GI

GI
• ESOPHAGUS
• STOMACH
• SMALL/LARGE BOWEL
• APPENDIX, PERITONEUM
•
ESOPHAGUS
Congenital Anomalies
• Achalasia
• Hiatal Hernia
• Diverticula
• Laceration
• Varices
• Reflux
• Barretts
• Esophagitis
• Neoplasm: Benign, Sq. Cell Ca., Adenoca.
 ANATOMY
• 25 cm.
• UES/LES
• Mucosa/Submucosa/Muscularis/Adventitia*
Inf. Thyroid Arts.

R. Bronch. Art.

Thoracic. Aor.

Variations:
Inf, Phrenic
Celiac
Splenic
Left Gastric Art.
Short Gast.
 DEFINITIONS
• Heartburn (GERD/Reflux)
• Dysphagia
• Hematemesis
• Esophagospasm (Achalasia)
 CONGENITAL ANOMALIES
• ECTOPIC TISSUE (gastric, sebaceous, pancreatic)
• Atresia/Fistula/Stenosis/”Webs”
• Schiatzki “Ring” in lower esophagus
MOST
COMMON
 MOTOR DISORDERS
• Achalasia
• Hiatal Hernia (sliding [95%],
paraesophageal)
• “ZENKER” diverticulum
• Esophagophrenic diverticulum
• Mallory-Weiss tear
 ACHALASIA
• “Failure to relax”
– Aperistalsis
– Incomplete relaxation of the LES
– Increased LES tone
• INCREASE: Gastrin, serotonin, acetylcholine,
Prostaglandin F2α, motulin, Substance P, histamine,
pancreatic polypeptide
• DECREASE: N.O., VIP
– Progressive dysphagia starting in teens
– Mostly UNCERTAIN etiology
 HIATAL HERNIA
• Diaphragmatic muscular defect
• WIDENING of the space which the lower
esophagus passes through
• IN ALL cases, STOMACH above
diaphragm
• Usually associated with reflux
• Very common Increases with age
• Ulceration, bleeding, perforation,
strangulation
 DIVERTICULA
•ZENKER (HIGH)
•TRACTION (MID)
•EPIPHRENIC (LOW)
•TRUE vs. FALSE?
DIVERTICULUM
 LACERATION
• Tears are LONGITUDINAL (lower esophagus)
• Usually secondary to severe VOMITING

• Usually in ALCOHOLICS
• Usually MUCOSAL tears
• By convention, they are all called:

MALLORY-WEISS
 VARICES
• THREE common areas of portal/caval anastomoses

–Esophageal
– Umbilical
– Hemorrhoidal
• 100% related to portal hypertension
• Found in 90% of cirrhotics
• MASSIVE, SUDDEN, FATAL hemorrhage is the most
feared consequence
VARICES
VARICES
 ESOPHAGITIS
• GERD/Reflux Barrett’s
• Barrett’s
• Chemical
• Infectious
 REFLUX/GERD
• DECREASED LES tone
• Hiatal Hernia
• Slowed reflux clearing
• Delayed gastric emptying
• REDUCED reparative ability of gastric
mucosa
 REFLUX/GERD
• Inflammatory Cells
–Eosinophils
–Neutrophils
–Lymphocytes
• Basal zone hyperplasia
• Lamina Propria papillae elongated
and congested, due to regeneration
REFLUX/GERD
 BARRETT’S
ESOPHAGUS
• Can be defined as intestinal metaplasia of a normally
SQUAMOUS esophageal mucosa. The presence of
GOBLET CELLS in the esophageal mucosa is
DIAGNOSTIC.
• SINGLE most common RISK FACTOR for esophageal
adenocarcinoma
• 10% of GERD patients get it
• “BREACHED” G-E junction
 BARRETT’S
ESOPHAGUS
 BARRETT’S
ESOPHAGUS
• INTESTINALIZED (GASTRICIZED) mucosa is AT RISK
for glandular dysplasia.
• Searching for dysplasia when BARRETT’s is present
is of utmost importance
• MOST/ALL adenocarcinomas arising in the
esophagus arise from previously existing
BARRETT’s
 ESOPHAGITIS
• CHEMICAL
– LYE (suicide attempts) with strictures
– Alcohol
– Extremely HOT drinks
– CHEMO (often harmful to ALL high turnover
mucosas)
• INFECTIOUS
– HSV, CMV, Fungal (especially CANDIDA)
ESOPHAGITIS
ESOPHAGITIS
 TUMORS
• BENIGN
• MALIGNANT
–Squamous cell carcinoma
–Adenocarcinoma
 BENIGN TUMORS
• LEIOMYOMAS
• FIBROVASCULAR
POLYPS
• CONDYLOMAS (HPV)
• LIPOMAS
• “GRANULATION”
TISSUE
(PSEUDOTUMOR)
 SQUAMOUS
CARCINOMA
• Nitrites/Nitrosamines
• Betel
• Fungi in food (nitrosamines)
• Tobacco
• Alcohol
• Esophagitis?
 SQUAMOUS
CARCINOMA
• DYSPLASIAIN-SITUINFILTRATION
 ADENOCARCINOMA
• BARRETT’s
• BARRETT’s
• BARRETT’s
• BARRETT’s
• BARRETT’s
• BARRETT’s
• BARRETT’s
• (heterotopic gastric or submucosal glands)
ADENOCARCINOMA
 STOMACH
NORMAL: Anat., Histo, Physio.
PATHOLOGY
CONGENITAL
GASTRITIS
PEPTIC ULCER
“HYPERTROPHIC” GASTRITIS
VARICES
TUMORS
BENIGN
ADENOCARCINOMA
OTHERS
 ANATOMY
Cardia (esoph), Fundus (diaph), Body (acid),
Antrum, Pylorus
Greater/Lesser Curvatures
1500-3000 ml
Rugae
INNERVATION: VAGUS, Sympathetic
VEINS: Portal
Blood Supply: RG, LG, RGE(O), LGE(O), SG, ALL 3
branches of the celiac, no matter what the
variations may be.
 CELLS

