Diseases of git

GI ESOPHAGUS STOMACH SMALL/LARGE BOWEL APPENDIX, PERITONEUM www.freelivedoctor.com

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

ANATOMY 25 cm. UES/LES Mucosa/Submucosa/Muscularis/Adventitia www.freelivedoctor.com

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

DEFINITIONS Heartburn (GERD/Reflux) ‏ Dysphagia Hematemesis Esophagospasm (Achalasia) ‏ www.freelivedoctor.com

CONGENITAL ANOMALIES ECTOPIC TISSUE (gastric, sebaceous, pancreatic) ‏ Atresia/Fistula/Stenosis/”Webs” Schiatzki “Ring” MOST COMMON www.freelivedoctor.com

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

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 www.freelivedoctor.com

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 www.freelivedoctor.com

DIVERTICULA ZENKER (HIGH) ‏ TRACTION (MID) ‏ EPIPHRENIC (LOW) ‏ TRUE vs. FALSE? www.freelivedoctor.com

DIVERTICULUM www.freelivedoctor.com

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

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 www.freelivedoctor.com

VARICES www.freelivedoctor.com

ESOPHAGITIS GERD/Reflux  Barrett’s Barrett’s Chemical Infectious www.freelivedoctor.com

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

REFLUX/GERD Inflammatory Cells Eosinophils Neutrophils Lymphocytes Basal zone hyperplasia Lamina Propria papillae elongated and congested www.freelivedoctor.com

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 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 INFECTIOUS HSV, CMV, Fungal (especially CANDIDA) ‏

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 Tobacco Alcohol Esophagitis?

SQUAMOUS CARCINOMA DYSPLASIA  IN-SITU  INFILTRATION

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

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 “ P EPTIC” 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 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 an immediate HIGH 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 • 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)

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

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. ( G astro- I ntestinal “ S tromal” T umor) CARCINOID (NEUROENDOCRINE)

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

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.

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

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

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

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

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

NEUROMUSCULAR AUTONOMIC ( VAGUS, Symp.)----- extrinsic INTRINSIC 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, FREQUENCY DIARRHEA: SECRETORY, OSMOTIC, EXUDATIVE, MALABSORPTION, 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

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

MALABSORPTION INTRALUMINAL BRUSH BORDER (TRANS)EPITHELIAL OTHER REDUCED MUCOSAL AREA: Celiac, CD 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

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

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

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 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

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 AGE L  R FIBER Weakening of wall

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

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)

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 PHYSIOLOGY ILEUS, esp. postsurgical INFARCTION MOTILITY DISEASES, esp., HIRSCHSPRUNG DISEASE

TUMORS NON-NEOPLASTIC (POLYPS) 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 PRE-MALIGNANT as well) SESSILE vs. PEDUNCULATED TUBULAR vs. VILLOUS

PEDUNCULATED vs VILLOUS vs SESSILE

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

“ FAMILIAL” NEOPLASMS POLYPOSIS (NON-NEOPLASTIC, hamartomatous) POLYPOSIS (NEOPLASTIC, i.e., cancer risk) 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, LOW transit time, refined carbs

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

GROWTH PATTERNS POLYPOID ANNULAR, CONSTRICTING DIFFUSE

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

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

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

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

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 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

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