GASTROINTESTINAL

TRACT
Anny Setijo Rahaju
 O r al C a v i t y
▶ ULCERATIVE AND INFLAMMATORY LESIONS
▶ LEUKOPLAKIA

▶ CANCER OF THE ORAL CAVITYAND TONGUE

▶ SALIVARY GLAND DISEASES
Sialadenitis
Salivary gland Tumor
ULCERATIVE AND INFLAMMATORY LESIONS
Aphthous Ulcers
(Canker Sores)
- common, small (<5 mm),
painful, shallow ulcers,
rounded, superficial erosions,
often covered with a gray-white
exudate and having an
erythematous rim
-the first 2 decades of
life triggered by stress, fever,
ingestion of certain foods, and
activation of inflammatory
bowel disease.
an autoimmune basis is
suspected.
self-limited may recur in the
same or a different location.
Acut Inflammation
-Minor inflammation of the
mouth are common due to
trauma, hot food or irritans.
-The lips and mouth are also
commonly involved as part of a
more general infection( such as
Measles)
Oral Candidiasis Herpes simplex virus
infection
-Candida albicans, found in causes a usually self-limited
30% to 40% of the population infection with vesicles (cold
-Pseudomembranous sores, fever blisters) that
candidiasis (thrush, moniliasis) typically rupture and heal but
>>fungal infection of the oral may leave latent virus in nerve
cavity diabetes mellitus, ganglia.
anemia, antibiotic or
glucocorticoid therapy,
immunodeficiency, acquired
immunodeficiency syndrome
(AIDS)
-takes the form of an adherent
white, curdlike, circumscribed
plaque anywhere within the oral
cavity
-The pseudomembrane can be
scraped off to reveal an
underlying granular
erythematous inflammatory
base.
-Histologically, composed of
fungal organisms
superficially attached to the
underlying mucosa.
-minimal ulceration - entire
mucosa
 LEUKOPLAKIA
leukoplakia refers to a whitish, well-defined mucosal patch or plaque caused by epidermal thickening
or hyperkeratosis.
(WHO) leukoplakia is a white patch or plaque that can not be scraped off and cannot be characterized
as any other disease.
3% to 25% may progress to squamous cell carcinoma.
Clinical appearance of leukoplakias : A. smooth and thin with well-demarcated borders.
B, diffuse and thick. C, irregular with a granular surface D, diffuse and corrugated.
(Courtesy of Drs. Neville, Damm, Allen, Bouquot [eds], Oral & Maxillofacial Pathology,
Philadelphia, WB Saunders, 2002.)
Salivary Gland Disease
S i a lad e niti s
➢ traumatic, viral, bacterial, or autoimmune origin.
➢ >>mucocele, resulting from blockage or rupture of a salivary

gland duct, saliva into the surrounding tissues.

