Ch27.pdf

CHAPTER

Alterations in

Gastrointestinal Function

Alterations in Intestinal Absorption

Malabsorption Syndrome

Neoplasms

Adenomatous Polyps

Colorectal Cancer

Disorders of the Esophagus

Dysphagia

Esophageal Diverticulum

Gastroesophageal Reﬂux Disease

Gastroesophageal Reﬂux in Children

Cancer of the Esophagus

Disorders of the Stomach

Gastric Mucosal Barrier

Gastritis

Acute Gastritis

Chronic Gastritis

Ulcer Disease

Peptic Ulcer Disease

Zollinger-Ellison Syndrome

Stress Ulcers

Cancer of the Stomach

Disorders of the Small and Large Intestines

Irritable Bowel Syndrome

Inﬂammatory Bowel Disease

Crohn’s Disease

Ulcerative Colitis

Infectious Colitis

Clostridium Difﬁcile Colitis

Escherichia Coli O157:H7 Infection

Diverticular Disease

Appendicitis

Alterations in Intestinal Motility

Diarrhea

Constipation

Intestinal Obstruction

Peritonitis

G astrointestinal disorders are not cited as the leading

cause of death in the United States, nor do they receive

the same publicity as heart disease and cancer. However,

according to government reports, digestive diseases rank third

in the total economic burden of illness, resulting in consider-

able human suffering, personal expenditures for treatment, lost

working hours, and a drain on the nation’s economy. It has

been estimated that 60 to 70 million Americans have digestive

disease. 1 Even more important is the fact that proper nutrition

or a change in health practices could prevent or minimize

many of these disorders.

DISORDERS OF THE ESOPHAGUS

The esophagus is a tube that connects the oropharynx with the

stomach. It lies posterior to the trachea and larynx and extends

through the mediastinum, intersecting the diaphragm at the

level of the 11th thoracic vertebra. The esophagus functions

primarily as a conduit for passage of food from the pharynx to

the stomach, and the structure of its wall is designed for this

purpose: the smooth muscle layers provide the peristaltic

movements needed to move food along its length, and the epi-

thelial layer secretes mucus, which protects its surface and aids

in lubricating food.

Dysphagia

The act of swallowing depends on the coordinated action of the

tongue and pharynx. These structures are innervated by cranial

nerves V, IX, X, and XII. Dysphagia refers to difﬁculty in swal-

lowing. If swallowing is painful, it is referred to as odynophagia .

Dysphagia can result from altered nerve function or from dis-

orders that produce narrowing of the esophagus. Lesions of the

central nervous system (CNS), such as a stroke, often involve

473

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Unit Seven: Alterations in the Gastrointestinal System

the cranial nerves that control swallowing. Strictures and can-

cer of the esophagus and strictures resulting from scarring can

reduce the size of the esophageal lumen and make swallowing

difﬁcult. Scleroderma, an autoimmune disease that causes ﬁ-

brous replacement of tissues in the muscularis layer of the

gastrointestinal tract, is another important cause of dysphagia. 2

Persons with dysphagia usually report choking, coughing, or an

abnormal sensation of food sticking in the back of the throat

or upper chest when they swallow.

In a condition called achalasia , the lower esophageal sphinc-

ter fails to relax; food that has been swallowed has difﬁculty

passing into the stomach, and the esophagus above the lower

esophageal sphincter becomes enlarged. One or several meals

may lodge in the esophagus and pass slowly into the stomach.

There is danger of aspiration of esophageal contents into the

lungs when the person lies down.

4.0) are

particularly damaging. There is controversy regarding the im-

portance of hiatal hernia ( i.e. , herniation of the stomach

through an enlarged hiatus in the diaphragm) in the patho-

genesis of reflux disease. Small hiatal hernias are common

and considered to be of no signiﬁcance in asymptomatic people.

However, in cases of severe erosive esophagitis where gastro-

esophageal reflux and large hiatal hernia coexist, the hernia

may retard esophageal acid clearance and contribute to the

disorder. 3,5

Reﬂux esophagitis involves mucosal injury to the esopha-

gus, hyperemia, and inﬂammation. The most common symp-

tom of gastroesophageal reﬂux is heartburn. It frequently is

severe, occurring 30 to 60 minutes after eating. It often is made

worse by bending at the waist and recumbency and usually is

relieved by sitting upright. The severity of heartburn is not in-

dicative of the extent of mucosal injury; only a small percent-

age of people who report heartburn have mucosal injury.

