Alteration in Gastrointestinal

functions

PEPTIC ULCER DISEASE

Peptic ulcer disease refers to ulcerations in the
mucosa of the lower esophagus, stomach, or
duodenum

acid.
Nocturnal epigastric, abdominal pain or
burning. May awaken patient at night,
usually around midnight to 3 a.m. hunger
like due to excessive acid production

Epigastric tenderness on examination

Early satiety, anorexia, weight loss,

heartburn, belching (may indicate reflux
disease)

Dizziness, syncope, hematemesis, or melena

(may indicate hemorrhage)

Anemia

Pathophysiology and Etiology

Stomach contains acidic secretions that can

digest substances, intrinsic defenses protect
the gastric mucosal membrane from injury.
A thick, tenacious layer of gastric mucus
protects the stomach from autodigestion,

Gastric ulcers may be a result of destruction

of the mucosal barrier.

The duodenum is protected from ulceration

by the function of Brunner's glands. These
glands produce a viscid, mucoid,alkaline
secretion that neutralizes the acid chyme.
Duodenal ulcers appear to result from
excessive acid protection.

Helicobacter pylori releases a toxin that

destroys the gastric and duodenal mucosa,
reducing the epithelium's resistance to acid
digestion and causing gastritis and ulcer
disease.

Salicylates and other NSAIDs inhibit the

secretion of prostaglandins (substances that
block ulceration).

Sudden, intense midepigastric pain radiating to the

right shoulder may indicate ulcer perforation.
Diagnostic Evaluation
Upper GI endoscopy with possible tissue
biopsy and cytology.
Upper GI radiographic examination (barium
study)

Serial stool specimens to detect occult blood

Serology to test for H. pylori antibodies

Appendicitis
APPENDICITIS
Appendicitis is inflammation of the vermiform
appendix caused by an obstruction of the intestinal
lumen from infection, stricture, fecal mass, foreign
body, or tumor.

Certain illnesses, such as pancreatitis,

hepatic disease, Crohn's disease, preexisting
gastritis, and Zollinger-Ellison syndrome,
also contribute to ulceration.

blood type (gastric ulcers and type A;

duodenal ulcers and type O) and other
genetic factors.

Exposure to irritants, such as alcohol,

coffee,and tobacco, may contribute by
accelerating gastric acid emptying and
promoting mucosal breakdown. Emotional
stress also contributes to ulcer formation
because of the increased stimulation of acid
and pepsin secretion and decreased mucosal
defense.

Causes

mucosal ulceration
fecal mass
stricture
barium ingestion
viral infection.

Pathophysiology

Mucosal ulceration triggers inflammation,

which temporarily obstructs the appendix.
The obstruction blocks mucus outflow.
Pressure in the now distended appendix
increases, and the appendix contracts.

Bacteria multiply, and inflammation and

pressure continue to increase, restricting
blood flow to the organ and causing severe
abdominal pain.
Obstruction is followed by edema, infection,
and ischemia.

Physical trauma and normal aging are

additional predisposing conditions.

Clinical Manifestations
Gnawing or burning epigastric pain
occurring 1 to 3 hours after a meal due to
stretching of the mucosa by food
pain relieved by food or antacids, but
usually recurring 2 to 4 hours later
secondary to food acting as a buffer for

Appendicitis may occur at any age and

affects both sexes equally; however,
between puberty and age 25,
Prevalent in men.
Since the advent of antibiotics, the incidence
and the death rate of appendicitis have
declined; if untreated, this disease is
invariably fatal.

As intraluminal tension develops, necrosis

and perforation usually occur.

Clinical Manifestations
Generalized or localized abdominal pain in
the epigastric or periumbilical areas and
upper right abdomen. Within 2 to 12 hours,
the pain localizes in the right lower quadrant
and intensity increases.
Anorexia, moderate malaise, mild fever,
nausea and vomiting.

Percussion: resonance and tympany due to

paralytic ileus; loss of liver dullness may
indicate free air in abdomen.