➢ viral disease : mumps, paramyxovirus, influenza and
parainfluenza viruses.
➢ Bacterial sialadenitis ductal obstruction resulting from stone
formation (sialolithiasis) : Staphylococcus aureus and
Streptococcus viridans.
suppurative necrosis or even abscess formation.
➢ The dominant cause is autoimmune sialadenitis, which is almost
invariably bilateral.
Salivary Gland Tumors
▶ About 80% the parotid glands and most of the others in the submandibular glands.
▶ Males and females equally, sixth or seventh decade of life.
▶ (parotids) 70% to 80% of these tumors are benign, whereas in the submaxillary glands only half
are benign.
▶ >>> pleomorphic adenoma = a mixed tumor of salivary gland origin.
▶ >> papillary cystadenoma lymphomatosum (Warthin tumor) these two types account for
three-fourths of parotid tumors.
▶ The most malignant tumor of the salivary gland is mucoepidermoid carcinoma, which occurs
mainly in the parotids.
▶ When primary or recurrent benign tumors are present for many (10-20) years malignant
transformation a malignant mixed salivary gland tumor.
S a l i v a r y G l a n d Tum o r s
Pleomorphic Adenoma (Mixed Tumor of Salivary Glands)
- more than 90% of benign tumors of the salivary glands.
-slow-growing, well-demarcated, apparently encapsulated lesion
rarely exceeding 6 cm in greatest dimension.
-Most often arising in the superficial parotid, painless swelling
histologic examination often reveals multiple sites where the
tumor penetrates the capsule recurrences.
- about 10% of excisions are followed by recurrence.
Morphology
- histologic feature of pleomorphic adenoma is heterogeneity. -
The tumor cells form ducts, acini, tubules, strands, or sheets of
cells.
-The epithelial cells are small and dark and range from cuboidal
to spindle forms. These epithelial elements are intermingled with
a loose, often myxoid connective tissue stroma sometimes
containing islands of apparent cartilage or, rarely, bone
Warthin Tumor (Papillary Cystadenoma Lymphomatosum,
Cystadenolymphoma)
-benign tumor occurs and arise from heterotopic salivary tissue
trapped within a regional lymph node during embryogenesis.
- This tumor is generally a small, well-encapsulated, round to
ovoid mass that on transection often reveals mucin-containing
cleftlike or cystic spaces within a soft gray background.
Morphology
two characteristic features:
(1) a two-tiered epithelial layer lining the branching, cystic,
or cleftlike spaces;
(2) well-developed lymphoid tissue sometimes forming
germinal centers.
- A recurrence rate of about 10% is attributed to incomplete
excision, multicentricity, or a second primary tumor.
Malignant transformation is rare; about half of reported
cases have had prior radiation exposure
 Pleomorphic adenoma.
A, Slowly enlarging neoplasm in the
parotid gland of many years duration.
B, The bisected, sharply circumscribed,
yellow-white tumor can be seen
surrounded by normal salivary gland tissue.

Pleomorphic adenoma.
A, Low-power view showing a well-
demarcated tumor with adjacent normal
salivary gland parenchyma.
B, High-power view showing epithelial
cells as well as myoepithelial cells
found within a chondroid matrix
material.
 Histologic Classification and Approximate Incidence of
Benign and Malignant Tumors of the Salivary Glands

Benign
▶ Pleomorphic adenoma(mixed tumor)
(50%)
▶ Warthin tumor (5%–10%)
▶ Oncocytoma (1%)
▶ Other adenomas (5%–10%)
• Basal cell adenoma
• Canalicular adenoma
• Ductal papillomas
Malignant
▶ Mucoepidermoid carcinoma (15%)
▶ Adenocarcinoma (NOS) (10%)
▶ Acinic cell carcinoma (5%)
▶ Adenoid cystic carcinoma (5%)
▶ Malignant mixed tumor (3%–5%)
▶ Squamous cell carcinoma (1%)
▶ Other carcinomas (2%)
▪ NOS, not otherwise specified.

Data from Ellis GL, Auclair PL: Tumors of the Salivary Glands. Atlas of Tumor
Pathology, Third Series. Washington, DC, Armed Forces Institute of Pathology, 1996.
Eso phag u s
▪ ANATOMIC AND MOTOR DISORDERS
▪ ESOPHAGITIS - GERD

▪ BARRETT’S ESOPHAGUS

▪ ESOPHAGEAL CARCINOMA
P a tholo g y
▶ produce similar symptoms, heartburn, dysphagia, pain, and/or
hematemesis.
▶ H e a r t b u r n (retrosternal burning pain) usually reflects
regurgitation of gastric contents into the lower esophagus.
▶ D y s p h a g i a (difficulty in swallowing) is encountered both with
deranged esophageal motor function and with diseases that
narrow or obstruct the lumen.
▶ Pa i n a n d h e m a t e m e s i s are sometimes evoked by esophageal
disease, particularly by those lesions associated with
inflammation or ulceration of the esophageal mucosa.
▶ E s o p h a g e a l varices, rupture is frequently followed by massive
hematemesis (vomiting of blood)

▶ esophagoscopy, radiographic barium studies, and manometry.

