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Chapter 36: Alterations of Digestive Function – Part 1
Disorders of the Gastrointestinal Tract
I. Clinical Manifestations of Gastrointestinal Dysfunction
A. Anorexia

A lack of desire to eat despite physiologic stimuli that would normally produce hunger.
B. Vomiting (emesis)

The forceful emptying of the stomach and intestinal contents through the mouth.

Stimuli that initiate vomiting reflex include:

o
Severe pain
o
Distention or chemical irritation of the stomach or duodenum
o
Activation of the chemoreceptor trigger zone in the medulla by circulating chemicals
o
Stimulation of the vomiting center in the medulla by emotional stimuli, nervous input, etc.
Vomiting is usually preceded by nausea and retching.
o
Retching - nonproductive vomiting; begins movement of gastric and duodenal contents up
through the esophagus toward the mouth.

Projectile vomiting - spontaneous vomiting that is not preceded by nausea or retching.
o
Associated with direct stimulation of the vomiting center in the medulla oblongata.
C. Constipation

Constipation is defined as infrequent or difficult defecation.

Causes - low fiber diet; dehydration; lack of exercise; drugs or disorders that impair intestinal
motility or obstruct the intestinal lumen; hypothyroidism.
D. Diarrhea

Increased frequency of bowl movements with increased volume, fluidity, and weight of feces.

More than three stools per day is considered abnormal.

Stool volume and consistency is determined by water content of the colon and the presence of
unabsorbed food, unabsorbable material, and intestinal secretions.

Large-volume diarrhea - caused by excessive amounts of water or secretions in the intestines.

Small-volume diarrhea - results from excessive intestinal motility, usually from inflammation.

Major mechanisms of diarrhea:
o
Osmotic diarrhea - nonabsorbable substance draws excess water into the intestine and
increases stool weight and volume.

Causes - inability to digest lactose due to lactase and pancreatic enzyme deficiency;
excessive ingestion of synthetic, nonabsorbable sugars.
o
Secretory diarrhea - excessive mucosal secretion of fluid and electrolytes.

o
Causes - bacterial enterotoxins, exotoxins, or neoplasms.
Motility diarrhea - food is not mixed properly, digestion is impaired, and motility is increased.

Causes - resection of the small intestine, fistula formation between loops of intestine, and
excessive motility of the intestine caused by diabetic neuropathy.
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ACTIVITY 1: Explain why factors that slow movement of feces through the colon cause constipation,
whereas factors the speed up movement of feces through the colon cause diarrhea.
E. Abdominal Pain

Abdominal pain is caused by stretching, inflammation, or ischemia.

Originates in the organs themselves (visceral pain) or in the peritoneum (parietal pain). Visceral
pain is often referred to the back.
o
Parietal pain - localized and intense pain from irritation of the parietal peritoneum.
o
Visceral pain - from the organs themselves; it is poorly localized with a radiating pattern.
o
Referred pain - visceral pain felt at some distance from a diseased or affected organ; felt in
skin or deeper tissues that share a sensory pathway with the affected organ.
F. Gastrointestinal Bleeding

Upper gastrointestinal bleeding - from the esophagus, stomach, or duodenum.
o
Causes - most commonly from bleeding varices in the esophagus; also peptic ulcers, or a
Mallory-Weiss tear at the esophageal gastric junction from severe retching.
o

Hematemesis - bright red bleeding or dark “coffee ground” material (affected by stomach acids).
Lower gastrointestinal bleeding - from the jejunum, ileum, colon, or rectum.
o
Causes - polyps, inflammatory disease, cancer, or hemorrhoids.
o
Melena - Black, sticky, tarry, foul-smelling stools caused by digestion of blood.
o
Hematochezia - fresh, bright red blood passed from the rectum.
o
Occult bleeding - traces of blood in normal-appearing stools; detectable only with guaiac test.

Acute, severe gastrointestinal bleeding is life threatening, depending on volume and rate of loss.

Chronic gastrointestinal bleeding can cause iron-deficiency anemia.
II. Disorders of Motility
A. Dysphagia

Dysphagia is difficulty swallowing.