Auscultation: decreased bowel sounds.

Nausea and vomiting often occur; peristalsis

diminishes; anorexia is present.

Usually constipation occurs; occasionally

diarrhea.

Elevation of temperature and pulse as well

as leukocytosis.

Rebound tenderness, involuntary guarding,

generalized abdominal rigidity.

Fever; thirst; oliguria; dry, swollen tongue;

signs of dehydration.

low-grade temperature from systemic

manifestation of inflammation and
leukocytosis

Weakness, pallor, diaphoresis, and cold skin

are a result of the loss of fluid, electrolytes,
and protein into the abdomen.

Hypotension, tachycardia, and hypokalemia

may occur.

Shallow respirations may result from

abdominal distention and upward
displacement of the diaphragm.

Complications
wound infection
intraabdominal abscess
fecal fistula
intestinal obstruction
incisional hernia
peritonitis
death.

Note: With generalized peritonitis, large

volumes of fluid may be lost into abdominal
cavity (can account for losses to 5 L/day).

Diagnostic Evaluation
WBC count reveals moderate leukocytosis
(10,000 to 16,000/mm3) with shift to the left
(increased immature neutrophils).

Urinalysis to rule out urinary disorders.

Abdominal X-ray may visualize shadow
consistent with fecalith in appendix;
perforation will reveal free air.

Abdominal ultrasound or CT scan can

visualize appendix and rule out other
conditions, such as diverticulitis and Crohn's
disease. Focused appendiceal CT can
quickly evaluate for appendicitis.

PERITONITIS
Peritonitis is a generalized or localized inflammation
of the peritoneum, the membrane lining the
abdominal cavity and covering visceral organs.
Pathophysiology and Etiology
Primary Peritonitis
Acute, (rare)
Escherichia coli.
streptococci, pneumococci, or gonococci.
Secondary Peritonitis
Contamination of peritoneal cavity by GI fluid and
microorganisms.
Clinical Manifestations
Initially, local type of abdominal pain tends
to become constant, diffuse, and more
intense.
Abdomen becomes extremely tender and
muscles become rigid; rebound tenderness
and ileus may be present; patient lies very
still, usually with legs drawn up.

Ascites

Complication of appendicitis
diverticulitis, peptic ulceration, biliary tract
disease, colon inflammation, volvulus,
strangulated obstruction, perforation,
abdominal cancers.
Diagnostic Evaluation
WBC to show leukocytosis (leukopenia if
severe).
ABG levels may show hypoxemia or
metabolic acidosis with respiratory
compensation.

Urinalysis may indicate urinary tract

problems as primary source.

Peritoneal aspiration (paracentesis) to

demonstrate blood, pus, bile, bacteria
(Gram's stain), amylase.

Abdominal X-rays may show free air in

peritoneal cavity, gas and fluid collection in
small and large intestines, generalized bowel
dilatation, intestinal wall edema.

CT scan of abdomen or sonography may

reveal intra-abdominal mass, abscess,
ascites.

Chest X-ray may show elevated diaphragm.

Exploratory laparotomy

CROHN'S DISEASE
Crohn's disease is a chronic idiopathic inflammatory
disease that can affect any part of the GI tract, usually
the small and large intestines.
As Crohn's disease progresses, fibrosis thickens the
bowel wall and narrows the lumen. Narrowing or
stenosis

can occur in any part of the intestine and cause

varying degrees of intestinal obstruction
Pathophysiology and Etiology
unknown
lymphatic obstruction, allergies, immune disorders,
genetic predisposition.
Environmental agents, such as infections (viral or
bacterial overload) or dietary factors,
Defect in the intestinal barrier that increases the
permeability of the bowel.
Defect in the repair of mucosal injury leading to
chronic condition.
Intestinal tissue is thickened and edematous;
ulcers enlarge, and deepen.The deep
penetration of these ulcers may form
fissures, abscesses, and fistulae. The healing
and fibrosis of these lesions may lead to
stricture