MUCOUS: MUCUS, PEPSINOGEN II

CHIEF: PEPSINOGEN I, II
PARIETAL: ACID
ENTEROENDOCRINE: HISTAMINE,
SOMATOSTATIN, ENDOTHELIN
 PHYSIOLOGY PHASES
(HCl Secretion)
CEPHALIC (VAGAL)
GASTRIC (STRETCH)
INTESTINAL (DUOD)
 ACID PROTECTION
MUCUS
HCO3-
EPITHELIAL BARRIERS
BLOOD FLOW
PROSTAGLANDIN E, I
 CONGENITAL
• ECTOPIC PANCREAS (ectopic pancreas tissue 
stomach), very common
• ECTOPIC GASTRIC (ectopic gastric tissue 
pancreas), not rare
• Diaphragmatic HERNIA Failure of diaphragm to
close, not rare
• PULMONARY SEQUESTER (rare) (foregut anomaly)
• …..and the #1 congenital gastric disease ?????
PYLORIC STENOSIS
• CONGENITAL: (1/500), Neonatal
obstruction symptoms, pyloric
splitting curative
• ACQUIRED: Secondary to extensive
scarring such as advanced peptic
ulcer disease
 GASTRITIS
• ACUTE
• CHRONIC
• AUTOIMMUNE
• OTHER
– EOSINOPHILIC
– ALLERGIC
– LYMPHOCYTIC
– GRANULOMATOUS
– GVH
 GASTRITIS
• ACUTE, HEMORRHAGIC
• (NSAIDs), particularly aspirin
• Excessive alcohol consumption
• Heavy smoking
• CHEMO
• Uremia
• Salmonella, CMV
• Severe stress (e.g., trauma, burns, surgery)
• Ischemia and shock
• Suicidal attempts, as with acids and alkali
• Gastric irradiation or freezing
• Mechanical (e.g., nasogastric intubation)
• Distal gastrectomy
 GASTRITIS
• ACUTE, HEMORRHAGIC
• HISTOLOGY: Erosion, Hemorrage,
NEUTROPHILS
 GASTRITIS
• CHRONIC, NO EROSIONS, NO HEMORRHAGE