Often, the heartburn occurs during the night. Antacids give

prompt, although transient relief. Other symptoms include

belching and chest pain. The pain usually is located in the epi-

gastric or retrosternal area and often radiates to the throat,

shoulder, or back. Because of its location, the pain may be

confused with angina. The reﬂux of gastric contents also may

produce respiratory symptoms such as wheezing, chronic

cough, and hoarseness. There is considerable evidence link-

ing gastroesophageal reﬂux with bronchial asthma. 7 The pro-

posed mechanisms of reﬂux-associated asthma and chronic

cough include aspiration, laryngeal injury, and vagal-mediated

bronchospasm.

Persistent gastroesophageal reﬂux produces a cycle of mu-

cosal damage that predisposes to strictures and a condition

called Barrett’s esophagus . Strictures are caused by a combina-

tion of scar tissue, spasm, and edema. They produce narrowing

of the esophagus and can cause dysphagia. Barrett’s esophagus

is characterized by a reparative process in which the squamous

mucosa that normally lines the esophagus gradually is replaced

by columnar epithelium resembling that in the stomach or in-

testines. 5,6 It is associated with increased risk for development

of esophageal cancer.

The diagnosis of gastroesophageal reﬂux depends on a his-

tory of reﬂux symptoms and selective use of diagnostic meth-

ods, including radiographic studies using a contrast medium

such as barium, esophagoscopy, and ambulatory esophageal

pH monitoring. 8

The treatment of gastroesophageal reﬂux usually focuses

on conservative measures. These measures include avoidance

of positions and conditions that increase gastric reflux. 8

Avoidance of large meals and foods that reduce lower eso-

phageal sphincter tone ( e.g. , caffeine, fats, chocolate), alcohol,

and smoking is recommended. Sleeping with the head elevated

helps to prevent reﬂux during the night. Weight loss usually is

recommended in overweight people.

Antacids or a combination of antacids and alginic acid also

are recommended for mild disease. Alginic acid produces a

foam when it comes in contact with gastric acid; if reflux oc-

curs, the foam, rather than acid, rises into the esophagus.

Histamine type 2 receptor-blocking drugs, which inhibit gas-

tric acid production, often are recommended when additional

treatment is needed. Proton pump inhibitors, which block the

ﬁnal pathway for acid secretion, may be used for persons who

in contact with mucosa. Acidic gastric fluids (pH

Esophageal Diverticulum

A diverticulum of the esophagus is an outpouching of the

esophageal wall caused by a weakness of the muscularis layer.

An esophageal diverticulum tends to retain food. Reports that

the food stops before it reaches the stomach are common, as

are reports of gurgling, belching, coughing, and foul-smelling

breath. The trapped food may cause esophagitis and ulceration.

Because the condition usually is progressive, correction of the

defect requires surgical intervention.

Gastroesophageal Reﬂux Disease

The term reflux refers to backward or return movement. In the

context of gastroesophageal reflux, it refers to the backward

movement of gastric contents into the esophagus, a condition

that causes heartburn. Often referred to as gastroesophageal

reflux disease (GERD), it probably is the most common dis-

order originating in the gastrointestinal tract. Most persons

experience heartburn occasionally as a result of reflux. Such

symptoms usually occur soon after eating, are short lived, and

seldom cause more serious problems. However, for some

persons, persistent heartburn can represent reflux disease with

esophagitis.

The lower esophageal sphincter regulates the ﬂow of food

from the esophagus into the stomach. Both internal and exter-

nal mechanisms function in maintaining the antireﬂux func-

tion of the lower esophageal sphincter. 3,4 Relaxation of the

lower esophageal sphincter is a brain stem reﬂex that is medi-

ated by the vagus nerve in response to a number of afferent

stimuli. Transient relaxation with reflux is common after

meals. Gastric distension and meals high in fat increase the fre-

quency of relaxation. Reﬂuxed material normally is returned to

the stomach by secondary peristaltic waves in the esophagus,

with swallowed saliva neutralizing and washing away the re-

ﬂuxed acid.