 ATRESIA A N D FISTULAS
▶incompatible with life cause immediate
regurgitation when feeding is attempted, usually
discovered soon after birth.
▶A b s e n c e ( a g e n e s i s ) of the esophagus is

extremely rare
▶atresia, a segment of the esophagus is represented

by only a thin, noncanalized cord, with a proximal

blind pouch connected to the pharynx and a lower
pouch leading to the stomach.
▶fistula : connecting the lower or upper pouch with

a bronchus or the trachea.

Figure 17-1 Esophageal atresia and tracheoesophageal fistula.
A, Blind upper and lower esophageal segments.
B, Fistula between blind upper segment and trachea.
C, Blind upper segment, fistula between blind lower segment and
trachea.
D, Blind upper segment only.
E, Fistula between patent esophagus and trachea.
Type C is the most common variety.
(Adapted from Morson BC, and Dawson IMP, eds.,
Gastrointestinal Pathology. Oxford, Blackwell Scientific
Publications, 1972, p. 8.)
esophageal motor
dysfunction

F i g u r e 17-2 M a j o r c ond i ti ons a s s o c i a t e d with

e s o p h a g e a l m o t o r dysfunction.
E s o p h a g e a l Varices
▶ Dilatedtertuous vessels
▶Varices the submucosa of the distal
esophagus and proximal stomach.
▶When the varix is unruptured, the mucosa

m a y be normal, but often it is eroded and

inflamed because of its exposed position,
further weakening the tissue support of the
dilated veins
▶Massive hemorrhage
F i g u r e 17-4 Esophageal varices. A, A view of the everted esophagus and gastroesophageal junction,
showing dilated submucosal veins (varices). The blue-colored varices have collapsed in this postmortem
specimen. B, Low-power cross-section of a dilated submucosal varix that has ruptured through the
mucosa. A small amount of thrombus is present within the point of rupture. C, Hepatic venogram after
injection of dye into portal veins (PV) to show a large tortuous gastroesophageal varix (arrow) extending
superiorly from the patent main portal vein.
(C, courtesy of Dr. Emily Sedgwick, Brigham and W o m e n' s Hospital, Boston, MA.)
Esophagitis
-Inflammation of the esophageal mucosa
-Reflux Esophagitis
(Gastroesophageal Reflux Disease) GERD
Histologic :
1. Eosinophils, with or without neutrophils, in
the epithelial layer
2. Basal zone hyperplasia
3. Elongation of lamina propia papillae
S t o m a ch
Stomach
▪ GASTRITIS
▪Chronic Gastritis
▪Acute Gastritis
▪ GASTRIC ULCERATION
▪Peptic Ulcers
▪Acute Gastric Ulceration
▪ TUMORS
▪Gastric Polyps
▪Gastric Carcinoma
▪Carcinoid Tumor
▪Lymphoma
▪GIST
S tom ach
▶ Gastric disorders frequently cause clinical disease,
▶Gastric infection with Helicobacter pylori represents

the most common gastrointestinal infection.

▶Gastric disorders give rise to symptoms similar to

esophageal disorders, primarily heartburn and vague

epigastric pain.
▶With breach of the gastric mucosa and bleeding,

hematemesis or melena may ensue.