•
Chronic infection by H. pylori
• Immunologic (autoimmune), e.g., PA
• Toxic, as with alcohol and cigarette smoking
• Postsurgical, reflux of bile
• Motor and mechanical, including obstruction, bezoars (luminal
concretions), and gastric atony
• Radiation
• Granulomatous conditions (e.g., Crohn disease)
• GVH, uremia
 GASTRITIS
• CHRONIC, NO EROSIONS, NO HEMORRHAGE
• Perhaps some neutrophils
• Lymphocytes, lymphoid follicles
• REGENERATIVE CHANGES
– METAPLASIA, intestinal
– ATROPHY, mucosal hypoplasia, “thinning”
– DYS-PLASIA
 GASTRITIS
• AUTOIMMUNE (10%)
• ANTIBODIES AGAINST
–acid producing enzyme H+
–K+ -ATPase
–gastrin receptor
–and intrinsic factor
 GASTRITIS
• OTHER
– EOSINOPHILIC, middle aged women
– ALLERGIC, children (also eosinophils)
– LYMPHOCYTIC, T-Cells, body, DIFFUSE
– GRANULOMATOUS, Crohn’s, other granulomas
– GVH, in bone marrow transplants
 “PEPTIC” ULCERS
• “PEPTIC” implies acid cause/aggravation
• ULCER vs. EROSION (muscularis mucosa intact)
• MUCSUBMUCMUSCULARISSEROSA
• Chronic, solitary (usually), adults
• 80% caused by H. pylori
• 100% caused by H. pylori in
duodenum
• NSAIDS
“STRESS”
 Helicobacter pylori
• Causes 80% of gastric peptic ulcers
• Causes 100% of duodenal peptic ulcers
• Causes chronic gastritis
• Causes gastric carcinomas
• Causes MALT lymphomas
 “PEPTIC” ULCERS
• Gnawing, burning, aching pain, epigastric
• Fe deficiency anemia
• Acute hemorrhage
• Penetration, perforation:
– Pain in BACK
– Pain in CHEST
– Pain in LUQ

• NOT felt to develop into malignancy

• Bleeding “PEPTIC” ULCERS
– Occurs in 15% to 20% of patients
– Most frequent complication
– May be life-threatening
– Accounts for 25% of ulcer deaths
– May be the first indication of an ulcer

• Perforation
– Occurs in about 5% of patients
– Accounts for two thirds of ulcer deaths
– Rarely, is the first indication of an ulcer
• Obstruction from edema or scarring
– Occurs in about 2% of patients
– Most often due to pyloric channel ulcers
– May also occur with duodenal ulcers
– Causes incapacitating, crampy abdominal pain
– Rarely, may lead to total obstruction with intractable vomiting
 “ACUTE” ULCERS
• NSAIDS
• “STRESS” ULCERS
– ENDOGENOUS STEROIDS
• SHOCK
• BURNS
• MASSIVE TRAUMA
• Intracranial trauma, Intracranial surgery
• SEPSIS
– EXOGENOUS STEROIDS
• CUSHING ULCER
 “ACUTE” ULCERS
• Usually small (<1cm), superficial, MULTIPLE
 GASTRIC DILATATION
• PYLORIC STENOSIS
• PERITONITIS ( pyloric stenosis)
• 1.5-3.0 liters NORMAL
• 10 liters can be present
• ACUTE RUPTURE is associated with
a HIGH immediate mortality rate
 BEZOARS
• PHYTO-bezoar (plant material)
• TRICHO-bezoar (hairball)
• NON-food material in PSYCH patients
– pins
– nails
– razor blades
– coins
– gloves
– leather wallets
“HYPERTROPHIC”* GASTROPATHY
RUGAL PROMINENCE (cerebriform)
NO INFLAMMATION
HYPERPLASIA of MUCOSA
 “HYPERTROPHIC” GASTROPATHY
• Inaccurate name “hypertrophic gastritis”
• Ménétrier disease, resulting from profound hyperplasia
of the surface mucous cells with accompanying
glandular atrophy, ass. w. CMV, H. Pylori, ↑TGF-α
• Hypertrophic-hypersecretory gastropathy, associated
with hyperplasia of the parietal and chief cells within
gastric glands (normal gastrin)