GERD is thought to be associated with a weak or incom-

petent lower esophageal sphincter that allows reflux to occur,

the irritant effects of the refluxate, and decreased clearance of

the refluxed acid from the esophagus after it has occurred. 5,6

Delayed gastric emptying also may contribute to reflux by

increasing gastric volume and pressure with greater chance

for reflux. Esophageal mucosal injury is related to the de-

structive nature of the refluxate and the amount of time it is

475

Chapter 27: Alterations in Gastrointestinal Function

continue to have daytime symptoms, recurrent strictures, or

large esophageal ulcerations. Surgical treatment may be indi-

cated in some people.

reﬂux, decrease crying and energy expenditure, and increase the

calorie density of the formula. 9,10 In infants, positioning on the

left side seems to decrease reﬂux. In older infants and children,

raising the head of the bed and keeping the child upright may

help. Medications usually are not added to the treatment regi-

men until pathologic reﬂux has been documented by diagnos-

tic testing.

Gastroesophageal Reﬂux in Children

Gastroesophageal reﬂux is a common problem in infants. The

small reservoir capacity of an infant’s esophagus coupled with

frequent spontaneous reductions in sphincter pressure con-

tributes to reﬂux. Regurgitation of at least one episode a day

occurs in as many as half of infants 0 to 3 months of age. By

6 months of age it becomes less frequent, and it abates by

2 years of age as the child assumes a more upright posture and

eats solid foods. 9,10 Although many infants have minor degrees

of reﬂux, complications occur in 1 of every 300 to 500 chil-

dren. 9,10 The condition occurs more frequently in children with

cerebral palsy, Down’s syndrome, and other causes of devel-

opmental delay.

In most cases, infants with simple reflux are thriving and

healthy, and symptoms resolve between 9 and 24 months of

age. Pathologic reﬂux is classiﬁed into three categories: (1) re-

gurgitation and malnutrition, (2) esophagitis, and (3) respira-

tory problems. Symptoms of esophagitis include evidence

of pain when swallowing, hematemesis, anemia caused by

esophageal bleeding, heartburn, irritability, and sudden or in-

consolable crying. Parents often report feeding problems in

their infants. 9 These infants often are irritable and demonstrate

early satiety. Sometimes the problems progress to actual resis-

tance to feeding. Tilting of the head to one side and arching of

the back may be noted in children with severe reﬂux. The head

positioning is thought to represent an attempt to protect the

airway or reduce the pain-associated reﬂux. Sometimes regur-

gitation is associated with dental caries and recurrent otalgia.

The ear pain is thought to occur through referral from the

vagus nerve in the esophagus to the ear. A variety of respira-

tory symptoms are caused by damage to the respiratory mu-

cosa when gastric reflux enters the esophagus. Reflux may

cause laryngospasm, apnea, and bradycardia. A relationship

between reﬂux and acute life-threatening events or sudden in-

fant death syndrome has been proposed. However, the associ-

ation remains a matter of controversy, and the linkage may be

coincidental. 9,10

Rumination is the repetitive gagging, regurgitation, mouth-

ing, and reswallowing of regurgitated material. Although the

cause of the disorder is unknown, it often is associated with

mental retardation or altered interaction with the environment

( e.g. , lack of stimulation in newborn intensive care units or be-

cause of altered relationships with caregivers). As with pure re-

ﬂux, rumination may produce severe esophagitis with signs of

iron deﬁciency anemia, failure to thrive, and head tilting. 10

Diagnosis of gastroesophageal reflux in infants and chil-

dren often is based on parental and clinical observations. The

diagnosis may be confirmed by esophageal pH probe studies

or barium ﬂuoroscopic esophagography. In severe cases, esoph-

agoscopy may be used to demonstrate reflux and obtain a

biopsy.