The clinical presentation can be divided into

three patterns:
o
o

Inflammatory
Fibrostenotic (stricturing)

Perforating (fistulizing)

Signs and symptoms

Signs and symptoms include:
steady, colicky pain in the right lower quadrant due to
acute inflammation and nerve fiber irritation
cramping intermittent pain due to acute
inflammation
tenderness due to acute inflammation

Diagnosis
Fecal occult test reveals minute amounts of blood in
stools.
Small bowel X-ray shows irregular mucosa,
ulceration, and stiffening.
Barium enema reveals the string sign (segments of
stricture separated by normal bowel) and possibly
fissures and narrowing of the bowel.
Sigmoidoscopy and colonoscopy reveal patchy areas
of inflammation (helps to rule out ulcerative colitis),
with cobblestone-like mucosal surface. With colon
involvement, ulcers may be seen.
Biopsy reveals granulomas in up to half of all
specimens.
Blood tests reveal increased white blood cell count
and erythrocyte sedimentation rate, and decreased
potassium, calcium, magnesium, and hemoglobin
levels.
Hemorrhoids
Hemorrhoids are varicosities in the superior(internal)
or inferior (external) hemorrhoidal venous plexus.
Dilation and enlargement
Incidence: both sexes.
highest between ages 20 and 50.
Pathophysiology
Hemorrhoids result from activities that increase
intravenous pressure, causing distention and
engorgement.

weight loss secondary to diarrhea and malabsorption

diarrhea due to bile salt malabsorption,
loss of healthy intestinal surface area, and bacterial
growth

The exact pathogenesis remains

controversial. Theories include:
o Abnormal dilatation of veins of
internal hemorrhoidal venous
plexus.
o

Abnormal distension of the

arteriovenous anastomoses.

Downward displacement or
prolapse of anal cushions.

Destruction of the anchoring

connective tissue system.

steatorrhea secondary to fat malabsorption

bloody stools secondary to bleeding from
inflammation and ulceration.
Fever may indicate infectious complication such as
abscess.
Fecal urgency and tenesmus (feeling of constantly
needing to pass stools, despite an empty colon feeling
of constantly needing to pass stools, despite an empty
colon)
anorexia, weight loss, malaise, nausea, arthralgias,
and hematochezia
Rectal examination may reveal a perirectal abscess,
fistula, fissure, or skin tags (which represent healed
perianal lesions).
Complications
anal fistula
perineal abscess
fistulas to the bladder or vagina or to the
skin in an old scar area
intestinal obstruction
nutrient deficiencies from poor digestion
and malabsorption of bile salts and vitamin
B 12
fluid imbalances.

Increased intra-abdominal pressure causes

engorgement in the vascular tissue lining the
anal canal.

Loosening of vessels from surrounding

connective tissue occurs with protrusion or
prolapse into anal canal.
Predisposing factors include:
o
o

Pregnancy, prolonged
sitting/standing.
Straining at stool, chronic
constipation/diarrhea.

Anal infection, rectal surgery, or

episiotomy.

Hereditary factor.

Exercise.

Coughing, sneezing, vomiting.

Loss of muscle tone due to age.

Anal intercourse.

Classification:
First-degree- anal canal.
Second-degree- prolapse during straining but reduce
spontaneously.
Third-degree- prolapsed hemorrhoids that require
manual reduction after each bowel movement.
Fourth-degree hemorrhoids are irreducible..
Clinical Manifestations
Bleeding during or after defecation, bright
red blood on stool due to injury of mucosa
covering hemorrhoid (most common)
Visible (if external) and palpable mass

Constipation, anal itching

Sensation of incomplete fecal evacuation

Infection or ulceration, mucus discharge

Pain noted more in external hemorrhoids

Sudden rectal pain due to thrombosis in

external hemorrhoids

Complications
Constipation
Local infection
Thrombosis of hemorrhoids
Secondary anemia from severe or recurrent bleeding.

lead to ulceration and

perforation

FIGURE 18-9 GI and systemic

complications of ulcerative colitis.
May manifest as a systemic disease with
inflammatory changes of connective tissue.
Most common in young adulthood and
middle-age, peak incidence at ages 20 to 40.
Incidence greatest in whites of Jewish
descent.