• Gastric gland hyperplasia secondary to excessive

gastrin secretion, in the setting of a gastrinoma
(Zollinger-Ellison syndrome)
 GASTRIC “VARICES”
• SAME SETTING AND ETIOLOGY AS
ESOPHAGEAL VARICES, i.e., PORTAL
HYPERTENSION
• NOT AS COMMON AS ESOPHAGEAL VARICES
• MAY LOOK LIKE PROMINENT RUGAE
• IF A PATIENT HAS GASTRIC VARICES, HE ALSO
PROBABLY HAS ESOPHAGEAL, (but probably
not vice versa)
 GASTRIC
• BENIGN:
TUMORS
*
– “POLYPS ” (HYPERPLASTIC vs. ADENOMATOUS)
– LEIOMYOMAS (Same gross and micro as smooth muscle)
– LIPOMAS (Same gross and micro as adipose tissue)
• MALIGNANT
– (ADENO)-Carcinoma
– LYMPHOMA
• POTENTIALLY MALIGNANT
– G.I.S.T. (Gastro-Intestinal “Stromal” Tumor)
– CARCINOID (NEUROENDOCRINE)
BENIGN TUMORS
BEBNIBGNB

MUCOSA
(POLYPS)
---HYPERPLASTIC
---Fundic
---Peutz-Jaeger
---Juvenile

---
ADENOMATOUS

MUSCLE
FAT
MALIG. TUMORS
BEBNIBGNB

MUCOSA
LYMPHS

(MUSCLE)
(FAT)
 WHO GASTRIC NEOPLASMS
• Epithelial Tumors: Adenomatous polyps,
Adenocarcinoma (papillary, tubular,
mucinous, signet ring, adenosquamous,
unclassified), Small cell, Carcinoid
(neuroendocrine)
• Nonepithelial Tumors: Leiomyo(sarc)oma,
Schwannoma, GIST, Granular Cell Tumor,
Kaposi sarcoma
• Malignant Lymphomas:
 ADENOCARCINOMA
• H. pylori associated, MASSIVELY!!!
• Japan, Chile, Costa Rica, Colombia,
China, Portugal, Russia, and Bulgaria
• M>>F
• Socioeconomically related*
 ADENOCARCINOMA
RISK FACTORS
• H. pylori
• H. pylori
• H. Pylori
• Nitrites, smoked meats, pickled, salted, chili
peppers, socioeconomic, tobacco
• Chronic gastritis, Barrett’s, adenomas
• Family history
ADENOCARCINOMA
GROWTH PATTERNS
ADENOCARCINOMA
GROWTH PATTERNS
PAPILLARY
TUBULAR
MUCINOUS
SIGNET RING
ADENOSQUAMOUS
• Can behave and/or look benign or malignant
G.I.S.T. TUMORS
• Usually look like smooth muscle, i.e., “stroma”, “spindly”
• Are usually POSITIVE for

c-KIT (CD117), i.e., express this antigen on immunochemical staining, the tumor cells are derived from the interstitial cells of Cajal, a “neural” type of cell, similar
to the neural plexi found in the intestines.
 SMALL/LARGE INTESTINE
• NORMAL: Anat., Vasc., Mucosa, Endocr., Immune,
Neuromuscular.
• PATHOLOGY:
– CONGENITAL
– ENTEROCOLITIS: DIARRHEA, INFECTIOUS, OTHER
– MALABSORPTION: INTRALUMINAL, CELL SURFACE, INTRACELL.
– (I)IBD: CROHN DISEASE and ULCERATIVE COLITIS
– VASCULAR: ISCHEMIC, ANGIODYSPLASIA, HEMORRHAGIC
– DIVERTICULOSIS/-ITIS
– OBSTRUCTION: MECHANICAL, PARALYTIC (ILEUS) (PSEUDO)
– TUMORS: BENIGN, MALIGNANT, EPITHELIAL, STROMAL
 ANATOMY
• SI = 6 meters (100% intraP, except for duodenum), LI = 1.5 meters (50%
retroP)
• Mucosa, submucosa, muscularis, serosa/adv.

2πr x L = ?
 BLOOD SUPPLY
• SI: SMA Jejunal, Ileal
• LI: SMA, IMA Ileocolic, R, M, L, colic, Sup. Rect
• RECTUM: Superior, Middle, Inferior

• SMA has anastomoses with CELIAC

(pancreatoduodenal), IMA (marginal)
 MUCOSA
• SI: ABSORPTIVE, MUCUS, PANETH (apical granules)
– VILLI
• LI: MUCUS, ABSORPTIVE, ENTEROENDOCRINE (basal
granules)
– CRYPTS (like stomach), NOT villi
 ENTEROENDOCRINE
• SECRETORY PEPTIDES
• Endocrine, Paracrine, Neurocrine
• Chemical messengers
• Regulate digestive functions
• Serotonin, somatostatin, motilin,
cholecystokinin, gastric inhibitory polypeptide,
neurotensin, vasoactive inhibitory peptide (VIP),
neuropeptides (generic), enteroglucagon
 IMMUNE SYSTEM
• MALT