Various treatment methods are available for infants and

children with gastroesophageal reﬂux. Small, frequent feedings

are recommended because of the association between gastric

volume and transient relaxation of the esophagus. Thickening

an infant’s feedings with cereal tends to decrease the volume of

Cancer of the Esophagus

Carcinoma of the esophagus accounts for approximately 6% of

all gastrointestinal cancers. This disease is more common in

persons older than 50 years, with a male-to-female ratio of

approximately 2

1. 11

There are two types of esophageal cancers: squamous cell

and adenocarcinomas. Fewer than 50% of esophageal tumors

are squamous cell cancers. These cancers are associated more

commonly with dietary and environmental inﬂuences. 11,12

Most squamous cell cancers in the United States and Europe are

attributable to alcohol and tobacco use. Adenocarcinomas,

which typically arise from Barrett’s esophagus, account for

more than 50% of esophageal cancers. The incidence of this

type of cancer appears to be increasing. Adenocarcinomas typ-

ically are located in the distal esophagus and may invade the

adjacent upper part of the stomach. Endoscopic surveillance in

people with Barrett’s esophagus may detect adenocarcinoma at

an earlier stage, when it is more amenable to curative surgical

resection. 12

Dysphagia is by far the most frequent complaint of persons

with esophageal cancer. It is apparent ﬁrst with ingestion of

bulky food, later with soft food, and ﬁnally with liquids. Un-

fortunately, it is a late manifestation of the disease. Weight loss,

anorexia, fatigue, and pain on swallowing also may occur.

Treatment includes surgical resection, which provides a

means of cure when done in early disease and palliation when

done in late disease. Irradiation is used as a palliative treat-

ment. Chemotherapy sometimes is used before surgery to de-

crease the size of the tumor, and it may be used along with

irradiation and surgery in an effort to increase survival. 12

The prognosis for persons with cancer of the esophagus,

although poor, has improved. However, even with modern

forms of therapy, the long-term survival is limited because, in

many cases, the disease has already metastasized by the time

the diagnosis is made.

In summary, the esophagus is a tube that connects the

oropharynx with the stomach; it functions primarily as a con-

duit for passage of food from the pharynx to the stomach.

Dysphagia refers to difﬁculty in swallowing; it can result from

altered nerve function or from disorders that produce narrow-

ing of the esophagus. A diverticulum of the esophagus is an

outpouching of the esophageal wall caused by a weakness of

the muscularis layer.

Gastrointestinal reﬂux refers to the backward movement

of gastric contents into the esophagus, a condition that

causes heartburn. Although most persons experience occa-

sional esophageal reﬂux and heartburn, persistent reﬂux can

cause esophagitis. Gastroesophageal reﬂux is a common

problem in infants. Reﬂux commonly corrects itself with age,

and symptoms abate in most children by 2 years of age.

476

Unit Seven: Alterations in the Gastrointestinal System

The gastric epithelial cells are connected by tight junctions

that prevent acid penetration, and they are covered with an im-

permeable hydrophobic lipid layer that prevents diffusion of

ionized water-soluble molecules. Aspirin, which is nonionized

and lipid soluble in acid solutions, rapidly diffuses across this

lipid layer, increasing mucosal permeability and damaging epi-

thelial cells. 14 Gastric irritation and occult bleeding caused by

gastric irritation occur in a signiﬁcant number of persons who

take aspirin on a regular basis (Fig. 27-1). Alcohol, which also

is lipid soluble, disrupts the mucosal barrier; when aspirin and

alcohol are taken in combination, as they often are, there is in-

creased risk of gastric irritation. Bile acids also attack the lipid

components of the mucosal barrier and afford the potential for

gastric irritation when there is reﬂux of duodenal contents into

the stomach.

Normally, the secretion of hydrochloric acid by the parietal

cells of the stomach is accompanied by secretion of bicarbon-

ate ions (HCO 3 – ). For every hydrogen ion (H + ) that is secreted,

a HCO 3 – is produced, and as long as HCO 3 – production is equal

to H + secretion, mucosal injury does not occur. Changes in

gastric blood ﬂow, as in shock, tend to decrease HCO 3 – pro-

duction. This is particularly true in situations in which de-

creased blood ﬂow is accompanied by acidosis. Aspirin and the

nonsteroidal anti-inﬂammatory drugs (NSAIDs) also impair

HCO 3 – secretion.