▶ Vomited blood hence has the appearance of coffee

grounds.
 Acute Gastritis
-Acute gastritis is a transient mucosal inflammatory process that
may be asymptomatic or cause variable degrees of epigastric pain,
nausea, and vomiting.
- severe cases there may be mucosal erosion, ulceration,
hemorrhage, hematemesis, melena, or, rarely, massive blood loss.
PATHOGENESIS
- The gastric lumen is strongly acidic more acidic than the blood.
- Mucin secreted by surface foveolar cells forms a thin layer of
mucus that prevents large food particles from directly touching the
epithelium.
-The mucus layer also promotes formation protects the mucosa
and has a neutral pH as a result of bicarbonate ion secretion by
surface epithelial cells.
- The rich vascular supply to the gastric mucosa delivers oxygen,
bicarbonate, and nutrients while washing away acid that has back-
diffused into the lamina propria.
- Acute or chronic gastritis can occur after disruption of any of these
protective mechanisms.
For example, reduced mucin synthesis in elderly persons is
suggested to be one factor that explains their increased susceptibility
to gastritis.
Nonsteroidal anti-inflammatory drugs (NSAIDs) cytoprotection
normally provided by prostaglandins or reduce bicarbonate
secretion, both of which increase the susceptibility of the gastric
mucosa to injury.
Chronic Gastritis
-The symptoms and signs less severe but more persistent than
those of acute gastritis.
- Nausea and upper abdominal discomfort may occur, sometimes
with vomiting, but hematemesis is uncommon.
- The most common bacillus Helicobacter pylori.
Autoimmune gastritis, the most common cause of atrophic gastritis,
represents less than 10% of cases of chronic gastritis and is the most
common form of chronic gastritis in patients without H. pylori
infection.
-Less common causes include radiation injury and chronic bile
reflux.
the presence of chronic inflammatory changes in the mucosa
leading eventually to mucosal atrophy and epithelial metaplasia.
Pathogenesis
the most important etiologic chronic infection by the bacillus H.
pylori.
- highest infection rates in developing countries.
-Most individuals with the infection also have the associated
gastritis but are asymptomatic.
Clinical Feat u r es
-few or no symptoms upper abdominal discomfort and nausea and
vomiting can occur.
-When severe parietal cell loss occurs in the setting of autoimmune
gastritis, hypochlorhydria or achlorhydria (referring to
concentrations of gastric luminal hydrochloric acid) and
hypergastrinemia are characteristically present.
-Most important is the relationship of chronic gastritis to the
development of peptic ulcer and gastric carcinoma.
-Most individuals with a peptic ulcer, whether duodenal or gastric,
have H. pylori infection.
-The long-term risk of gastric carcinoma for persons with H. pylori-
associated chronic gastritis is increased about fivefold relative to the
 A c u t e Peptic Ulceration Peptic Ulcer D i s e a s e
Focal, acute peptic injury is a well-known complication of -Peptic ulcer disease (PUD) most often is associated with H.
therapy with NSAIDs as well as severe physiologic stress. pylori infection or NSAID use.
Such lesions include :
•Stress ulcers, most commonly affecting critically ill patients Clinical Features
with shock, sepsis, or severe trauma -chronic, recurring lesions that occur most often in middle-aged
• Curling ulcers, occurring in the proximal duodenum and to older adults
associated with severe burns or trauma -A majority epigastric burning or aching pain, manifest
•Cushing ulcers, arising in the stomach, duodenum, or with complications such as iron deficiency anemia, frank
esophagus of persons with intracranial disease, have a high hemorrhage, or perforation.
incidence of perforation -The pain tends to occur 1 to 3 hours after meals during the day,
is worse at night, and is relieved by alkali or food.
PATHOGENESIS -Nausea, vomiting, bloating, and belching may be present. -
Healing may occur with or without therapy, but the tendency to
The pathogenesis of acute ulceration is complex and develop ulcers later remains.
incompletely understood
NSAID-induced ulcers :
as cyclooxygenase inhibition, which prevents prostaglandin
synthesis.
This eliminates the protective effects of prostaglandins,
which include enhanced bicarbonate secretion and increased
vascular perfusion.
- direct stimulation of vagal nuclei, which causes gastric acid
hypersecretion intracranial injury
-Systemic acidosis lowering the intracellular pH of mucosal
cells.
- Hypoxia and reduced blood flow caused by stress- induced
splanchnic vasoconstriction acute ulcer pathogenesis
Small and Large Intestines
▪ DEVELOPMENTALANOMALIES
▪Hirschprung disease : Congenital Megacolon
▪ BOWEL OBSTRUCTION
▪ VASCULAR DISORDERS