Clinical Manifestations
Diarrhea may be bloody or contain pus and
mucus.
Tenesmus (painful straining), sense of
urgency, and frequency.

Increased bowel sounds; abdomen may

appear flat, but, as condition continues,
abdomen may appear distended.

There often is weight loss, fever,

dehydration, hypokalemia, anorexia, nausea
and vomiting, iron-deficiency anemia, and
cachexia (general lack of nutrition and
wasting with chronic disease).

Crampy abdominal pain.

The disease usually begins in the rectum and

sigmoid and spreads proximally, at times,
involving the entire colon. Anal area may be
irritated and reddened; left lower abdomen
may be tender on palpation.

Diagnosis
Physical examination confirms external hemorrhoids.
Anoscopy and flexible sigmoidoscopy visualizes
internal hemorrhoids

There is a tendency for the patient to

experience remissions and exacerbations.

Increased risk of developing colorectal

cancer.

Ulcerative colitis

May inhibit extracolonic manifestations of

eye (iritis, uveitis), joint (polyarthritis), and
skin complaints (erythema nodosum,
pyoderma gangrenosum).

Ulcerative colitis is a chronic idiopathic

inflammatory disease of the mucosa and, less
frequently, the submucosa of the colon and rectum. If
only the rectum is involved, it may be called
ulcerative proctitis.
Pathophysiology and Etiology
The exact cause of ulcerative colitis is
unknown. Possible theories include:
o Genetic predisposition.

Diagnostic Evaluation
Diagnosis is based on a combination of laboratory,
radiologic, endoscopic, and histologic findings.
Laboratory Tests
Stool examination to rule out enteral
pathogens; fecal analysis positive for blood
during active disease.
Complete blood count hemoglobin and
hematocrit may be low due to bleeding;
WBC may be increased.

Environmental factors may trigger

disease (viral or bacterial
pathogens, dietary).

Immunologic imbalance or
disturbances.

Elevated erythrocyte sedimentation rate

(ESR).

Defect in intestinal barrier causing

hypersensitive mucosa and
increased permeability.

Decreased serum levels of potassium,

magnesium, and albumin may be present.

Defect in repair of mucosal injury,

which may develop into a chronic
condition.

Multiple crypt abscesses

develop in intestinal mucosa
that may become necrotic and

Other Diagnostic Tests

Barium enema to assess extent of disease
and detect pseudopolyps, carcinoma, and
strictures. May show absence of haustral
markings; narrow, lead-pipe appearance;
superficial ulcerations.
Flexible proctosigmoidoscopy/colonoscopy
findings reveal mucosal erythema and

edema, ulcers, inflammation that begins

distally in the rectum and spreads
proximally for variable distances.
Pseudopolyps and friable tissue may be
present.

Changes in crypt height, loss of crypts, crypt

abscess with neutrophils infiltrates on
biopsy.

CT scan can identify complications such as

toxic megacolon.

Rectal biopsy differentiates from other

inflammatory diseases or cancer.

