Alexander C.

Florentino, RMT, MD, DPSP

Small and Large intestines

Appendix
 Outline
• Small intestine – Inflammatory
– Congenital bowel disease
disorders – Vascular diseases
– Infections • Large intestine – Polyps – colon and
– Vascular diseases rectum
– Congenital
– Malabsorption disorders – Malignant tumors
– Mechanical – Infections • Appendix
obstruction – Diverticular disease – Appendicitis
– Neoplasms – Neoplasms
SMALL INTESTINE
Atresia
Stenosis
Meckel diverticulum
Meconium ileus

CONGENITAL DISORDERS
 Atresia
• Complete occlusion of the
intestinal lumen, may manifest
as:
– Thin intraluminal diaphragm
– Blind proximal and distal sacs
joined by a cord
– Disconnected blind ends
 Stenosis
• Incomplete stricture  narrows
the lumen, but does not occlude
• Usually symptomatic in infancy
 Atresia and stenosis
• Diagnosed on the basis of:
1. Persistent vomiting of bile-containing fluid within the first day
of life
2. Meconium is not passed
3. Obstructed intestine is dilated and filled with fluid (xray)

* Surgical correction is usually successful

 Meckel diverticulum
• Caused by persistence of vitelline duct
• Outpouching of the gut on the antimesenteric border of the ileum, 60-100cm
from the ileocecal valve (adults)
• “RULE OF 2”:
– 2% of the population
– Present within 2ft (85cm) from the ileocecal valve
– Approximately 2 inches (5cm) long
– M:F = 2:1
– Symptomatic by age 2

• Most common and most clinically significant congenital anomaly of the small
intestine
 Meckel diverticulum
• True diverticulum
• Most are asymptomatic
• If symptomatic, about ½ has ectopic
gastric, duodenal, pancreatic,
biliary, or colonic tissue

• Complications:
– Hemorrhage
– Perforation
– Obstruction
– Diverticulitis
 Meconium ileus
• Accumulation of tenacious
meconium in the small intestine
– Neonatal intestinal obstruction in
cystic fibrosis

• In half of patients, it is
complicated by
– Volvulus
– Perforation with meconium
peritonitis
– Intestinal atresia
INFECTIONS OF THE
SMALL INTESTINE
 Bacterial diarrhea
• Most significant factor in infectious diarrhea is increased
intestinal secretion
– Stimulated by bacterial toxins and enteric hormones
• Agents:
– Toxigenic organisms
• V. cholera, some E. coli strains
– Adherent or invasive bacteria
• Shigella, Salmonella, some E. coli strains, Yersinia, and Campylobacter
 Viral gastroenteritis
• Most common causes:
• ROTAVIRUS
– Common cause of infantile diarrhea
– Hospitalized children <2y/o
– Injury to surface epithelium of duodenum (for up to 2 months)

• NORWALK VIRUS
– 1/3 of viral gastroenteritis epidemics in US
– Targets upper small intestine
– Causes patchy mucosal lesions and malabsorption
– Vomiting and diarrhea  resolve w/in 2 days
Decreased intestinal blood flow can lead to ISCHEMIC BOWEL DISEASE

VASCULAR DISEASES
 Acute intestinal ischemia
ARTERIAL OCCLUSION
• Occlusion of the superior mesenteric artery (SMA) is the most
common cause
• Infarct may be segmental or may lead to gangrene of entire SI
• Less commonly, caused by vasculitis w/c involves small arteries
• Other causes: volvulus, intussusception, incarceration in
hernial sac
 Acute intestinal ischemia
NONOCCLUSIVE INTESTINAL ISCHEMIA
• May be extensive
• Seen in hypoxic patients w/ reduced cardiac output sec. to
shock
– Hemorrhage
– Sepsis
– AMI
 Acute intestinal ischemia
THROMBOSIS OF MESENTERIC VEINS
• Causes:
– Hypercoagulable state
– Stasis
– Inflammation (pylephlebitis)
• Almost all affect superior mesenteric vein
 Acute intestinal ischemia

