This document provides an overview of the gastrointestinal system, with a focus on the esophagus and stomach. It discusses the anatomy, blood supply, congenital anomalies, motor disorders like achalasia and hiatal hernia, and common pathologies for each organ. For the esophagus, it covers topics like esophagitis, Barrett's esophagus, varices, and cancers. For the stomach, it discusses gastritis, peptic ulcers, hypertrophic gastropathy, gastric varices, benign and malignant tumors, and adenocarcinoma.

1. GI

2. GI
• ESOPHAGUS
• STOMACH
• SMALL/LARGE BOWEL
• APPENDIX, PERITONEUM

3. ESOPHAGUS
• Congenital Anomalies
• Achalasia
• Hiatal Hernia
• Diverticula
• Laceration
• Varices
• Reflux
• Barretts
• Esophagitis
• Neoplasm: Benign, Sq. Cell Ca., Adenoca.

4. ANATOMY
• 25 cm.
• UES/LES
• Mucosa/Submucosa/Muscularis/Adventitia

5. Inf. Thyroid Arts.
R. Bronch. Art.
Thoracic. Aor.
Left Gastric Art.
Variations:
Inf, Phrenic
Celiac
Splenic
Short Gast.

7. DEFINITIONS
• Heartburn (GERD/Reflux)
• Dysphagia
• Hematemesis
• Esophagospasm (Achalasia)

8. CONGENITAL ANOMALIES
• ECTOPIC TISSUE (gastric, sebaceous, pancreatic)
• Atresia/Fistula/Stenosis/”Webs”
• Schiatzke “Ring”
MOST
COMMON

9. MOTOR DISORDERS
• Achalasia
• Hiatal Hernia (sliding [95%],
paraesophageal)
• “ZENKER” diverticulum
• Esophagophrenic diverticulum
• Mallory-Weiss tear

11. 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: NO, VIP
– Progressive dysphagia starting in teens
–Mostly UNCERTAIN etiology

12. 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

15. DIVERTICULA
•ZENKER (HIGH)
•TRACTION (MID)
•EPIPHRENIC (LOW)
•TRUE vs. FALSE?

16. DIVERTICULUM

17. LACERATION
• Tears are LONGITUDINAL
• Usually secondary to severe VOMITING
• Usually in ALCOHOLICS
• Usually MUCOSAL tears
• By convention, they are all called:
MALLORY-WEISS

19. 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

20. VARICES

21. VARICES

22. ESOPHAGITIS
•GERD/Reflux Barrett’s
• Barrett’s
•Chemical
•Infectious

23. REFLUX/GERD
• DECREASED LES tone
• Hiatal Hernia
• Slowed reflux clearing
• Delayed gastric emptying
• REDUCED reparative ability of gastric
mucosa

24. REFLUX/GERD
• Inflammatory Cells
–Eosinophils
–Neutrophils
–Lymphocytes
• Basal zone hyperplasia
• Lamina Propria papillae elongated
and congested

25. REFLUX/GERD

26. 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

27. BARRETT’S
ESOPHAGUS

29. 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

31. ESOPHAGITIS
• CHEMICAL
– LYE (suicide attempts) with strictures
– Alcohol
– Extremely HOT drinks
–CHEMO
• INFECTIOUS
– HSV, CMV, Fungal (especially CANDIDA)

32. ESOPHAGITIS

33. ESOPHAGITIS

34. TUMORS
• BENIGN
• MALIGNANT
–Squamous cell carcinoma
–Adenocarcinoma

35. BENIGN TUMORS
• LEIOMYOMAS
• FIBROVASCULAR
POLYPS
• CONDYLOMAS (HPV)
• LIPOMAS
• “GRANULATION”
TISSUE
(PSEUDOTUMOR)

36. SQUAMOUS
CARCINOMA
• Nitrites/Nitrosamines
• Betel
• Fungi in food
• Tobacco
• Alcohol
• Esophagitis?

37. SQUAMOUS
CARCINOMA
• DYSPLASIAIN-SITUINFILTRATION

41. ADENOCARCINOMA
• BARRETT’s
• BARRETT’s
• BARRETT’s
• BARRETT’s
• BARRETT’s
• BARRETT’s
• BARRETT’s
• (heterotopic gastric or submucal glands)

42. ADENOCARCINOMA

44. STOMACH
NORMAL: Anat., Histo, Physio.
PATHOLOGY
CONGENITAL
GASTRITIS
PEPTIC ULCER
“HYPERTROPHIC” GASTRITIS
VARICES
TUMORS
BENIGN
ADENOCARCINOMA
OTHERS