• PEYER PATCHES, mucosa, submucosa, 1˚, 2 ˚

• IgGAMDE
 NEUROMUSCULAR
• AUTONOMIC ( VAGUS, Symp.)-----extrinsic
• INTRINSIC (gut has it’s own brain)
–Meissner (submucosa)
– Auerbach (between circular and longitudinal)
 CONGENITAL
• DUPLICATION
• MALROTATION
• OMPHALOCELE
• GASTROSCHISIS
• ATRESIA/STENOSIS SPECTRUM
• MECKEL (terminal ileum, “vitelline” duct)
• AGANGLIONIC MEGACOLON
(HIRSCHSPRUNG DISEASE)
 ENTEROCOLITIS
• DEFINITION of diarrhea: INCREASE in MASS,
FLUIDITY, and/or FREQUENCY
• DIARRHEA is merely a SYMPTOM: 1) SECRETORY, 2)
OSMOTIC, 3) EXUDATIVE, 4) MALABSORPTION, 5)
MOTILITY
– INFECTIOUS (Viral, Bacterial, Parasitic)
– NECROTIZING
– COLLAGENOUS
– LYMPHOCYTIC
– AIDS
– After BMT
– DRUG INDUCED
– RADIATION
– “SOLITARY” RECTAL ULCER
 SECRETORY DIARRHEA
• Viral damage to mucosal epithelium
• Entero-toxins, bacterial
• Tumors secreting GI hormones
• Excessive laxatives
 OSMOTIC DIARRHEA
• Disaccharidase deficiencies
• Bowel preps
• Antacids, e.g., MgSO4
 EXUDATIVE DIARRHEA
• BACTERIAL DAMAGE to GI MUCOSA
• IBD
• TYPHLITIS (immunosuppression
colitis)
MALABSORPTION DIARRHEA
• INTRALUMINAL
• MUCOSAL CELL SURFACE
• MUCOSAL CELL FUNCTION
• LYMPHATIC OBSTRUCTION
• REDUCED FUNCTIONING BOWEL
SURFACE AREA
 MOTILITY DIARRHEA
• DECREASED TRANSIT TIME
– Reduced gut length
– Neural, hyperthyroid, diabetic
– Carcinoid syndrome
• INCREASED TRANSIT TIME
– Diverticula
– Blind loops
– Bacterial overgrowth
 INFECTIOUS enterocolitis
• VIRAL
– Rotavirus (69%), Calciviruses, Norwalk-like, Sapporo-
like, Enteric adenoviruses, Astroviruses
• BACTERIAL
– E. coli, Salmonella, Shigella, Campylobacter, Yersinia, Vibrio,
Clostridium difficile, Clostridium perfringens, TB
– Bacterial “overgrowth”
• PARASITIC
– Ascaris, Strongyloides, Necator, Enterobius, Tricuris
– Diphyllobothrium, Taenia, Hymenolepsis
– Amebiasis (Entamoeba histolytica)
– Giardia
 VIRAL enterocolitis
• Rotavirus most common, by far
– Selectively infects and destroys
mature enterocytes in the small
intestine
– Crypts spared
• Most have a 3-5 day course
• Person to person, food, water
 BACTERIAL enterocolitis
• Ingestion of bacterial toxins
– Staph
– Vibrio
– Clostridium
• Ingestion of bacteria which produce toxins
– Montezuma’s revenge (traveller’s diarrhea), E.coli
• Infection by enteroinvasive bacteria
– Enteroinvasive E. coli (EIEC)
– Shigella
– Clostridium difficile
 E. coli
• Toxin, invasion, many subtypes
• Food, water, person-to-person
• Usually watery, some hemorrhagic
• INFANTS often, in epidemics
 SALMONELLA
Food, not hemorrhagic