▪Ischemic Bowel Disease

▪Hemorrhoids
▪ DIARRHEAL DISEASES

▪Diarrhea and Dysentery

▪Infectious Enterocolitis
▪ IDIOPATHIC INFLAMMATORY BOWEL DISEASE
▪ Crohn's Disease
▪ Ulcerative Colitis
▪ COLONIC DIVERTICULOSIS
SMALL AND LARGE INTESTINES
▶ The small intestine and colon account for
most of the length of the gastrointestinal
tract nutrient and water transport.
▶ Perturbation of these processes can cause
malabsorption and diarrhea.
▶the small intestine and colon frequently are
involved by infectious and inflammatory
processes.
▶ the colon is the most common site of
gastrointestinal neoplasia in Western
populations.
Congenital Anomalies
In the small intestine
- Atresia or stenosis
✓ Duplication
✓ Meckel’s diverticulum
✓ Omphalocele
In the large intestine
✓ Malrotation
✓ Hirschsprung disease
 MORPHOLOGY HIRSCHSPRUNG
DISEASE
▶Most cases are limited to the rectum and sigmoid
colon, but It can involve the entire colon.
▶The aganglionic region m a y have a grossly normal

or contracted appearance, while the normally

innervated proximal colon m a y undergo
progressive dilation a s a result of the distal
obstruction
▶Diagnosis of Hirschsprung disease requires

demonstrating the absence of ganglion cells in the

affected segment.
 PATH O G E N E S IS
▶Hirschsprung disease, also known a s
c o n g e n i t a l a g a n g l i o n i c megacolon, results
when the normal migration of neural crest cells
from cecum to rectum is disrupted.
▶This produces a distal intestinal segment that

lacks both the M e i s s n e r s u b m u c o s a l p l e x u s

and t he A u e r b a c h m yen t eric p l e x u s
(“aganglionosis”).
Figure 14–19 Hirschsprung disease.
A, P r e op e ra ti v e b a r i u m e n e m a study showing constricted
rectum (bottom of the image) and dilated sigmoid colon. Ganglion
cells were absent in the rectum, but present in the sigmoid colon.
B, C o r r e s p o n d i n g intraoperative a p p e a ra n c e of the dilated
sigmoid colon.
(Courtesy of Dr. Aliya Husain, The University of Chicago, Chicago,
INTESTINAL OBSTRUCTION
▶Mechanical Obstruction
◦ Hernias, internal or external
◦ Adhesions
◦ Intussusception
◦ Volvulus
▶O t h e r L e s s F re q u e n t C o n d i t i o n s
◦ Tumors
◦ Inflammatory strictures
◦ Obstructive gallstones, fecaliths, foreign bodies
◦ Congenital stricture, atresias
◦ Congenital bands
◦ Meconium in cystic fibrosis
◦ Imperforate anus
S c h e m a t i c d e p i c t i n g the four major c a u s e s of intestinal
obstruction:
(1) Herniation of a segment in the umbilical or inguinal regions;
(2)adhesion between loops of intestine;
(3) intussusception;
(4) volvulus formation.
33
 Abdominal Hernia
▶ Any weakness or defect in the wall of the peritoneal cavity may
permit protrusion of a serosa-lined pouch of peritoneum called a
hernia sac.
▶Acquired hernias : anteriorly, the inguinal and femoral canals or

umbilicus, or at sites of surgical scars. These are of concern because

of visceral protrusion (external herniation).
▶Small bowel loops are herniated most often, but portions of omentum

or large bowel also protrude, and any of these may become

entrapped.
▶ impair venous drainage, leading to stasis and edema.
▶ permanent entrapment, or incarceration, and over time, arterial

and venous compromise, or strangulation, can result in infarction.

VASCULAR D I S O R D E R S OF
BOWEL
▶The greater portion of the gastrointestinal tract is supplied by
the celiac, superior mesenteric, and inferior mesenteric
arteries.
▶As they approach the intestinal wall, the superior and inferior

mesenteric arteries fan out to form the mesenteric arcades.