45. ANATOMY
Cardia, Fundus, Body, 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

51. CELLS
MUCOUS: MUCUS, PEPSINOGEN II
CHIEF: PEPSINOGEN I, II
PARIETAL: ACID
ENTEROENDOCRINE: HISTAMINE,
SOMATOSTATIN, ENDOTHELIN

52. PHYSIOLOGY PHASES
CEPHALIC (VAGAL)
GASTRIC (STRETCH)
INTESTINAL (DUOD)

53. ACID PROTECTION
MUCUS
HCO3-
EPITHELIAL BARRIERS
BLOOD FLOW
PROSTAGLANDIN E, I

54. 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)
• …..and the #1 congenitnal gastric disease

55. PYLORIC STENOSIS
• CONGENITAL: (1/500), Neonatal
obstruction symptoms, pyloric
splitting curative
• ACQUIRED: Secondary to extensive
scarring such as advanced peptic
ulcer disease

56. GASTRITIS
• ACUTE
• CHRONIC
• AUTOIMMUNE
• OTHER
– EOSINOPHILIC
– ALLERGIC
– LYMPHOCYTIC
–GRANULOMATOUS
–GVH

57. 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

58. GASTRITIS
• ACUTE, HEMORRHAGIC
• HISTOLOGY: Erosion, Hemorrage,
NEUTROPHILS

59. 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

60. GASTRITIS
• CHRONIC, NO EROSIONS, NO HEMORRHAGE
• Perhaps some neutrophils
• Lymphocytes, lymphoid follicles
• REGENERATIVE CHANGES
– METAPLASIA, intestinal
– ATROPHY, mucosal hypoplasia, “thinning”
– DYS-PLASIA

62. GASTRITIS
•AUTOIMMUNE (10%)
• ANTIBODIES AGAINST
–acidproducing enzyme H+
–K+ -ATPase
–gastrin receptor
–and intrinsic factor

63. 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

65. “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”

66. Helicobacter pylori
• Causes 80% of gastric peptic ulcers
• Causes 100% of duodenal peptic ulcers
• Causes chronic gastritis
• Causes gastric carcinomas
• Causes MALT lymphomas

67. “PEPTIC” ULCERS
• Gnawing, burning, aching pain
• Fe deficiency anemia
• Acute hemorrhage
• Penetration, perforation:
– Pain in BACK
– Pain in CHEST
– Pain in LUQ
•NOTfelt to develop into malignancy

68. • 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

69. “ACUTE” ULCERS
• NSAIDS
• “STRESS” ULCERS
–ENDOGENOUS STEROIDS
• SHOCK
• BURNS
• MASSIVE TRAUMA
• Intracranial trauma, Intracranial surgery
• SEPSIS
– EXOGENOUS STEROIDS
• CUSHING ULCER

70. “ACUTE” ULCERS
• Usually small (<1cm), superficial, MULTIPLE

71. GASTRIC DILATATION
• PYLORIC STENOSIS
• PERITONITIS ( pyloric stenosis)
• 1.5-3.0 liters NORMAL
• 10 liters can be present
• ACUTE RUPTURE is associated with
an immediate HIGH mortality rate

72. BEZOARS
• PHYTO-bezoar (plant material)
• TRICHO-bezoar (hairball)
• NON-food material in PSYCH patients
– pins
– nails
– razor blades
– coins
– gloves
– leather wallets

74. “HYPERTROPHIC” GASTROPATHY
RUGAL PROMINENCE (cerebriform)
NO INFLAMMATION
HYPERPLASIA of MUCOSA

75. “HYPERTROPHIC” GASTROPATHY
• Inaccurate name “hypertrophic gastritis”
• Ménétrier disease, resulting from profound hyperplasia
of the surface mucous cells with accompanying
glandular atrophy
• Hypertrophic-hypersecretory gastropathy, associated
with hyperplasia of the parietal and chief cells within
gastric glands
• Gastric gland hyperplasia secondary to excessive
gastrin secretion, in the setting of a gastrinoma
(Zollinger-Ellison syndrome)

77. GASTRIC “VARICES”
• SAME SETTING AND ETIOLOGY AS
ESOPHAGEAL VARICES, i.e., PORTAL
HYPERTENSION
• NOT AS COMMON AS ESOPHAGEAL VARICES
• MAY LOOK LIKE RUGAE
• IF A PATIENT HAS GASTRIC VARICES, HE ALSO
PROBABLY HAS ESOPHAGEAL