Results from mechanical obstruction of the esophagus or a disorder that impairs its motility.

Mechanical obstructions - tumors, strictures, and diverticular herniations (outpouchings).

Functional obstructions - neurological or muscular disorders that interfere with voluntary
swallowing or peristalsis.
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
Achalasia - form of functional dysphagia caused by denervation of smooth muscle in the
esophagus; results in loss of esophageal peristalsis and failure of the lower esophageal sphincter
(LES) to relax.
B. Gastroesophageal Reflux Disease (GERD)

GERD - reflux of chyme from the stomach to the esophagus.

Reflux esophagitis - inflammation of the esophagus due to repeated exposure to acids and enzymes.

Normally the lower esophageal sphincter (LES) prevents reflux of acidic chyme.

Causes - loss of muscle tone in LES or increased abdominal pressures.

Manifestations - heartburn, dysphagia, and upper abdominal pain within 1 hour of eating.

Sequealae - GERD may cause esophageal ulcerations and strictures, and possibly cancer.
C. Hiatal Hernia

Protrusion of the upper part of the stomach through the diaphragm at the gastroesophageal junction.

Sliding hiatal hernia - stomach slides into the thoracic cavity through the esophageal hiatus.

Paraesophageal hiatal hernia - greater curvature of the stomach herniates through a secondary
opening in the diaphragm and lies alongside the esophagus.
o

Strangulation of the hernia is a major complication.
Manifestations - may be asymptomatic; but often exhibit gastroesophageal reflux, dysphagia,
heartburn, and epigastric pain; regurgitation and substernal discomfort after eating.
D. Pyloric Obstruction

Blocking or narrowing of the opening between the stomach and the duodenum.

Causes - congenital defect, inflammation and scarring secondary to a gastric ulcer, or tumor growth.

Manifestations - epigastric pain and fullness after eating, nausea, succussion splash, vomiting,
and, with a prolonged obstruction, malnutrition, dehydration, and extreme debilitation.
E. Intestinal Obstruction and Ileus

Intestinal obstruction - any condition that prevents the flow of chyme through the intestinal
lumen or failure of normal intestinal motility in the absence of an obstructing lesion.

Ileus - an obstruction of the intestines.

Simple obstruction - mechanical blockage of the lumen, often by torsion, herniation, or a tumor.

Functional obstruction - failure of motility (paralytic ileus), often occurring after abdominal surgery.

Intussusception - telescoping of a section of small intestine into the distal portion of the bowel.

Volvulus (torsion)- twisted loop of intestine and mesentery.

Pathophysiology:
o
Fluid and gas accumulate upstream of blockage, causing distension of the intestinal wall.
o
Pressure from distension reduces blood flow, resulting in ischemic damage, which allows
intestinal contents and bacteria to leak into peritoneum; fluids shift into peritoneal cavity.
o
Blockage reduces absorption of fluids and electrolytes.
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
Manifestations - colicky pain that occurs intermittently as a peristaltic wave of muscle contraction
meets the obstruction; vomiting; and abdominal distension.

Sequealae - fluid and electrolyte losses cause acidosis, hypokalemia, dehydration, hypovolemia,
hypotension and shock; ischemia causes necrosis, perforation of intestinal wall and peritonitis.
III. Gastritis

Acute or chronic inflammation of the gastric mucosa.
A. Acute gastritis

Inflammation that erodes the surface epithelium in a diffuse or localized pattern.

Usually due to injury of the protective mucosal barrier caused by drugs or chemicals.
o
NSAIDs cause gastritis by inhibiting prostaglandins, which stimulate secretion of mucus.
o
Alcohol, histamine, digitalis, and metabolic disorders can contribute.

Manifestations - vague abdominal discomfort, epigastric tenderness, and bleeding.

Treatment - healing usually occurs spontaneously within a few days. Discontinuing injurious
drugs, using antacids, or decreasing acid secretion with cimetidine (Tagamet®, a histamine H2receptor antagonist) facilitates healing.
B. Chronic gastritis

More complex and serious than acute gastritis.

Characterized by atrophy of the gastric mucosa.