• Infarcted bowel is edematous and

diffusely purple
• Sharp demarcation between
infarcted and normal bowel
– Venous occlusion has diffuse appearance
• Extensive hemorrhage in mucosa and
submucosa
– Prominent in venous occlusion
• Irregular white sloughs on mucosa
• Thin, distended walls
• Cloudy serosa covered by
 Acute intestinal ischemia
• Adynamic ileus – bowel proximal to the lesion is dilated and
filled with fluid

• If px survives episode of hypoperfusion

– Bowel may be completely repaired OR
– May heal with granulation tissue and fibrosis  stricture formation
 Acute intestinal ischemia
• Abrupt onset of abdominal pain
• Bloody diarrhea, hematemesis, shock
• Perforation is frequent
• Occlusion of SMA  extensive infarction  resection of entire
SI
 Chronic intestinal ischemia
• Atherosclerotic narrowing of major splanchnic arteries
• Intestinal (abdominal) angina – Intermittent abdominal pain
– Pain begins w/in 30mins after eating and lasts for a few hrs

• May promote fibrosis and stricture formation  obstruction

• Malabsoprtion due to stasis and bacterial overgrowth

• Submucosa is thickened and fibrotic with granulation tissue,

may involve muscular layer
Clinical conditions in which important nutrients are inadequately absorbed by the Gastrointestinal tract

MALABSORPTION
• Only absorption from the small intestine, mainly the proximal
portion, is clinically important

• Normal intestinal absorption, characterized by:

1. Luminal phase
2. Intestinal phase
• LUMINAL PHASE
– Processes occur within lumen of SI
– Pancreatic enzymes and bile acids  secreted in duodenal lumen

• INTESTINAL PHASE
– Processes that occur in cells and transport channels
 Luminal phase malabsorption
• Interruption of the normal continuity of the distal stomach and
duodenum – i.e. gastroduodenal surgery
• Pancreatic dysfunction – chronic pancreatitis, cancer, cystic
fibrosis
• Deficient or ineffective bile salts, causes:
1. Impaired excretion of bile – liver disease
2. Bacterial overgrowth – blind-loop syndrome, multiple diverticula,
muscular/neurogenic defects
• Defective GI motility causes deconjugation of bile salts by excess bacterial
flora  cannot form micelles  cannot be absorbed
 Intestinal phase malabsorption
• Reflects specific enzyme defects or impaired transport

PATHOGENESIS:
• Microvilli – binds disaccharidases and oligopeptidases
– Disaccharidases – essential for sugar absorption  only
monosaccharides can be absorbed by intestinal epithelial cells
– Abnormal function:
• Primary – disaccharidase deficiency
• Secondary – damage to villi (celiac disease/sprue)
 Intestinal phase malabsorption
PATHOGENESIS:
• Absorptive area – Severe diminution of small bowel surface
area
1. Small bowel resection (short bowel syndrome)
2. Gastrocolic fistula – SI is bypassed
3. Mucosal damage – celiac disease, tropical sprue, Whipple dse
 Intestinal phase malabsorption
PATHOGENESIS:
• Metabolic function of the absorptive cells – monoglycerides
and FFAs are reassembled into TG and coated with apoproteins
 form chylomicrons and lipoproteins
– Abetalipoproteinemia – absorptive cells cannot synthesize the
apoprotein required for the assembly of lipoproteins and
chylomicrons
– Nonspecific damage – celiac dse, tropical sprue, Whipple dse,
hyperacidity due to gastrinoma
 Intestinal phase malabsorption
PATHOGENESIS:
• Transport – impaired transport through conduits like blood
capillaries and lymphatic vessels
– Whipple dse, intestinal lymphomas, congenital lymphangiectasia
 Clinical features
• Specific or isolated malabsorption
– Identifiable molecular defect that causes malabsorption of a single
nutrient
• Disaccharidase deficiency – i.e. Lactase deficiency
• Deficiency of gastric intrinsic factor – vitamin B12 malabsorption 
pernicious anemia
– Generalized malabsorption – several or all nutrient classes 
malnutrition
 Lactase deficiency
• Intolerance to milk products
• Abdominal distention, flatulence, and diarrhea
• Injury to intestinal mucosa  acquired lactase deficiency
 Celiac disease
• Aka celiac sprue, gluten-sensitive enteropathy
• Characterized by:
1. Generalized malabsorption
2. Small intestinal mucosal lesions
3. Prompt clinical and histopathologic response to the withdrawal of
gluten-containing foods from the diet
• M:F = 1:1.3
• Dx during childhood – seen after introducing cereals into the
diet
 PATHOGENESIS (Celiac disease)
• Cereals (wheat, barley, rye flour), and Gliadin (alcohol soluble
fraction of gluten)  active dse
• Genetics: 90% of px w/ celiac dse carry HLA-B8, HLA DQ2 and
DQ8
• Immunologic factors:
– Characterized by:
• damage to epithelial cells
• marked increase in CD8+ T lymphocytes in w/in epithelium and plasma cells
in lamina propria
– Diagnostic HALLMARK of celiac dse  serum IgA antibodies to gluten
 PATHOGENESIS (Celiac disease)
• Association with dermatitis
herpetiformis
– Vesicular skin dse – affects extensor
surfaces and exposed parts of the body
– IgA deposits in BM and autoantibodies
to tissue transglutaminase