78. GASTRIC TUMORS
• BENIGN:
– POLYPS (HYPERPLASTIC vs. ADENOMATOUS)
– LEIOMYOMAS (Same gross and micro as sm. 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)

79. BENIGN TUMORS
BEBNIBGNB
MUCOSA
(POLYPS)
---HYPERPLASTIC
---Fundic
---Peutz-Jaeger
---Juvenile
---ADENOMATOUS
MUSCLE
FAT

80. MBAEBLNIIBGG.N BTUMORS
MUCOSA
LYMPHS
(MUSCLE)
(FAT)

81. 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:

82. ADENOCARCINOMA
• H. pylori associated, MASSIVELY!!!
• Japan, Chile, Costa Rica, Colombia,
China, Portugal, Russia, and Bulgaria
• M>>F
• Socioeconomically related

83. 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

84. ADENOCARCINOMA
GROWTH PATTERNS

85. ADENOCARCINOMA
GROWTH PATTERNS

86. PAPILLARY

87. TUBULAR

88. MUCINOUS

89. SIGNET RING

90. ADENOSQUAMOUS

91. G.I.S.T. TUMORS
• Can behave and/or look benign
or malignant
• Usually look like smooth muscle,
i.e., “stroma”
• 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.

92. 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/-IT IS
– OBSTRUCTION: MECHANICAL, PARALYTIC (ILEUS) (PSEUDO)
– TUMORS: BENIGN, MALIGNANT, EPITHELIAL, STROMAL

93. ANATOMY
• SI = 6 meters, LI = 1.5 meters
• Mucosa, submucosa, muscularis, serosa/adv.

94. 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)

95. MUCOSA
• SI: ABSORPTIVE, MUCUS, PANETH (apical granules)
– VILLI
• LI: MUCUS, ABSORPTIVE, ENTEROENDOCRINE
(basal granules)
– CRYPTS

97. ENTEROENDOCRINE
• SECRETORY PEPTIDES
• Endocrine, Paracrine, Neurocrine
• Chemical messengers
• Regulate digestive functions
• Serotonin, somatostatin, motilin,
cholecystokinin, gastric inhibitory peptide,
neurotensin, vasoactive inhibitory peptide (VIP),
neuropeptide, enteroglucagon

98. IMMUNE SYSTEM
• MALT
• PEYER PATCHES, mucosa, submucosa, 1˚, 2 ˚
• IgGAMDE

99. NEUROMUSCULAR
• AUTONOMIC (VAGUS, Symp.)-----extrinsic
• INTRINSIC
– Meissner (submucosa)
– Auerbach (between circular and longitudinal)

100. CONGENITAL
• DUPLICATION
• MALROTATION
• OMPHALOCELE
• GASTROSCHISIS
• ATRESIA/STENOSIS SPECTRUM
• MECKEL (terminal ileum, “vitelline” duct)
• AGANGLIONIC MEGACOLON
(HIRSCHSPRUNG DISEASE)

102. ENTEROCOLITIS
• DEFINITION of diarrhea: INCREASE in MASS,
FLUIDITY, FREQUENCY
• DIARRHEA: SECRETORY, OSMOTIC, EXUDATIVE,
MALABSORPTION, MOTILITY
– INFECTIOUS (Viral, Bacterial, Parasitic)
– NECROTIZING
– COLLAGENOUS
– LYMPHOCYTIC
– AIDS
– After BMT
– DRUG INDUCED
– RADIATION
– “SOLITARY” RECTAL ULCER

103. SECRETORY DIARRHEA
• Viral damage to mucosal epithelium
• Entero toxins, bacterial
• Tumors secreting GI hormones
• Excessive laxatives

104. OSMOTIC DIARRHEA
• Disaccharidase deficiencies
• Bowel preps
• Antacids, e.g., MgSO4

105. EXUDATIVE DIARRHEA
• BACTERIAL DAMAGE to GI MUCOSA
• IBD
• TYPHLITIS (immunosuppression
colitis)

106. MALABSORPTION DIARRHEA
• INTRALUMINAL
• MUCOSAL CELL SURFACE
• MUCOSAL CELL FUNCTION
• LYMPHATIC OBSTRUCTION
• REDUCED FUNCTIONING BOWEL
SURFACE AREA

107. MOTILITY DIARRHEA
• DECREASED TRANSIT TIME
– Reduced gut length
– Neural, hyperthyroid, diabetic
– Carcinoid syndrome
• INCREASED TRANSIT TIME
– Diverticula
– Blind loops
– Bacterial overgrowth

108. 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

109. 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

110. 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

111. E. coli
• Toxin, invasion, many subtypes
• Food, water, person-to-person
• Usually watery, some hemorrhagic
• INFANTS often

