremia, hypokalemia
Metabolic acidosis
Malnutrition
Infants and elderly at greatest risk
© 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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 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
© 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
© 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
© 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
© 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
© 2007 Thomson - Wadsworth
Pathophysiology:
Lower GI Tract
• Malabsorption - Fat - Nutrition
Restrict fat 25-50 g/day
Use of MCT supplements
Pancreatic enzymes
© 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.
© 2007 Thomson - Wadsworth
Pathophysiology:
Lower GI Tract
• Malabsorption - protein
Protein-losing enteropathy –
excessive protein loss
Reduced serum protein
Peripheral edema d/t oncotic pressure
© 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
© 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
© 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…
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 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
© 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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 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
© 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
© 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
© 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
© 2007 Thomson - Wadsworth
Pathophysiology:
Lower GI Tract
• IBS - Nutrition Therapy
Can lead to nutrient deficiency,
underweight, malnutrition
Decrease anxiety, normalize dietary
patterns
© 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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 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
© 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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Pathophysiology:
Lower GI Tract
• IBD - pathophysiology
UC - ulcerations lead to toxic
megacolon; thin, ulcerated colon
Crohn’s – fistulas, strictures,
obstruction
© 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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 2007 Thomson - Wadsworth
Pathophysiology:
Lower GI Tract
• IBD - Treatment
Antibiotics
Immunosupressants
Immunomodulators
Biologic therapies
Surgery
© 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
© 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
© 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 – B12, iron, zinc, calcium,
magnesium, copper, antioxidants
© 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
© 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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 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
© 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
© 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
© 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
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
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
© 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
© 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 B12 supplementation
© 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
© 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
© 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
© 2007 Thomson - Wadsworth
Short Bowel Syndrome
• Short bowel syndrome - treatment
Manage fluid and electrolytes
Oral rehydration solutions
Medications for motility, diarrhea and
gastric hypersecretion
© 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
© 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
© 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
© 2007 Thomson - Wadsworth