• Malabsorption also involves

– Reduce intestinal mucosal surface
(blunting of villi and microvilli)
– Impaired intracellular metabolism
 PATHOLOGY (Celiac dse)
• Flat mucosa
• Blunting or total disappearance of villi
• Damaged mucosal surface epithelial cells with numerous
intraepithelial lymphocytes (T cells)
• Increased plasma cells and lymphocytes in lamina propria (not
in deeper layers)
• Usually occur in duodenum and proximal jejunum
 Clinical features
• Char.: generalized malabsorption
• Manifested in older children and adults – growth retardation in
children
• Dx: Test for IgA antigliadin and antitissue transglutaminase
antibodies
• Late complications:
– Ulcerative jejunitis
– Small bowel T-cell lymphoma
– Other GI malignancies
 WHIPPLE DISEASE
• Malabsorption – most prominent feature
• Male, 30-40 y/o
• Systemic dse:
– Fever, increased skin pigmentation, anemia, lymphadenopathy,
arthritis, pericarditis, pleurisy, endocarditis, CNS involvement
 WHIPPLE DISEASE
• Mucosal infiltration by macrophages packed with small, rod-
shaped bacilli.
• Tropheryma whippelii – causative agent, actinomycete
• Macrophages exhibit decreased ability to degrade intracellular
microorganisms
• Tx: antibiotics
 WHIPPLE DISEASE

• Thickened, edematous bowel wall

• Enlarged mesenteric lymph nodes
• Flat and thick villi
• Lamina propria is extensively infiltrated
with large foamy macrophages – stain
(+) for PAS  glycoprotein granules
– Granules  engorged lysosomes with bacilli
in various stages of degeneration
Can be caused by:
1. Luminal mass
2. Intrinsic lesion of the bowel wall
3. Extrinsic compression

MECHANICAL OBSTRUCTION
 Intussusception

• A segment of bowel (intussusceptum)

protrudes distally into a surrounding
outer portion (intussuscipiens)
• Occurs in infants and young children 
Cause: unknown
• In adults, caused by Meckel’s
diverticulum or tumor
• May become infarcted
 Volvulus

• Segment of a gut twists on its

mesentery, kinking the bowel and
usually interrupting its blood supply
 Cause of an acute abdomen
• Segment distal to volvulus 
ischemic necrosis
• Often indicates an underlying
congenital abnormality
 Hernias
• Loops of small bowel 
incarcerate in inguinal/femoral
hernia
– Luminal obstruction
– Compromised vascular supply
<5% of GI tumors arise in the small intestine

NEOPLASMS
BENIGN
 Adenomas
• Resemble those of the colon
– Tubular, villous, tubulovillous
• Villous adenoma is rare in SI – usually in duodenum
(periampullary region); may undergo malignant transformation
 Peutz-Jeghers syndrome
• Autosomal dominant hereditary disorder
• Characterized by:
– intestinal hamartomatous polyps – occur mostly in proximal SI
– mucocutaneous melanin pigmentation – face, buccal mucosa, hands,
feet, perianal and genital areas; usually fade at puberty (except
buccal)
• Associated with inactivating mutations of a gene (LKB1) on
chromosome 19p
– Increased risk for cancers of the breast, pancreas, testis, ovary
 Peutz-Jeghers syndrome