Prostaglandins, chemical messengers derived from cell mem-

brane lipids, play an important role in protecting the gastro-

intestinal mucosa from injury. The prostaglandins probably

exert their effect through improved blood flow, increased

bicarbonate ion secretion, and enhanced mucus production.

The fact that drugs such as aspirin and the NSAIDs inhibit

prostaglandin synthesis may contribute to their ability to pro-

duce gastric irritation. 14 Smoking and older age have been asso-

Although many infants have minor degrees of reﬂux, some in-

fants and small children have signiﬁcant reﬂux that interferes

with feeding, causes esophagitis, and results in respiratory

symptoms and other complications.

Carcinoma of the esophagus, which accounts for 6% of all

cancers, is more common in persons older than 50 years, and

the male-to-female ratio is approximately 2:1. There are two

types of esophageal cancer: squamous cell and adenocarci-

noma. Most squamous cell cancers are attributable to alcohol

and tobacco use, whereas adenocarcinomas are more closely

linked to esophageal reﬂux and Barrett’s esophagus.

DISORDERS OF THE STOMACH

The stomach is a reservoir for contents entering the digestive

tract. While in the stomach, food is churned and mixed with

hydrochloric acid and pepsin before being released into the

small intestine. Normally, the mucosal surface of the stomach

provides a barrier that protects it from the hydrochloric acid

and pepsin contained in gastric secretions. Disorders of the

stomach include gastritis, peptic ulcer, and gastric carcinoma.

Gastric Mucosal Barrier

The stomach lining usually is impermeable to the acid it se-

cretes, a property that allows the stomach to contain acid and

pepsin without having its wall digested. Several factors con-

tribute to the protection of the gastric mucosa, including an im-

permeable epithelial cell surface covering, mechanisms for the

selective transport of hydrogen and bicarbonate ions, and the

characteristics of gastric mucus. 13 These mechanisms are col-

lectively referred to as the gastric mucosal barrier .

KEY CONCEPTS

DISRUPTION OF THE GASTRIC MUCOSA

AND ULCER DEVELOPMENT

The stomach is protected by tight cellular junctions,

a protective mucus layer, and prostaglandins that

serve as chemical messengers to protect the stom-

ach lining by improving blood ﬂow, increasing bicar-

bonate secretion, and enhancing mucus production.

■

Two of the major causes of gastric irritation and

ulcer formation are aspirin or nonsteroidal anti-

inﬂammatory drugs (NSAIDs) and infection

with Helicobacter pylori .

■

Aspirin and NSAIDs exert their destructive effects by

damaging epithelial cells, impairing mucus produc-

tion, and inhibiting prostaglandin synthesis.

■

H. pylori is an infectious agent that thrives in the acid

environment of the stomach and disrupts the mu-

cosal barrier that protects the stomach from the

harmful effects of its digestive enzymes.

■

■ FIGURE 27-1 ■ Erosive gastritis. This endoscopic view of the

stomach in a patient who was ingesting aspirin reveals acute he-

morrhagic lesions. (From Rubin E., Farber J.L. [1999]. Pathology

[3rd ed., p. 683]. Philadelphia: Lippincott Williams & Wilkins)

477

Chapter 27: Alterations in Gastrointestinal Function

ciated with reduced gastric and duodenal prostaglandin con-

centrations; these observations may explain the predisposition

to ulcer disease in smokers and older persons. 15

Chronic autoimmune gastritis and multifocal atrophic

gastritis cause few symptoms related directly to gastric changes.

Persons with autoimmune chronic gastritis may have signs of

pernicious anemia. More important is the development of pep-

tic ulcer and increased risk of peptic ulcer and gastric carcinoma.

Approximately 2% to 4% of persons with atrophic gastritis

eventually experience gastric carcinoma. 11

H. pylori gastritis is the most common type of chronic non-

erosive gastritis in the United States. H. pylori are small, curved,

gram-negative rods that can colonize the mucus-secreting

epithelial cells of the stomach 16,17 (Fig. 27-2). H. pylori have

multiple ﬂagella, which allow them to move through the mu-

cous layer of the stomach, and they secrete urease, which en-

ables them to produce sufﬁcient ammonia to buffer the acidity

of their immediate environment. Because the organism ad-

heres only to the mucus-secreting cells of the stomach, it does

not usually colonize other parts of the gastrointestinal tract.