Cholecystitis
Cholecystitis acute or chronic inflammation
causing painful distention of the gallbladder is
usually associated with a
gallstone impacted in the cystic duct. Cholecystitis
accounts for 10% to 25% of all patients requiring
gallbladder surgery.
The acute form is most common among middle-aged
women; the chronic form, among the elderly. The
prognosis is good
with treatment.
Causes
Gallstones (the most common cause)
Poor or absent blood flow to the gallbladder
Abnormal metabolism of cholesterol and bile salts.
Pathophysiology
In acute cholecystitis, inflammation of the
gallbladder wall usually develops after a gallstone
lodges in the cystic duct. When bile flow is blocked,
the gallbladder becomes inflamed and distended.
Bacterial growth, usually Escherichia coli, may
contribute to the inflammation. Edema of the
gallbladder (and sometimes
the cystic duct) obstructs bile flow, which chemically
irritates the gallbladder. Cells in the gallbladder wall
may become oxygen starved and die as the distended
organ presses on vessels and impairs blood flow. The
dead cells slough off, and an exudate covers ulcerated
areas, causing the gallbladder to adhere to
surrounding structures.
Signs and symptoms
Acute abdominal pain in the right upper quadrant that
may radiate to the back, between the shoulders, or to
the
front of the chest secondary to inflammation and
irritation of nerve fibers
Colic due to the passage of gallstones along the bile
duct
Nausea and vomiting triggered by to the
inflammatory response
Chills related to fever
Low-grade fever secondary to inflammation
Jaundice from obstruction of the common bile duct
by stones.
Complications
Perforation and abscess formation
Fistula formation
Gangrene
Empyema
Cholangitis
Hepatitis
Pancreatitis
Gallstone ileus
Carcinoma.
Diagnosis
X-ray reveals gallstones if they contain enough
calcium to be radiopaque; also helps disclose
porcelain gallbladder

(hard, brittle gall bladder due to calcium deposited in

wall), limy bile, and gallstone ileus.
Ultrasonography detects gallstones as small as 2 mm
and distinguishes between obstructive and
nonobstructive
jaundice.
Levels of serum alkaline phosphate, lactate
dehydrogenase, aspartate aminotransferase, and total
bilirubin are high; serum amylase slightly elevated;
and icteric index elevated. White blood cell counts
are slightly elevated during cholecystitis attack.

Vincent's angina:
A reoccurring periodontal disease which results in
necrosis and ulceration of the gums.
Symptoms may include fever, bone loss, breath
odor and enlarge neck and throat lymph nodes.
Also called trench mouth, acute necrotizing
ulcerative gingivitis or Vincent's infection.
An acute or chronic GINGIVITIS characterized
by redness and swelling, NECROSIS extending
from the interdental papillae along the gingival
margins, PAIN; HEMORRHAGE, necrotic odor,
and often a pseudomembrane. The condition may
extend to the ORAL MUCOSA; TONGUE;
PALATE; or PHARYNX.
Vincent gingivitis, also called Vincent
infection, Vincent stomatitis, acute necrotizing
ulcerative gingivitis, Vincent angina, or trench
mouth,
acute and painful infection of the tooth margins and
gums that is caused by the symbiotic
microorganismsBacillus fusiformis and Borrelia
vincentii. The chief symptoms are painful, swollen,
bleeding gums; small, painful ulcers covering the
gums and tooth margins; and characteristic fetid
breath. The ulcers may spread to the throat and
tonsils. Fever and malaise may also be present.
Vincent gingivitis can occur after a prolonged failure
to brush ones teeth, though there are many other
predisposing factors, such as vitamin deficiencies,
emotional stress, and so on.

GASTROESOPHAGEAL REFLUX DISEASE AND

ESOPHAGITIS
Gastric contents flow back into the esophagus in
gastroesophageal reflux disease (GERD) due to
incompetent lower esophageal sphincter (LES).
Esophagitis, or inflammation of the esophageal
mucosa, may result.
Pathophysiology and Etiology
Gastroesophageal reflux associated with an
incompetent LES gastric contents reflux
(flow backward) through the LES into the
esophagus.
Can be the result of impaired gastric
emptying from gastroparesis or partial
gastric outlet obstruction.

The acidity of gastric content and amount of

time in contact with esophageal mucosa are
related to the degree of mucosal damage.

Inflammation and ulceration of the

esophagus may result, causing esophagitis.

Clinical Manifestations
GERD
The most common symptom is heartburn
(pyrosis), typically occurring 30 to 60
minutes after meals and with reclining
positions. May have complaints of
spontaneous reflux (regurgitation) of sour or
bitter gastric contents into the mouth.
Other typical symptoms include globus
(sensation of something in throat), mild
epigastric pain, dyspepsia, and nausea
and/or vomiting.