SHIGELLA
(person-to-person, invasive,
i.e., often hemorrhagic)
 CAMPLYOBACTER
• Toxins, Invasion
• Food spread
YERSINIA (enterocolitica)
• Food
• Invasion
• LYMPHOID REACTION
 VIBRIO cholerae
• Water, fish, person-to-person
• Cholera epidemics
• NO invasion (watery)
• ENTEROTOXIN
 CLOSTRIDIUM DIFFICILE
• CYTOTOXIN (lab test readily available)
• NOSOCOMIAL
• PSEUDOMEMBRANOUS (ANTIBIOTIC
ASSOCIATED) COLITIS
 BACTERIAL OVERGROWTH
SYNDROME
• One of the main reasons why “normal” gut flora
is NOT usually pathogenic, is because, they are
constantly cleared by a NORMAL transit time.
• BLIND LOOPS
• DIVERTICULA
• OBSTRUCTION
• Bowel PARALYSIS
 PARASITES
• NEMATODES (ROUNDWORMS)
– Ascaris, Strongyloides, Hookworms (Necator &
Anklyostoma), Enterobius, Trichuris
• CESTODES (TAPEWORMS)
– FISH (DIPHYLLOBOTHRIUM latum)
– PORK (TAENIA solium)
– DWARF (HYMENOLEPSIS nana)
• PROTOZOANS: AMOEBA (ENTAMOEBA
histolytica), Giardia lamblia
ENTAMOEBA HISTOLYTICA
GIARDIA LAMBLIA
•
MISC. COLITIS (OTHER)
NECROTIZING ENTEROCOLITIS (neonate) (Cause unclear)
• COLLAGENOUS (Cause unclear)
• LYMPHOCYTIC (Cause unclear)
• AIDS
• GVHD after BMT, as in stomach
• DRUGS (NSAIDS, etc., etc., etc.)
• RADIATION, CHEMO
• NEUTROPENIC (TYPHLITIS), (cecal, caecitis)
• “DIVERSION” (like overgrowth)
• “SOLITARY” RECTAL ULCER (anterior, motor dysfunction)
 MALABSORPTION
• INTRALUMINAL
• BRUSH BORDER (microvilli)
• (TRANS)EPITHELIAL
• OTHER
– REDUCED MUCOSAL AREA: Celiac, Crohns
– LYMPHATIC OBSTRUCTION: Lymphoma, TB
– INFECTION
– IATROGENIC: Surgical
 INTRALUMINAL
• PANCREATIC
• DEFECTIVE/REDUCED BILE
• BACTERIAL OVERGROWTH
 BRUSH BORDER
• DISACCHARIDASE DEFICIENCY
• BRUSH BORDER DAMAGE, e.g., by bacteria
 (Trans)EPITHELIAL
• ABETALIPOPROTEINEMIA
• BILE ACID TRANSPORTATION DEFECTS
 CELIAC DISEASE
• Also called SPRUE
• Also called NON-tropical SPRUE
• Also called GLUTEN-SENSITIVE ENTEROPATHY
– Sensitivity to GLUTEN, a wheat protein, gliadin
– Immobilizes T-cells
– Also in oat, barley, rye
– Progressive mucosal “atrophy”, i.e. villous flattening
– Relieved by gluten withdrawal
CELIAC DISEASE
 “TROPICAL” SPRUE
• Epidemic forms
• NOT related to gluten, cause UN-
known
• RECOVERY with antibiotics
 WHIPPLE’s DISEASE
• DISTENDED MACROPHAGES in the LAMINA
PROPRIA
• PAS positive
• ROD SHAPED BACILLI
WHIPPLE’s DISEASE
DISACCHARIDASE DEFICIENCY
• LACTASE by far MOST COMMON
• ACQUIRED, NOT CONGENITAL
• LACTOSE GLUCOSE + GALACTOSE
• LACTOSE (fermented)XXXXXXXXX
• OSMOTIC DIARRHEA
 ABETALIPOPROTEINEMIA
• Autosomal recessive
• Rare
• Inability to make chylomicrons from
FFAs and MONOGLYCERIDES
• Infant failure to thrive, diarrhea,
steatorrhea
 (I) IBD
• CROHN DISEASE (granulomatous colitis)
• ULCERATIVE COLITIS
 (I) IBD
• COMMON FEATURES
–IDIOPATHIC
–DEVELOPED COUNTRIES
–COLONIC INFLAMMATION
–SIMILAR Rx
–BOTH have increased CANCER RISK
 (I) IBD DIFFERENCES
• CROHN (CD)
– TRANSMURAL, THICK WALL
– NOT LIMITED to COLON
– GRANULOMAS
– FISTULAE COMMON
– TERMINAL ILEUM OFTEN
– SKIP AREAS
– “CRYPT” ABSCESSES NOT COMMON
– NO PSEUDOPOLYPS
– MALABSORPTION
• ULCERATIVE (UC)
– MUCOSAL, THICK MUCOSA
– LIMITED to COLON
– NO GRANULOMAS
– FISTULAE RARE
– TERMINAL ILEUM NEVER
– NO SKIP AREAS
– “CRYPT” ABSCESSES COMMON
– PSEUDOPOLYPS
– NO MALABSORPTION
CROHN vs. UC
UC or CD?
 VASCULAR DISEASES
• ISCHEMIA/INFARCTION
• ANGIO-”DYSPLASIA”*
• HEMORRHOIDS
 ISCHEMIA/INFARCTION
• HEMORRHAGE is the main HALLMARK of
ischemic bowel disease
– ARTERIAL THROMBUS
– ARTERIAL EMBOLISM
– VENOUS THROMBUS
– CHF, SHOCK
– INFILTRATIVE, MECHANICAL