Most commonly a result of chronic infection by H. pylori bacteria; also autoimmune conditions.
1. Chronic fundal gastritis (atrophic gastritis) - affects fundus and body; most severe form.
o
Can result in gastric atrophy and decreased secretion of hydrochloric acid, pepsinogen, and
intrinsic factor, which can lead to pernicious anemia.
o
This is a risk factor for developing gastric carcinoma.
2. Chronic antral gastritis - affects pyloric antrum; most common type; not usually associated with
impaired secretion or gastric atrophy.

Manifestations - symptoms often do not correlate with the severity; symptoms are often vague,
including anorexia, fullness, nausea, vomiting, and epigastric pain; clinical signs include
diminished secretion of hydrochloric acid (achlorhydria) and gastric bleeding.
ACTIVITY 2: What treatments would be appropriate for treating chronic gastritis (including its sequelae)?
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IV. Peptic Ulcer Disease

Break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum.

Caused by excessive secretion of gastric acid, disruption of the protective mucosal barrier, or both.

Risk factors - smoking, advanced age, habitual use of nonsteroidal anti-inflammatory drugs
(NSAIDs), alcohol, psychological stress, and Helicobacter pylori infection, chronic diseases
such as emphysema, rheumatoid arthritis, cirrhosis, and diabetes.
A. Duodenal ulcers

Ulceration of the duodenal mucosa and submucosa layers.

Most common of the peptic ulcers.

Causes:

o
Infection with H. pylori - releases toxins and enzymes that promote inflammation and ulceration.
o
Nonsteroidal anti-inflammatory drugs (NSAIDs) - inhibit mucosal prostaglandin synthesis.
o
Hypersecretion of acid and pepsin by stomach - due to high gastrin levels and smoking.
o
Inadequate secretion of bicarbonate by the duodenal mucosa.
Clinical manifestations - epigastric pain that begins 2 to 3 hours after eating, most often at night.
o
Ingestion of food or antacids usually relieves the pain.

Complications - perforation of the duodenal wall with development of peritonitis.

Treatment - avoidance of smoking, NSAIDs, and alcohol; antibiotics to treat the H. pylori infection;
and proton pump inhibitors (PPIs) to prevent gastric acid production.
B. Gastric Ulcers

Tend to develop in the antral region of stomach, adjacent to the acid-secreting mucosa of the body.

Less common than duodenal ulcers.

Causes are similar to those of duodenal ulcers, including chronic H. pylori infection and NSAID use.

Pathophysiology:
o
The primary defect is reduced mucus secretion an increased mucosal permeability to H+ ions.
o
Gastric secretion tends to be normal or less than normal.

Clinical manifestations - epigastric pain immediately after eating, anorexia, vomiting, and weight loss.

Treatment - same as for duodenal ulcers.
C. Stress Ulcers

Peptic ulcers that result from severe physiologic stress such as burns, head injury, multiple trauma,
severe infection, and mechanical ventilation.

Types:
1. Ischemic ulcers - develop suddenly after severe illness, systemic trauma, or neural injury.
o
Ulceration follows mucosal damage caused by decreased blood flow to the gastric mucosa.
2. Curling ulcers - ischemic ulcers that develop as a result of burn injury.
3. Cushing ulcers - caused by head trauma or brain surgery.
o
Ulceration follows hypersecretion of gastric acid due to overstimulation of the vagal nuclei.
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
Clinical manifestations - often form multiple painless ulcers in the stomach and duodenum which
present as occult bleeding in fecal tests.
o
Life-threatening hemorrhage may be the first indication of their presence.
 Ulcer surgery - peptic ulcers may be treated surgically if the patient suffers recurrent or uncontrolled
bleeding or perforation of the stomach or duodenum.
 Gastrectomy - resection of all or part of the stomach.
o
Anemia can result due to decreased production of intrinsic factor (which decreases B12 absorption).
V. Malabsorption Syndromes

Malabsorption syndromes result in impaired digestion or absorption of nutrients.
o
Maldigestion - failure of the chemical processes of digestion.
o
Malabsorption - failure of the intestinal mucosa to absorb digested nutrients.
o
Maldigestion and malabsorption frequently occur together.
A. Pancreatic Insufficiency

Insufficient pancreatic enzyme production causes malabsorption associated with impaired digestion.
o
The pancreas does not produce sufficient amounts of the enzymes that digest protein,
carbohydrates, and fats into components that can be absorbed by the intestine.