• Hamartomas
• Branching networks of smooth
muscle fibers continuous with
the muscularis mucosae that
support glandular epithelium
 Gastrointestinal stromal tumors (GIST)
• Occur mostly in jejunum
• Intramural mass covered by
intact mucosa
• Behave more aggressively than
their gastric counterparts
(benign)
Uncommon in small intestine

MALIGNANT
 Adenocarcinoma
• Minute proportion of all GI tumors
• But account for half of all malignant small bowel tumors
• Mostly in duodenum and jejunum
• Middle-age; male predominance
• Crohn disease of SI is a risk factor
• FAP, HNPCC/Lynch syndrome, celiac disease
 Adenocarcinoma
• Polypoid, ulcerative, annular, stenosing
• Originate from crypt epithelium  resemble colorectal cancers
• By the time px becomes symptomatic
– Most have metastasized to local lymph nodes
– Overall 5-year survival rate - <20%
 Neuroendocrine tumor (carcinoid tumor)
• All considered MALIGNANT; with LOW metastatic potential
• 20% of all small intestinal malignancies
• Sites of origin;
1. Appendix – most common
2. Rectum
• #1&2 – small, rarely aggressive
3. Ileum – often multiple, more aggressive

• Associated with MEN syndromes, usually MEN type 1

 Neuroendocrine tumor (carcinoid tumor)
• Submucosal nodules covered by
intact mucosa
– May be polypoid, intramural or
annular
– May invade muscularis and
penetrate serosa
– Metastasize first to regional lymph
nodes; then hematogenous  liver
mets
 Neuroendocrine tumor (carcinoid tumor)
• Microscopically:
– Nests, cords, rosettes of uniform,
small, round cells
– Nuclei: regular
– Mitoses: rare
– Cytoplasm: abundant, eosinophilic
 Carcinoid syndrome
• Occur in px with extensive hepatic metastases
• Classic symptoms:
– Diarrhea – most distressing symptom
– Episodic flushing
– Bronchospasm
– Cyanosis
– Telangiectasia
– Skin lesions
 Metastatic tumors
• MOST COMMON MALIGNANT TUMORS IN THE SMALL
INTESTINE ARE METASTASES FROM OTHER SITES
• Spread by direct extension
• Lung, FGT organs, and skin (melanomas) – most frequent
primary site of small intestinal metastases
LARGE INTESTINE
Hirschsprung disease
Anorectal malformations

CONGENITAL DISORDERS
 Hirschsprung disease (congenital megacolon)

• Dilation of the colon

• Congenital absence of ganglion cells in
rectal wall
– Aganglionic segment always starts at the
rectum
– Permanently contracted – absent relaxation
stimuli  proximal bowel becomes dilated
• Incidence: 10x increase in Down
syndrome
 Hirschsprung disease (congenital megacolon)
• Constricted spastic segment –
aganglionic zone
• Proximal bowel is dilated
• Definitive diagnosis: ABSENCE OF
GANGLION CELLS IN A RECTAL
BIOPSY specimen
• Neural hyperplasia
 Hirschsprung disease (congenital megacolon)
• MOST COMMON CAUSE OF CONGENITAL INTESTINAL
OBSTRUCTION
• Clinical signs:
– Delayed passage of meconium
– Vomiting in first few days
• Most serious complication: enterocolitis
• Tx: surgical removal
 Anorectal malformations
• Result from arrested development of the caudal region of the
gut in the first 6 months
• Include anorectal agenesis/stenosis, imperforate anus
• Fistulas may occur between bladder, urethra, vagina, skin
Principal infections: TB and amebiasis

INFECTIONS
 Pseudomembranous colitis
• Generic term for an inflammatory disease of the colon,
characterized by exudative plaques on the mucosa
• Clostridium difficile – usually the offending organism
– Also implicated in neonatal necrotizing enterocolitis (NEC)
– Associated with antibiotic therapy
– Not invasive; produces toxins  damage the colonic mucosa
 Pathology

• Rectosigmoid region – raised yellowish

plaques up to 2cm in diameter, adhere
to underlying mucosa
• Intervening mucosa – congested,
edematous
• Pseudomebrane – consists of debris of
necrotic epithelial cells, mucus, fibrin,
and neutrophils