Dysphagia is a less common symptom.

Atypical symptoms include chest pain,

hoarseness, recurrent sore throat, frequent
throat clearing, chronic cough, dental
enamel loss, bronchospasm
(asthma/wheezing), and odynophagia (sharp
substernal pain on swallowing).

Symptoms that may suggest other disease

etiologies need further evaluation: atypical
chest pain (rule out possible cardiac causes),
dysphagia, odynophagia, GI bleeding,
shortness of breath, or weight loss (rule out
cancer or esophageal stricture).

Esophagitis
Esophagitis is an acute or chronic
inflammation of the esophagus. Severity of
symptoms may be unrelated to the degree of
esophageal tissue damage.
Symptoms vary according to etiology of
esophagitis. Symptoms include dysphagia,
odynophagia, severe burning, chest pain.

positive. This test differentiates between

cardiac and noncardiac chest pain.

May be caused by motility disorders

achalasia, scleroderma, esophageal spasm.

Causes of esophagitis other than GERD

o

Infectious Candida, herpes, human

immunodeficiency virus,
cytomegalovirus

Chemical (alkali or acid) or

radiation therapy

Medication-induced may include

doxycycline, ascorbic acid,
quinidine, potassium chloride,
bisphosphonates

Diagnostic Evaluation
Uncomplicated GERD may be diagnosed on
patient history of typical symptoms.
Endoscopy can visualize inflammation,
lesions, or erosions. Biopsy can confirm
diagnosis.

Esophageal manometry measures LES

pressure and determines if esophageal
peristalsis is adequate. This study should be
used before patients undergo surgical
treatment for reflux. This test is also done
before a pH probe for determination of
correct catheter placement.

Acid perfusion (Bernstein test) onset of

symptoms after ingestion of dilute
hydrochloric acid and saline is considered

Ambulatory 24-hour pH monitoring is

frequently performed for diagnosing GERD
or reflux esophagitis. It determines the
amount of gastroesophageal acid reflux and
has a 70% to 90% specificity rate. The
Bravo pH capsule system is a catheter-free
system in which a capsule containing a
radiotelemetry pH sensor is inserted into the
esophagus. This sensor transmits signals to
an external pager-size receiver, allowing the
patient to be catheter-free during the 24
hours of pH testing.

Barium esophagography use of barium with

radiographic studies to diagnose mechanical
and motility disorders. This test is rarely
useful in diagnosing GERD.

ESOPHAGEAL DIVERTICULUM
An esophageal diverticulum is an outpouching of the
esophageal wall, usually in the cervical posterior
side, secondary to an obstructive or inflammatory
process.
Pathophysiology and Etiology
Zenker's diverticulum protrusion of
pharyngeal mucosa at the
pharyngoesophageal junction between the
interior pharyngeal constrictor and
cricopharyngeal muscle.
Mid or distal esophageal diverticula may
develop above strictures or may be
secondary to motility disorders.

Clinical Manifestations
Zenker's Diverticulum
Difficulty in swallowing, fullness in neck,
throat discomfort, a feeling that food stops
before it reaches the stomach, and
regurgitation of undigested food
Belching, gurgling, or nocturnal coughing
brought about by diverticulum becoming
filled with food or liquid, which is
regurgitated and may irritate the trachea

Halitosis and foul taste in mouth caused by

food decomposing in a pouch (diverticulum)

Weight loss due to nutritional depletion

GERONTOLOGIC ALERT
Hoarseness, asthma, and pneumonitis may be
the only signs of esophageal diverticula in
elderly patients.
Mid or Distal Esophageal Diverticula
Generally no symptoms.
Diagnostic Evaluation
Barium esophagogram outlines
diverticulum.
Endoscopy is not indicated and may be
dangerous due to the possibility of rupture.