▶Interconnections between arcades, as well as collateral

supplies from the proximal celiac and distal pudendal and

iliac circulations, make it possible for the small intestine and
colon to tolerate slowly progressive loss of the blood supply
from one artery.
H e m o r rh o id s
▶Hemorrhoids affect about 5 % of the general
population.
▶Simply put, hemorrhoids are dilated anal and

perianal collateral vessels that connect the portal

and caval venous systems to relieve elevated
venous pressure within the hemorrhoid plexus.
▶Thus, although hemorrhoids are both more common

and less serious than esophageal varices, the

pathogenesis of these lesions is similar.
▶ increase intra-abdominal and venous pressures,
venous stasis of pregnancy, and portal
hypertension.
M O R P H O LO G Y
▶Collateral vessels within the inferior hemorrhoidal
plexus are located below the anorectal line and are
termed external hemorrhoi ds, while t h o s e that
result f rom dilation of the superior hemorrhoidal
plexus within the distal rectum are referred to as
internal hemorrhoi ds.
▶O n histologic examination, hemorrhoids consist of

thin-walled, dilated, submucosal vessels that protrude

beneath the anal or rectal mucosa. In their exposed
position, they are subject to trauma and tend to
become inflamed, thrombosed, and, in the course of
time, recanalized. Superficial ulceration ma y occur.
 Diarrhea
▶Diarrhea = an increase in stool mass, frequency, or fluidity, typically to volumes
greater than 200 mL per day.
▶In severe cases stool volume can exceed 14 L per day and, without fluid

resuscitation, result in death.

▶Painful, bloody, small-volume diarrhea is known as dysentery.

▶Diarrhea can be classified into four major categories:

✓ Secretory diarrhea is characterized by isotonic stool and persists during fasting.

✓ Osmotic diarrhea, such as that occurring with lactase deficiency, is due to
osmotic forces exerted by unabsorbed luminal solutes.
✓ Malabsorptive diarrhea caused by inadequate nutrient absorption is associated
with steatorrhea and is relieved by fasting.
✓ Exudative diarrhea is due to inflammatory disease and characterized by purulent,
bloody stools that continue during fasting.
In fe ctio us Enterocolitis
▶Enterocolitis can manifest with a broad range of signs and
symptoms including diarrhea, abdominal pain, urgency,
perianal discomfort, incontinence, and hemorrhage.
▶Bacterial infections, such as enterotoxigenic Escherichia coli,
frequently are responsible, but the most common pathogens
vary with age, nutrition, and host immune status, as well as
environmental influences
▶For example, epidemics of cholera are common in areas with
poor sanitation, as a result of inadequate public health
measures, or as a consequence of natural disasters (e.g., the
Haiti earthquake of 2010) or war.
▶Pediatric infectious diarrhea, which may result in severe
dehydration and metabolic acidosis, commonly is caused by
enteric viruses.
Table 15-7. M a j o r C a u s e s of
Diarrheal Illnesses
S e cr e t o r y D ia r r he a
▶ Infectious: viral damage to surface epithelium
Mal absorption
▶ Rotavirus
▶D efective intraluminal digestion
▶Norwalk virus ▶D efective m ucosal-cell absorption :
▶Enteric adenoviruses
▶ Reduced small intestinal surface area
▶Infectious: enterotoxin-mediated
▶Lymphatic obstruction
▶ Vibrio cholerae

▶Escherichia coli ▶Infectious: impaired mucosal-cell

▶ Bacillus cereus
absorption
▶ Clostridium perfringens
▶Giardia lam blia
▶Neoplastic: tumor elaboration of peptides or

serotonin
▶Excessive laxative use De r a n g e d Motility
▶Decreased intestinal retention time
O s m o t i c D ia r r he a Surgical reduction of gut length
▶Lactulose therapy (for hepatic encephalopathy, ▶Neural dysfunction, including irritable
constipation)
▶ Prescribed gut lavage for diagnostic procedures bowel syndrome
▶ Antacids ( Mg S O 4 and other magnesium salts) ▶Hyperthyroidism