• Always accompanied by diarrhea

 Neonatal necrotizing enterocolitis (NEC)
• One of the most common
acquired surgical emergencies in
newborns
• Common in premature infants
• Ischemia  bacterial
colonization (C. difficile)
• Can cause perforation
Diverticulosis
Diverticulitis

DIVERTICULAR DISEASE
 Diverticulosis
• Acquired herniation of mucosa and submucosa through the
muscular layer of colon
– Pseudodiverticula
• Sigmoid colon – 95% of cases
• Most appear in parallel rows between the mesenteric and
lateral taeniae
• Flask-like structure – extends from lumen through the muscle
layers
• Episodic abdominal pain, alternating constipation and diarrhea
 Diverticulitis
• Irritation caused by retained fecal material
• Inflammation of wall of diverticulum
• Most common symptoms:
– Persistent lower abdominal pain
– Fever
– Changes in bowel habit
– Leukocytosis
Crohn disease
Ulcerative colitis

INFLAMMATORY
BOWEL DISEASE
 Crohn disease
• Most common sites involved – terminal ileum, ileocecal valve,
and cecum
• Cause: unknown
• Adolescents or young adults
• M:F = 1:1.6
• Multiple, separate, sharply delineated areas of disease SKIP
LESIONS (characteristic)
 Crohn disease
Two major characteristics:
1. Inflammation involves ALL LAYERS of the
bowel wall  Transmural inflammatory
disease
2. Discontinuous involvement of the
intestine – alternating normal and
inflamed tissue

• Macroscopic patterns:
1. Ileum and cecum – 50%
2. Small intestine only – 15%
3. Colon only – 20%
4. Anorectal region – 15%
 Crohn disease
• Earliest lesion – aphthous ulcer/s  coalesce into elongated,
serpentine ulcers along the axis of the bowel
• Sparing of interspersed mucosa  COBBLESTONE
APPEARANCE
• Fissures may lead to fistula form’n
• Bowel wall – thick and rubbery
– Transmural edema, inflammation, submucosal fibrosis, muscularis
propria hypertrophy  stricture form’n
– Mesenteric fat extends around serosal surface – creeping fat
 Crohn disease

• Abundant neutrophils  damage

crypt epithelium  crypt abscesses
• Repeated cycles of crypt destruction
and regeneration  Mucosal
architecture distortion
• Noncaseating granulomas –
HALLMARK OF CROHN

• Intestinal obstruction and fistulas -

most common intestinal
complication
 Clinical manifestation
• Intermittent mild diarrhea, fever and abdominal pain
• Iron deficiency anemia
• Fibrosing strictures
• Fistula formation
• Extra-intestinal manifestation: uveitis, migratory polyarthritis,
sacroiliitis, ankylosing spondylitis, erythema nodosum,
clubbing of fingertips

• Increased risk for adenocarcinoma

 Ulcerative colitis
• Limited to colon and rectum
• Extra-intestinal manifestation:
– migratory polyarthritis
– Sacroiliitis
– ankylosing spondylitis
– Uveitis
– skin lesions
– Pericholangitis
– primary sclerosing cholangitis
 Ulcerative colitis
• always involves the rectum
• extends proximally in a continuous fashion to involve part or all of the
colon
– Pancolitis – entire colon
– Left-sided disease – up to transverse colon only
 Ulcerative colitis
• broad-based ulcers  abrupt transition
between diseased and uninvolved colon
• Isolated islands of regenerating mucosa
often bulge into the lumen to create
pseudopolyps
– tips of these polyps may fuse to create
mucosal bridges
• Toxic megacolon – damage of muscularis
propria  neuromuscular function
disturbance
 Ulcerative colitis

• Chronic dse  mucosal

atrophy
• Inflammatory process is
diffuse and generally limited to
the mucosa and superficial
submucosa
• Granulomas are not present
 Ulcerative colitis
• Bloody diarrhea, with stringy, mucoid material, lower
abdominal pain, and cramps that are temporarily relieved by
defecation