H. pylori produce an enzyme that degrades mucin and has the

capacity to interfere with the local protection of the gastric mu-

cosa against acid. It also may produce toxins that directly dam-

age the mucosa and produce ulceration in other ways. Chronic

infection with H. pylori can lead to gastric atrophy and intesti-

nal metaplasia. H. pylori also can cause peptic ulcer (to be dis-

cussed) and has been linked to the development of gastric ade-

nocarcinoma.

Chemical gastropathy is a chronic gastric injury resulting from

reﬂux of alkaline duodenal contents, pancreatic secretions, and

bile into the stomach. It is most commonly seen in persons

who have had gastroduodenostomy or gastrojejunostomy

surgery. A milder form may occur in persons with gastric ulcer,

Gastritis

Gastritis refers to inﬂammation of the gastric mucosa. There are

many causes of gastritis, most of which can be grouped under

the headings of acute or chronic gastritis.

Acute Gastritis

Acute gastritis refers to a transient inﬂammation of the gastric

mucosa. It is most commonly associated with local irritants

such as bacterial endotoxins, caffeine, alcohol, and aspirin.

Depending on the severity of the disorder, the mucosal re-

sponse may vary from moderate edema and hyperemia to he-

morrhagic erosion of the gastric mucosa.

The complaints of persons with acute gastritis vary. Persons

with aspirin-related gastritis can be totally unaware of the con-

dition or may report only heartburn or sour stomach. Gastritis

associated with excessive alcohol consumption is a different sit-

uation; it often causes transient gastric distress, which may lead

to vomiting and, in more severe situations, to bleeding and

hematemesis. Gastritis caused by the toxins of infectious or-

ganisms, such as the staphylococcal enterotoxins, usually has

an abrupt and violent onset, with gastric distress and vomiting

ensuing approximately 5 hours after the ingestion of a contam-

inated food source. Acute gastritis usually is a self-limiting dis-

order; complete regeneration and healing usually occur within

several days.

Chronic Gastritis

Chronic gastritis is a separate entity from acute gastritis. It is

characterized by the absence of grossly visible erosions and the

presence of chronic inﬂammatory changes leading eventually

to atrophy of the glandular epithelium of the stomach. The

changes may become dysplastic and possibly transform into

carcinoma. Factors such as chronic alcohol abuse, cigarette

smoking, and chronic use of NSAIDs may contribute to the

development of the disease.

There are four major types of chronic gastritis: (1) auto-

immune gastritis, (2) multifocal atrophic gastritis, (3) Helicobac-

ter pylori gastritis, and (4) chemical gastropathy. 16 Autoimmune

gastritis is the least common form of chronic gastritis. Most per-

sons with the disorder have circulating antibodies to parietal

cells and intrinsic factor, so this form of chronic gastritis is con-

sidered to be of autoimmune origin. Autoimmune destruction

of the parietal cells leads to hypochlorhydria or achlorhydria,

a high intragastric pH, and hypergastrinemia. Pernicious ane-

mia is a megaloblastic anemia that is caused by malabsorption

of vitamin B 12 caused by a deﬁciency of intrinsic factor (see

Chapter 13). This type of chronic gastritis frequently is associ-

ated with other autoimmune disorders, such as Hashimoto’s

thyroiditis and Addison’s disease.

Multifocal atrophic gastritis is a disorder of unknown etiology.

It is more common than autoimmune gastritis and is seen

more frequently in whites than in other races. It is particularly

common in Asia, Scandinavia, and parts of Europe and Latin

America. As with autoimmune gastritis, it is associated with re-

duced gastric acid secretion, but achlorhydria and pernicious

anemia are less common.

■ FIGURE 27-2 ■ Infective gastritis. H. pylori appears on silver stain-

ing as small, curved rods on the surface of the gastric mucosa.

(From Rubin E., Farber J.L. [1999]. Pathology [3rd ed., p. 687].

Philadelphia: Lippincott Williams & Wilkins)

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