▶Decreased motility (increased intestinal

Ex udative D i s e a s e s retention time)
▶ Infectious:
destruction of the epithelial layer ▶Surgical creation of a "blind" intestinal
▶Shigella spp.
▶ Salmonella spp.
loop
▶Bacterial overgrowth in the small intestine
▶ Campylobacter spp.
▶ Entamoeba histolytica
▶ Idiopathic inflammatory bowel disease
Entamoeba histolytica in colon. High-power view of the organisms. Note some
of the organisms ingesting red blood cells.

Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 24 March 2005 09:49 AM)
© 2005 Elsevier
Inflammatory Bowel Disease
▶ Inflammatory bowel disease (IBD) is a chronic condition
resulting from inappropriate mucosal immune activation.
▶Crohn disease and ulcerative colitis are idiopathic inflammatory

bowel diseases believed to result from abnormal local immune

responses against unknown microbes and/or self antigens in the
intestine.
▶Both Crohn disease and ulcerative colitis are more common in
females and frequently present during adolescence or in young
adults.
▶ This predilection is at least partly due to genetic factors,
▶ The hygiene hypothesis suggests
F i g u r e 17-43 C o m p a r i s o n of the distribution p a t t e r n s of
C r o h n d i s e a s e a n d ulcerative colitis, a s well a s the different
c o n f o r m a t i o n s of the ulcers a n d wall thickenings.
▶ Tumors of the Sma l l Intestine a n d Colon
Non-neoplastic (Benign) Polyps
▶ Hyperplastic polyps
▶ Hamartomatous polyps
• Juvenile polyps
• Peutz-Jeghers polyps Inflammatory polyps
▶ Lymphoid polyps

Neoplastic Epithelial Lesions

▶ Benign

• Adenoma *
▶ M alig nant

• Adenocarcinoma *
• Carcinoid tumor
• Anal zone carcinoma
Mes enchymal Lesions
▶ Gastrointestinalstromal tumor (GIST) (gradation from benign to malignant)
▶ Other benign lesions
• Lipoma
• Neuroma
• Angioma
▶ Kaposi sarcoma

Lymphoma
* Benign and malignant counterparts of the most common neoplasms in the intestines;
virtually all lesions are in the colon.
Figure. S c h e m a t i c of the m o r p h o l o g i c a n d molecular c h a n g e s in
the a d e n o m a - c a r c i n o m a s e q u e n c e . It i s p o s t u l a t e d t h a t l o s s of o n e
n o r m a l c o p y of the t u m o r s u p p r e s s o r g a t e k e e p e r g e n e A P C oc c u r s
early.
F i g u r e 1 4 – 3 3 Colonic a d e n o m a s .
A, Pe d u n c u l a t e d a d e n o m a ( e n d o s c o p i c v iew).
B, A d e n o m a with a velvety surface.
C, L ow - m a gn i fi c a t i on p h o t o m i c r o g ra p h of a pedunculated
tubular adenoma.
F i g u r e 17-61 C a r c i n o m a of the
cecum. The f u n g a t i n g c a r c i n o m a
projects into the l u m e n b u t h a s
n o t c a u s e d obstruction.
F i g u r e 17-62 C a r c i n o m a of the
d e s c e n d i n g colon. This
circumferential t u m o r h a s
e aped-up edges and an
ulcerated central portion. The
Figure 14–38 Colorectal carcinoma.
A, Circumferential, ulcerated rectal cancer. Note the anal mucosa at the bottom of the image.
B, Cancer of the sigmoid colon that has invaded through the muscularis propria and is present
within subserosal adipose tissue (left). Areas of chalky necrosis are present within the colon
wall
Figure 14–39 Histologic appearance of colorectal carcinoma.
A, Well-differentiated adenocarcinoma. Note the elongated, hyperchromatic nuclei.
Necrotic debris, present in the gland lumen, is typical.
B, Poorly differentiated adenocarcinoma forms a few glands but is largely composed of
infiltrating nests of tumor cells.
C, Mucinous adenocarcinoma with signet ring cells and extracellular mucin pools.
Path for colon