• Increased risk for adenocarcinoma

VASCULAR DISEASES
 Ischemic injury
• Chronic segmental disease is the rule
– Extensive infarction is uncommon (unlike SI)
• Most cases due to atherosclerosis
• >50y/o
• Watershed areas (i.e. splenic flexure) –
most vulnerable areas
 Ischemic injury
• Do not require immediate surgical intervention
• Multiple ulcers, hemorrhagic nodular lesions or
pseudomembranes
• Histo: mucosal ulceration, crypt abscesses, edema,
hemorrhage

• Manifest as abdominal pain, rectal bleeding, change in bowel

habits
 Angiodysplasia (vascular ectasia)

• Localized AV malformation, mainly in cecum

and ascending colon
– Lower GI bleeding
• 60y/o; younger pxs may present lesions in
rectum, stomach, small bowel
• Surgical removal: curative
• Histo: submucosal veins and capillaries are
tortuous, thin walled, dilated
 Hemorrhoids

• Dilated venous channels of the

hemorrhoidal plexuses
• External - located below the anorectal line
• Internal - dilation of the superior
hemorrhoidal plexus within the distal
rectum
• Histo: thin-walled, dilated, submucosal
vessels that protrude beneath the anal or
rectal mucosa
• Pain and rectal bleeding
POLYPS
 Adenomatous polyps
• >65 y/o, M:F=1.4:1
• Rectosigmoid region - 50% of cases
• Classified as:
1. Tubular
2. Villous
3. Tubulovillous
 Tubular adenoma

• Smooth surface, with a stalk

(pedunculated)
• Histo: closely packed epithelial tubules,
excessively branched, embedded in a
fibrovascular stroma
• If >2cm, 35% are cancerous
 Villous adenoma
• Rectosigmoid region
• Large, broad-based, elevated
• Shaggy, cauliflower-like surface
• Most are >2cm
• Histo: thin, tall, finger-like processes –
resemble villi of the SI
• Contain foci of carcinoma more often
 Tubulovillous adenoma
• Have both tubular and villous features
• Intermediate in size, distribution, and risk for invasive
carcinoma
 Pathogenesis
• Neoplastic alteration of crypt epithelial homeostasis
1. Diminished apoptosis
2. persistent cell replication
3. Failure to mature and differentiate as the epithelial cells migrate
toward the surface of the crypts

• Size is the most important characteristic that correlates with

risk of malignancy.
 Hyperplastic polyps

• 60-70 y/o
• these lesions are without malignant
potential.
• Most commonly found in left colon
• <5mm
• Histo: composed of mature goblet
and absorptive cells.
• crowding creates the serrated
surface architecture that is the
morphologic hallmark of these
lesions
 Juvenile polyps
• focal malformations of the mucosal epithelium and lamina
propria
• sporadic or syndromic
– Sporadic – solitary, retention polyp
– Syndromic – autosomal dominant; 3-100 hamartomatous polyps 
colectomy
• children less than 5 years of age
• Majority in rectum  rectal bleeding
 Juvenile polyps

• <3cm
• Pedunculated, smooth-surfaced
• Char.: cystic spaces at sectioning
• Histo: cysts are dilated glands filled
with mucin and inflammatory
debris
 Inflammatory polyps
• Elevated nodules of inflamed regenerating epithelium
• Commonly found in Crohn and UC
• Histo: distorted and inflamed mucosal glands, intermixed with
granulation tissue
MALIGNANT TUMORS
 Colorectal adenocarcinoma
• Most common cause of cancer deaths that are not directly
attributable to tobacco use (western countries)
• Peak – 60-70y/o
• M>F
• Dietary factors: low intake of unabsorbable vegetable fiber,
high intake of refined carbohydrates and fat (i.e. fastfood)
 Pathogenesis
• Multistep carcinogenesis
• APC/β-catenin pathway – associated with WNT and classic
adenocarcinoma sequence
• Microsatellite instability pathway – defects in DNA mismatch
repair
 Molecular genetics
• APC gene – germline mutations in APC (adenomatous
polyposis coli) lead to FAP
– Normal APC is a negative regulator of β-catenin
– Mutant APC  β-catenin accumulation in nucleus  activate
proliferation genes (cyclin D1, MYC)
– APC is mutated in most SPORADIC colorectal cancers

• Ras oncogene – activation occur early in tubular adenomas

 Molecular genetics
• “Deletion in Colon Cancer” (DCC) gene – tumor suppressor gene,
located in chromosome 18
– Missing in colon Ca