Causes - pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis.

Clinical manifestations - fatty stools, diarrhea, weight loss, and failure to thrive.

Treatment - oral replacement of pancreatic enzymes during meals.
B. Lactase Deficiency


Deficient lactase production in the brush border of the small intestine results in lactose intolerance.
o
Inhibits the breakdown of lactose (milk sugar) and prevents its absorption.
o
Fermentation of lactose by bacteria causes gas (cramping, pain, flatulence, etc.).
o
Excess lactose in lumen draws fluid in and increases gut motility, causing osmotic diarrhea.
Causes - can be genetic (more common in certain ethnic groups) or caused by diseases of the
intestine such as gluten-sensitive enteropathy.
o

Generally does not develop until adulthood.
Treatment - avoidance of lactose-containing foods.
C. Bile Salt Deficiency

Bile salts are needed to emulsify and absorb fats and fat-soluble vitamins.
o
Synthesized from cholesterol in the liver.

Bile salt deficiency causes fat malabsorption and steatorrhea (fatty stools).

Causes - liver disease, obstruction of the bile duct, intestinal hypomotility, and Crohn disease.

Clinical manifestations:
o
Poor intestinal absorption of lipids causes fatty stools and diarrhea.
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o

Malabsorption of fat-soluble vitamins causes vitamin deficiencies.

Vitamin A - night blindness

Vitamin D - decreased calcium absorption, bone pain, osteoporosis, fractures.

Vitamin K - prolonged prothrombin time, purpura, and petechiae

Vitamin E - uncertain; may cause testicular atrophy and neurologic defects in children.
Treatment - increase medium-chain triglycerides in the diet (coconut oil); oral bile salts; injections of
Vitamins A, D, and K.
VI. Inflammatory Bowel Diseases

Chronic, relapsing inflammatory bowel disorders of unknown origin.
A. Ulcerative Colitis

Chronic inflammatory disease that causes ulceration of the colonic mucosa, usually in the rectum
and sigmoid colon.

Possible causes - although the specific cause is unknown it is related to a number of factors:
o
Genetics - runs in families and more common is certain ethnic groups (Caucasians, Jews).
o
Autoimmunity - associated with other autoimmune diseases such as systemic lupus
erythematosus (SLE); immune cells cause inflammation of mucosa.

Pathophysiology:
o
Injury to the colon is mediated by macrophages, T cytotoxic cells, and the production of
anticolon antibodies.
o
These cause inflammatory ulceration in the large intestine with mucosal erythema and edema.
o
Ulceration and swelling cause narrowing of the colonic lumen, diarrhea, and significant
bleeding (hematochezia).
o
Process begins in the rectum and advances up through the colon in a continuous manner and
does not "skip" parts of the mucosa.


Clinical manifestations:
o
Most often presents in early adulthood.
o
Usually of sudden onset, with severe signs and symptoms.
o
Frequent loose bowel movements (10 to 20 stools per day) with bloody stools.
o
Crampy abdominal pain and dehydration.
o
Bleeding can cause iron-deficiency anemia.
o
A course of frequent remissions and exacerbations is common.
o
Increased risk of infection, perforation, strictures, and colon cancer.
Treatment - anti-inflammatory drugs; colonic resection with colostomy placement may be necessary.
B. Crohn Disease

Similar to ulcerative colitis, but it affects both the large and small intestines.
o
Most often involves ascending and transverse colon and distal ileum; rarely involves rectum.

Ulceration tends to involve all the layers of the intestinal wall (not just the mucosa).

“Skip lesion” fissures (affected areas separated by normal ones) and granulomas are characteristic.
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
Similar risk factors and theories of causation as ulcerative colitis.