51
Table 1 4 – 8 AJCC T u m o r - N o d e - M e t a s t a s i s ( T N M )
Classification of Colorectal C a r c i n o m a

Tumor (T)
▶T0 = none evident
▶Tis = in situ dysplasia or intramucosal carcinoma

▶T1 = Tumor invades submucosa

▶T2 = Tumor invades into, but not through muscularis propria
▶T3 = Tumor invades through muscularis propria
▶T4 = Tumor invades adjacent organs or visceral peritoneum

Ly m p h N o d e s ( N )
▶N x = Lymphenodes cannot be assessed
▶N 0 = N o regional lymph node metastasis
▶N 1 = Metastasis in one to three regional lymph nodes
▶N 2 = Metastasis in four or more regional lymph nodes

Distant Metastases (M)

▶M X = Distant metastasis cannot be assessed
▶M 0 = No distant metastasis
▶M 1 = Distant metastasis or seeding of abdominal organs
▶The detection and diagnosis of colorectal digital rectal
examination and fecal testing for occult blood loss. Barium
enema, sigmoidoscopy, and colonoscopy require confirmatory
biopsy for diagnosis. Computed tomography and other
radiographic studies are usually used to assess metastatic spread.
▶Serum markers for disease carcinoembryonic antigen, are of
little diagnostic value, because they reach significant levels only
after the tumor has achieved considerable size and has very
probably spread.
▶The single most important prognostic indicator of colorectal

carcinoma is the extent (stage) of the tumor at the time of

diagnosis.
▶The American Joint Commission on Cancer uses the TNM

classification
The a p p e n d i x
▶a normal true diverticulum of the cecum.
▶ acute and chronic inflammation, and acute appendicitis is a relatively
common entity.
▶Other lesions, including tumors, can also occur in the appendix but are far

less common.
ACUTE APPENDICITIS
▶Acute appendicitis is most common in adolescents and young adults but

may occur in any age group.

▶males are affected slightly more often than females.

▶ Despite the prevalence of acute appendicitis, the diagnosis can be

difficult to confirm preoperatively, and the condition may be confused

with mesenteric lymphadenitis (often secondary to unrecognized Yersinia
infection or viral enterocolitis), acute salpingitis, ectopic pregnancy,
mittelschmerz (pain associated with ovulation), and Meckel diverticulitis.
PATHOGENESIS
▶Acute appendicitis is thought to be initiated by
progressive increases in intraluminal pressure that
compromises venous outflow.
▶In 5 0 % to 8 0 % of cases, acute appendicitis is

associated with overt luminal obstruction, usually by

a small, stonelike m a s s of stool, or fecalith, or, l e s s
c o m m o n l y, a g a l l s t o n e , tumor, or m a s s of worms.
▶Ischemic injury and stasis of luminal contents, which

favor bacterial proliferation, trigger inflammatory

responses including tissue edema and neutrophilic
infiltration of the lumen, muscular wall, and
periappendiceal soft tissues.
Clinical F e a t u r e s
▶Typically, early acute appendicitis produces periumbilical
pain that ultimately localizes to the right lower quadrant,
followed by nausea, vomiting, low-grade fever, and a
mildly elevated peripheral white cell count.
▶ A classic physical finding is McBurney’s sign, deep

tenderness noted at a location two thirds of the distance

from the umbilicus to the right anterior superior iliac spine
(McBurney’s point).
▶These signs and symptoms often are absent, however,

creating difficulty in clinical diagnosis.

W h a t is the m o s t c o m m o n abdominal
e m e r g e n c y s u r g e r y in t h e U . S ?

58
TER I M A
KASIH