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.

Left Gastric Art.

Variations:

Inf, Phrenic

Celiac

Splenic

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

• DYSPLASIAIN-SITUINFILTRATION

ADENOCARCINOMA• BARRETT’s• BARRETT’s• BARRETT’s• BARRETT’s• BARRETT’s• BARRETT’s• BARRETT’s• (heterotopic gastric or submucosal glands)

ADENOCARCINOMA

STOMACHSTOMACHNORMAL: Anat., Histo, Physio.PATHOLOGY

CONGENITALGASTRITISPEPTIC ULCER“HYPERTROPHIC” GASTRITISVARICESTUMORS

BENIGNADENOCARCINOMAOTHERS

ANATOMYANATOMYCardia (esoph), Fundus (diaph), Body (acid), Antrum, PylorusGreater/Lesser Curvatures1500-3000 mlRugaeINNERVATION: VAGUS, SympatheticVEINS: PortalBlood 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 IICHIEF: PEPSINOGEN I, IIPARIETAL: ACIDENTEROENDOCRINE: HISTAMINE, SOMATOSTATIN, ENDOTHELIN

PHYSIOLOGY PHASES(HCl Secretion)

CEPHALIC (VAGAL)

GASTRIC (STRETCH)

INTESTINAL (DUOD)

ACID PROTECTIONMUCUSHCO3-EPITHELIAL BARRIERSBLOOD FLOWPROSTAGLANDIN 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)• MUCSUBMUCMUSCULARISSEROSA• 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

“PEPTIC” ULCERS• Bleeding– 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 INFLAMMATIONHYPERPLASIA 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 TUMORS• BENIGN:

– “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)

BEBNIBGNB

BENIGN TUMORS

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

---ADENOMATOUS

MUSCLEFAT

BEBNIBGNBMALIG. TUMORS

MUCOSALYMPHS

(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*

ADENOCARCINOMARISK FACTORS

• H. pylori• H. pylori• H. Pylori• Nitrites, smoked meats, pickled, salted, chili

peppers, socioeconomic, tobacco• Chronic gastritis, Barrett’s, adenomas• Family history

ADENOCARCINOMAGROWTH PATTERNS

ADENOCARCINOMAGROWTH PATTERNS

PAPILLARY

TUBULAR

MUCINOUS

SIGNET RING

ADENOSQUAMOUS

G.I.S.T. TUMORS• Can behave and/or look benign or malignant• 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

SALMONELLAFood, 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– LR (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

• DYSPLASIAINFILTRATIONMETASTASIS

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

APPENDIX

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: NEUTROPHILSMucosa,

submucosa

• NEED NEUTROPHILS in the MUSCULARIS to confirm the DIAGNOSIS

• 25% normal rate, usually• Perforationperitonitis 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