Clinical manifestations - symptoms vary considerably from person to person.

o
Usually develops slowly.
o
Diarrhea, abdominal pain, and weight loss are typical.
o
Anemia due to deficiency of vitamin B12 and folic acid absorption.
o
Weight loss due to inadequate absorption of nutrients.
o
Fistulae formation.
o
Bloody diarrhea is less common than in ulcerative colitis.
Treatment - similar to ulcerative colitis.
C. Diverticular Disease of the Colon

Diverticula - outpouchings of colonic mucosa through the muscle layers of the colon wall.
o

Most common in sigmoid colon.
Diverticulosis - asymptomatic condition characterized by presence of diverticula.
o
Associated with a diet low in fiber and high in refined foods, constipation, and increased
pressure on weakened colon walls.

Diverticulitis - inflammation of the diverticula.
o
Caused by a fecolith (impacted fecal matter) that blocks the opening of a diverticulum,
causing irritation and bacterial growth.
o
Clinical manifestations - lower left quadrant abdominal pain (since sigmoid colon is usually
involved), fever, and episodes of diarrhea and/or constipation.
o
Sequelae - bleeding, necrosis of wall, perforation, peritonitis, fistula formation, and stenosis
of the colon causing obstruction.
VII. Appendicitis

Inflammation and infection of an outpouching of the vermiform appendix.

Usually develops during early adulthood, although it can occur in children.

Cause - obstruction of the appendix with fecal matter causes inflammation, infection, edema, and
ischemia of the appendix.

Clinical manifestations:
o
Initially pain is in epigastric or umbilical region, but swelling causes contact with the sensitive
parietal peritoneum, causing pain to move to lower right quadrant.

o
Anorexia (from pain), nausea and vomiting.
o
Low grade fever.
o
Leukocyte count moderately elevated.
Treatment - surgical removal of the appendix and administration of antibiotics.
o
Without surgical resection, inflammation may progress to gangrene, perforation, and peritonitis.
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ACTIVITY 3: What are some similarities between appendicitis and diverticulitis?
VIII. Irritable Bowel Syndrome

IBS is a functional disorder with no known structural or biochemical alterations

“Spastic colon”

Involved in up to half of the GI problems for which people seek help.

Symptoms vary, but can include cramping, fatigue, and constipation alternating with diarrhea.


o
Diarrhea symptoms are due to increased intestinal motility, reducing the time for fluid absorption.
o
Cramping is due to a loss of peristaltic coordination with conflicting waves of peristalsis.
Factors involved:
o
Alterations in the brain-gut axis with intestinal hypersensitivity
o
Abnormal GI motility and secretion
o
Intestinal infection
o
Changes in composition of intestinal flora
o
Food allergy or intolerance
o
Psychosocial factors such as emotional stress
Treatment - no cure; treatments aim at easing the symptoms, including antidepressants,
antispasmotics, visceral analgesics, antidiarrheals, laxatives, and fiber.
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Answer Key to Activities
ACTIVITY 1: Explain why factors that slow movement of feces through the colon cause constipation,
whereas factors the speed up movement of feces through the colon cause diarrhea.
As material moves through the GI tract, fluid and nutrients are removed by transport across the GI
wall from the lumen into the blood. The longer material is in contact with the wall, the more fluid
is removed and the more solid the fecal matter will become. This favors constipation.
The more quickly material passes through the GI tract (or the more damage there is to the wall),
the less fluid is removed and the more watery the feces become. This favors diarrhea.
ACTIVITY 2: What treatments would be appropriate for treating chronic gastritis (including its sequelae)?
Antibiotics to eliminate the H. pylori infections are generally used along with proton pump inhibitors
and other drugs to inhibit secretion of gastric acid.
If anemia symptoms are present, injections of vitamin B12 or high oral doses should be given.
(Since this can be caused by an autoimmune attack on the gastric mucosa, one might expect that
immune suppressants would be used, but this is not recommended in most cases.)
ACTIVITY 3: What are some similarities between appendicitis and diverticulitis?
Both involve obstruction of a pouch in the wall of the intestines, which creates a situation where
intestinal bacteria can grow and cause inflammation of the wall, compression of vessels and
necrosis.
Both can result in perforation of the wall, allowing fecal matter to enter the peritoneal space and
cause peritonitis.