112. SALMONELLA
Food, not hemorrhagic
SHIGELLA
(person-to-person, invasive,
i.e., often hemorrhagic)

113. CAMPLYOBACTER
• Toxins, Invasion
• Food spread

114. YERSINIA (enterocolitica)
• Food
• Invasion
• LYMPHOID REACTION

115. VIBRIO cholerae
• Water, fish, person-to-person
• Cholera epidemics
• NO invasion (watery)
• ENTEROTOXIN

116. CLOSTRIDIUM DIFFICILE
• CYTOTOXIN (lab test readily available)
• NOSOCOMIAL
• PSEUDOMEMBRANOUS (ANTIBIOTIC
ASSOCIATED) COLITIS

117. 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

118. PARASITES
• NEMATODES (ROUNDWORMS)
– Ascaris, Strongyloides, Hookworms (Necator &
Anklyostoma), Enterobius, Trichuris
• CESTODES (TAPEWORMS)
– FISH (DIPHYLLOBOTHRIUM latum)
– PORK (TAENIA solium)
– DWARF (HYMENOLEPSIS nana)
• AMOEBA (ENTAMOEBA histolytica), Giardia
lamblia

119. ENTAMOEBA HISTOLYTICA

120. GIARDIA LAMBLIA

121. 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
• NEUTROPENIC (TYPHLITIS), (cecal)
• DIVERSION (like overgrowth)
• “SOLITARY” RECTAL ULCER (anterior, motor dysfunction)

122. MALABSORPTION
• INTRALUMINAL
• BRUSH BORDER
• (TRANS)EPITHELIAL
• OTHER
– REDUCED MUCOSAL AREA: Celiac, CD
– LYMPHATIC OBSTRUCTION: Lymphoma, TB
– INFECTION
– IATROGENIC: Surgical

123. INTRALUMINAL
• PANCREATIC
• DEFECTIVE/REDUCED BILE
• BACTERIAL OVERGROWTH

124. BRUSH BORDER
• DISACCHARIDASE DEFICIENCY
• BRUSH BORDER DAMAGE, e.g., by bacteria

125. (Trans)EPITHELIAL
• ABETALIPOPROTEINEMIA
• BILE ACID TRANSPORTATION DEFECTS

126. 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

127. CELIAC DISEASE

128. “TROPICAL” SPRUE
• Epidemic forms
• NOT related to gluten
• RECOVERY with antibiotics

129. WHIPPLE’s DISEASE
• DISTENDED MACROPHAGES in the LAMINA
PROPRIA
• PAS positive
• ROD SHAPED BACILLI

130. WHIPPLE’s DISEASE

131. DISACCHARIDASE DEFICIENCY
• LACTASE by far MOST COMMON
• ACQUIRED, NOT CONGENITAL
• LACTOSE GLUCOSE + GALACTOSE
• LACTOSE (fermented)XXXXXXXXX
• OSMOTIC DIARRHEA

132. ABETALIPOPROTEINEMIA
• Autosomal recessive
• Rare
• Inability to make chylomicrons from
FFAs and MONOGLYCERIDES
• Infant failure to thrive, diarrhea,
steatorrhea

133. (I) IBD
• CROHN DISEASE (granulomatous colitis)
• ULCERATIVE COLITIS

134. (I) IBD
• COMMON FEATURES
–IDIOPATHIC
–DEVELOPED COUNTRIES
–COLONIC INFLAMMATION
–SIMILAR Rx
–BOTH have CANCER RISK

135. (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

136. CROHN vs. UC

137. UC or CD?

138. VASCULAR DISEASES
• ISCHEMIA/INFARCTION
• ANGIO-”DYSPLASIA”*
•HEMORRHOIDS

139. ISCHEMIA/INFARCTION
• HEMORRHAGE is the main HALLMARK of
ischemic bowel disease
– ARTERIAL THROMBUS
– ARTERIAL EMBOLISM
– VENOUS THROMBUS
– CHF, SHOCK
– INFILTRATIVE, MECHANICAL
MUCOSAL TRANSMURAL

141. ANGIODYSPLASIA
• NOT really “dysplasia”
• NOT neoplastic
• TWISTED, DILATED SUBMUCOSAL VESSELS, can
rupture!
• Common X-ray finding

142. HEMORRHOIDS
• INCREASED INTRABDOMINAL PRESSURE
• i.e., VALSALVA
• INTERNAL vs. EXTERNAL

143. DIVERTICULOSIS/-ITIS
• FULL THICKNESS BOWEL
OUTPOCKETING
• Assoc. w.:
– INCREASED LUMINAL PRESSURE
–AGE
– LR
– FIBER
– Weakening of wall