MUCOSAL TRANSMURAL
 ANGIODYSPLASIA
• NOT really “dysplasia”
• NOT neoplastic
• TWISTED, DILATED SUBMUCOSAL VESSELS, can
rupture!
• Common X-ray finding
 HEMORRHOIDS
• INCREASED INTRABDOMINAL PRESSURE
• i.e., VALSALVA
• INTERNAL vs. EXTERNAL
 DIVERTICULOSIS/-ITIS
• FULL THICKNESS BOWEL OUTPOCKETING
• Assoc. w.:
– INCREASED LUMINAL PRESSURE, ↑transit
time
– AGE
– LR (decreased liquidity)
– Decreased dietary FIBER
– Weakening of wall
 DIVERTICULOSIS/-IT IS
(CLINICAL)
• IMPACTION
• INFLAMMATION (“appendicitis” syndrome)
• PERFORATION Peritonitis, local, diffuse
• BLEED, silently, even fatally
• OBSTRUCT
• EXTREMELY EXTREMELY COMMON

• NOT assoc. w. neoplasm, but mimic carcinomas

clinically, radiologically, surgically, and grossly!
 Formation of colonic diverticuli

• The most commonly known colonic diverticuli are pseudo

diverticuli – composed of only mucosa on the luminal side and
serosa externally. Why are these called “pseudo” or false?
• Diverticuli resemble hernias of the colonic wall in that they occur @
sites of entry of mucosal arteries as they pass through the
muscularis – this represents a weak spot that leads to a
diverticulum if the individual generates high colonic intraluminal
pressure (low fiber diet)
DIVERTICULOSIS
DIVERTICULITIS
DIVERTICULITIS
 OBSTRUCTION
• ANATOMY
– ADHESIONS (post-surgical)
– IMPACTION
– HERNIAS
– VOLVULUS
– INTUSSUSCEPTION
– TUMORS
– INFLAMMATION, such as IBD (Crohn) or divertics
– STRICTURES/ATRESIAS
– STONES, FECALITHS, FOREIGN BODIES
– CONGENITAL BANDS, MECOMIUM, INPERF. ANUS
OBSTRUCTION
 OBSTRUCTION
• PHYSIOLOGY
– ILEUS, esp. postsurgical
– INFARCTION
– MOTILITY DISEASES, esp., HIRSCHSPRUNG DISEASE
 TUMORS
• NON-NEOPLASTIC
• EPITHELIAL
• MESENCHYMAL (STROMAL)
• LYMPHOID
• BENIGN
• MALIGNANT
 POLYPS
• ANY mucosal bulging, blebbing, or bump

• HYPERPLASTIC (NON-NEOPLASTIC)
• HAMARTOMATOUS (NON-NEOPLASTIC)

• ADENOMATOUS (TRUE NEOPLASM, and regarded

by many as “potentially” PRE-MALIGNANT as well)

• SESSILE vs. PEDUNCULATED

• TUBULAR vs. VILLOUS
POLYPS
PEDUNCULATED vs VILLOUS vs SESSILE
 BENIGN vs. MALIGNANT
• Usual, atypia, pleo-, hyper-, mitoses, etc.
• Stalk invasion!!!
HPERPLASTIC POLYP
ADENOMATOUS POLYP (TUBULAR)
ADENOMATOUS POLYP (VILLOUS)
 “FAMILIAL” NEOPLASMS
• 1) POLYPOSIS (NON-NEOPLASTIC,
hamartomatous)
• 2) POLYPOSIS (NEOPLASTIC, i.e.,
cancer risk)
• 3) HNPCC: (Hereditary Non
Polyposis Colorectal Cancer)
 CANCER GENETICS
• Loss of APC gene
• Mutation of K-RAS
• Loss of SMADs (regulate transcription)
• Loss of p53
• Activation of TELOMERASE
CANCER RISK FACTORS