• p53 gene – adenoma to carcinoma, a late event in carcinogenesis

• MisMatch Repair (MMR) genes –

– Impaired DNA repair  deficient correction of spontaneous replication
errors, especially in microsatellites  MICROSATELLITE INSTABILITY
– Occur in HNPCC (Lynch) syndrome (hereditary), MLH1 gene inactivation
(sporadic)
 Risk factors
• Increasing age – single most important risk factor
• Chronic inflammatory bowel dse
• prior colorectal cancer
• Diet
• genetic factors
 Pathology
• Polypoid, ulcerating or infiltrative, may be annular and
constrictive
– Polypoid – more common in right colon, esp. cecum
– Annular – more common in distal colon
• Spread by direct extension or vascular/lymphatic invasion
– Venous invasion  liver metastasis
• Prognosis: degree of tumor invasion to the bowel wall
– NOT size and histopathologic characteristics
 Clinical features
• Most common sign – occult blood in feces
• Obstructive symptoms – left side tumor – narrow lumen, more
solid feces  manifested as changes in bowel habits and
abdominal pain
– may perforate early  peritonitis
• Right side tumor (cecum) – lumen is large, fecal contents liquid
 tumors can grow to a large size w/o symptoms
– May cause iron-deficiency anemia

• TX: resection
 Hereditary nonpolyposis colon cancer
• HNPCC or Warthin-Lynch syndrome
• Autosomal dominant; 3-5% of all colorectal cancers
• Characterized by:
1. Young age at onset
2. Few adenomas (hence, nonpolyposis)
3. High frequency of Ca proximal to splenic flexure
4. Multiple synchronous or metachronous Ca
5. Extracolonic cancers – endometrial, ovarian, stomach, SI,
hepatobiliary tract, renal pelvis and ureters (TCC)
 Pathology
• Germline mutation followed by somatic mutation (LOH) in DNA
mismatch repair genes
– hMSH2 on chromosome 2p
– hMLH1 on chromosome 3p
• Microsatellite instability
• High frequency of mucinous signet ring cell and solid
(medullary) carcinomas
ANAL CANAL
 Anal canal

• Upper third: columnar rectal epithelium 

adenocarcinoma
• Middle third: transitional epithelium 
basaloid carcinoma
• Lower third: stratified squamous
epithelium  squamous cell carcinoma
– Frequently associated with HPV; precursor is
condyloma accuminatum
Normal true diverticulum of the cecum

APPENDIX
 Acute appendicitis
• M>F
• Commonly confused clinically with acute salpingitis, ectopic
pregnancy, Meckel’s etc
• Progressive increase in intraluminal pressure  venous
outflow compromise
• 50-80% - cause by fecalith
 Morphology
• Early: congestion, perivascular neutrophilic infiltrate
• Histologic hallmark: neutrophilic infiltration of the muscularis
propria
• Acute suppurative appendicitis – focal abscesses w/in the wall
• Acute gangrenous appendicitis - large areas of hemorrhagic
ulceration and gangrenous necrosis that extends to the serosa
– Followed by rupture  peritonitis
 Clinical features
• Periumbilical pain  RLQ pain
• Nausea, vomiting, low-grade fever, mildly elevated WBC count
• McBurney’s sign – deep tenderness at McBurney’s point
 Tumors of the appendix

• Most common tumor: carcinoid tumor

– Frequently at distal tip
• Adenomas and adenocarcinoma
• Mucocele – dilated appendix filled with mucin
– May be due to obstruction OR
– A consequence of mucinous
cystadenoma/cystadenocarcinoma  invasion may
cause intraperitoneal seeding  pseudomyxoma
peritonei
PERITONEUM
 Peritonitis
• Usually caused by intestinal organisms  acute abdomen with
severe abdominal pain and tenderness
• Nausea, vomiting, high fever
• Perforation – most common cause of bacterial peritonitis
 Neoplasms
• Mesotheliomas – most common primary
peritoneal tumor
– Associated with exposure to asbestos

• Primary peritoneal carcinoma – tumor masses

involving the omentum and peritoneum

• Metastatic carcinoma – most common

malignancy of the peritoneum
– Ovarian, gastric, pancreatic
(natapos din…)

SALAMAT!