144. DIVERTICULOSIS/-IT IS
(CLINICAL)
• IMPACT
• INFLAME (“appendicitis” syndrome)
• PERFORATE Peritonitis, local, diffuse
• BLEED, silently, even fatally
• OBSTRUCT
• EXTREMELY EXTREMELY COMMON
• NOT assoc w. neoplasm

145. 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)

146. DIVERTICULOSIS

147. DIVERTICULITIS

148. DIVERTICULITIS

149. 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

150. OBSTRUCTION

151. OBSTRUCTION
• PHYSIOLOGY
– ILEUS, esp. postsurgical
– INFARCTION
– MOTILITY DISEASES, esp., HIRSCHSPRUNG DISEASE

152. TUMORS
• NON-NEOPLASTIC (POLYPS)
• EPITHELIAL
• MESENCHYMAL (STROMAL)
• LYMPHOID
• BENIGN
• MALIGNANT

154. POLYPS
• ANY mucosal bulging, blebbing, or bump
•HYPERPLASTIC(NON-NEOPLASTIC)
• HAMARTOMATOUS (NON-NEOPLASTIC)
•ADENOMATOUS(TRUE NEOPLASM, and
regarded by many as PRE-MALIGNANT as well)
• SESSILE vs. PEDUNCULATED
• TUBULAR vs. VILLOUS

155. POLYPS

156. PEDUNCULATED vs VILLOUS vs SESSILE

157. BENIGN vs. MALIGNANT
• Usual, atypia, pleo-, hyper-, mitoses, etc.
• Stalk Invasion

158. HPERPLASTIC POLYP

159. ADENOMATOUS POLYP (TUBULAR)

160. ADENOMATOUS POLYP (VILLOUS)

161. “FAMILIAL” NEOPLASMS
• POLYPOSIS (NON-NEOPLASTIC,
hamartomatous)
• POLYPOSIS (NEOPLASTIC, i.e., cancer
risk)
• HNPCC: (Hereditary Non Polyposis
Colorectal Cancer)

162. CANCER GENETICS
• Loss of APC gene
• Mutation of K-RAS
• Loss of SMADs (regulate transcription)
• Loss of p53
• Activation of TELOMERASE

163. CANCER RISK FACTORS
• Family history
• Age (rare <50)
• LOW fiber, HIGH meat, LOW
transit time, refined carbs

164. PATHOGENESIS
• From existing ADENOMATOUS POLYPS
• DE-NOVO
• DYSPLASIAINFILTRATIONMETASTASIS

165. GROWTH PATTERNS
• POLYPOID
• ANNULAR, CONSTRICTING
• DIFFUSE

167. PAPILLARY

168. TUBULAR

169. MUCINOUS

170. SIGNET RING

171. ADENOSQUAMOUS

172. Tumor Stage Histologic Features of the Neoplasm
Tis Carcinoma in situ (high-grade dysplasia) or intramucosal
carcinoma (lamina propria invasion)
T1 Tumor invades 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

173. OTHER TUMORS
• CARCINOID, with or without
syndrome
• LYMPHOMA (MALTOMAS, B-Cell)
• LEIOMYOMA/-SARCOMA
• LIPOMA/-SARCOMA

174. ANAL CANAL CARCINOMAS
• MORE LIKELY TO BE SQUAMOUS, or
“basaloid”
• WORSE IN PROGNOSIS
• HPV RELATED

175. A
P
P
E
N
D
I
X

176. 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

177. 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

178. ACUTE APPENDICITIS

180. Mucus “TUMORS”
• Mucocele (common)
• Mucinous Cystadenoma (rather rare)
• Mucinous Cystadenocarcinoma (rare)

181. MUCOCELE
• COMMON CYST on APPENDIX filled with
MUCIN
• Can RUPTURE to become:
PSEUDOMYXOMA PERITONEII

183. MUCINOUS CYSTADENO(CARCINO)MA
ADENOMA CARCINOMA

184. 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
– Ruptured bowel due to any reason
– Perforating abdominal wall injuries

185. PERITONITIS
• E. coli
• STREP
• S. aureus
• ENTEROCOCCUS

186. PERITONITIS, outcomes:
• Complete RESOLUTION
• Walled off ABSCESS
• ADHESIONS

187. SCLEROSING RETROPERITONITIS
• Unknown cause (autoimmune?)
• Generalized retroperitoneal fibrosis,
progressive hydronephrosis

188. 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