• Family history
• Age (rare <50)
• LOW fiber, HIGH meat, LONG
transit time, refined carbs
 PATHOGENESIS
• From existing ADENOMATOUS POLYPS
• DE-NOVO

• DYSPLASIAINFILTRATIONMETASTASIS
 GROWTH PATTERNS
• POLYPOID
• ANNULAR, CONSTRICTING
• DIFFUSE
PAPILLARY
TUBULAR
MUCINOUS
SIGNET RING
ADENOSQUAMOUS
Tumor Stage Histologic Features of the Neoplasm
Tis Carcinoma in situ (high-grade dysplasia) or intramucosal
carcinoma (lamina propria invasion)

T1 Tumor breaches the musc. muc. invades into submucosa

T2 Extending into the muscularis propria but not penetrating
through it
T3 Penetrating through the muscularis propria into subserosa

T4 Tumor directly invades other organs or structures

Nx Regional lymph nodes cannot be assessed

N0 No regional lymph node metastasis
N1 Metastasis in 1 to 3 lymph nodes
N2 Metastasis in 4 or more lymph nodes
Mx Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
 OTHER TUMORS
• CARCINOID, with or without syndrome
• LYMPHOMA (MALTOMAS, B-Cell)
• LEIOMYOMA/-SARCOMA
• LIPOMA/-SARCOMA
ANAL CANAL CARCINOMAS

• MORE LIKELY TO BE SQUAMOUS, or

“basaloid”
• WORSE IN PROGNOSIS
• HPV RELATED
A
P
P
E
N
D
I
X
 ANATOMY
• Junction of 3 tenia coli, variable in location
• All 4 layers, true serosa
• Thickest layer is submucosal lymphoid tissue

• APPENDICITIS (ACUTE)
• MUCOCELE
• MUCUS CYSTADENOMA
• MUCUS CYSTADENOCARCINOMA
 ACUTE APPENDICITIS
• GENERALLY, a disease of YOUNGER people
• OBSTRUCTION by FECALITH the classic cause but
fecaliths present only about half the time
• EARLY APPENDICITIS: NEUTROPHILSMucosa,
submucosa
• NEED NEUTROPHILS in the MUSCULARIS
to confirm the DIAGNOSIS
• 25% normal rate, usually
• Perforationperitonitis the rule, if no surgery
ACUTE APPENDICITIS
 Mucus “TUMORS”
• Mucocele (common)
• Mucinous Cystadenoma (rather rare)
• Mucinous Cystadenocarcinoma (rare)
 MUCOCELE
• COMMON CYST on APPENDIX filled with
MUCIN
• Can RUPTURE to become:
PSEUDOMYXOMA PERITONEII
(Jelly Belly)
MUCINOUS CYSTADENO(CARCINO)MA
ADENOMA CARCINOMA
 PERITONEUM
• Visceral, Parietal: all lined by mesothelium
• Peritonitis, acute:
– Appendicitis, local or with rupture
– Peptic ulcer, local or ruptured
– Cholecystitis, local or ruptured
– Diverticulitis, local or with rupture
– Salpingitis gonococcal or chlamydial, retrograde
or perforated
– Ruptured bowel due to any reason
– Perforating abdominal wall injuries
 PERITONITIS
• E. coli
• STREP
• S. aureus
• ENTEROCOCCUS
PERITONITIS, outcomes:
• Complete RESOLUTION
• Walled off ABSCESS

•ADHESIONS
SCLEROSING RETROPERITONITIS
• Unknown cause (autoimmune?)
• Generalized retroperitoneal fibrosis,
progressive hydronephrosis
 TUMORS
• MESOTHELIOMAS (solitary nodules or
diffuse constricting growth pattern, also
asbestos caused)
• METASTATIC, usually diffuse, often
looking very much like pseudomyxoma
peritoneii, but containing tumor cells,
usually adenocarcinoma