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Flashcards in Gastrointestinal Deck (144):

GI Embryology

Foregut - Pharynx to duodenum
Midgut - duodenum to transverse colon
Hindgut - distal transverse colon to rectum


Developmental Defects of anterior abdominal wall due to failure of?

-Rostral fold closure: sternal defects
-Lateral fold closure: omphalocele, gastroschisis
-Caudal fold closure: bladder exstrophy


Duodenal atresia?

failure to recanalize (trisomy 21)


Jejunal, ileal, colonic atresia?

due to vascular accident (apple peel atresia)


Midgut Development?

-6th week: midgut herniates through umbilical ring
-10th week: returns to abdominal cavity + rotates around SMA


Pathology of GI Embryology

-malrotation of midgut
-intestinal atresia or stenosis



-extrusion of abdominal contents through abdominal folds; not covered by peritoneum



-persistence of herniation of abdominal contents into umbilical cord, covered by peritoneum


Tracheoesophageal Anomalies

-Esophageal atresia (EA) with distal tracheoesophageal fistula (TEF) is the most common (85%)
-Results in drooling, choking, & vomiting with first feeding
-TEF allows air to enter stomach (visible on CXR)
-Cyanosis is secondary to laryngospasm (to avoid reflux-related aspirations)
-Clinical test: failure to pass NG tube into stomach
-In H-type it is a fistula alone, in pure atresia (isolated) EA the CXR shows gasless abdomen


Congenital Pyloric Stenosis

-Hypertrophy of the pylorus causes obstruction
-Palpable "olive" mass in epigastric region & nonbilious projectile vomiting at ~2weeks of age
-Treatment: surgical incision
-occurs in 1/600 live births, more often in firstborn males


Pancreas Embryology

Pancreas-derived from foregut, ventral pancreatic buds contribute to the pancreatic head & main pancreatic duct
-the uncinate process is formed by the ventral bud alone
-the dorsal pancreatic bud becomes everything else (Body, tail, isthmus, & accessory pancreatic duct)


Annular Pancreas

Ventral pancreatic bud abnormally encircles 2nd part of duodenum; forms a ring of pancreatic tissue that may cause duodenal narrowing


Pancreas Divisum

Ventral & dorsal parts fail to fuse at 7 weeks


Spleen Embryology

Arises in mesentery of stomach (hence is mesodermal) but it supplied by foregut (celiac artery)


Retroperitoneal Structures

-include GI structures that lack a mesentery & non-GI structures
-Injuries to retroperitoneal structures can cause blood or gas accumulation in retroperitoneal structures can cause blood or gas accumulation in retroperitoneal space
-Suprarenal (adrenal) gland
-Aorta & IVC
-Duodenum (2nd & 3rd parts)
-Pancreas (except tail)
-Colon (descending & ascending)
-Esophagus (lower 2/3)
-Rectum (lower 2/3)


Falciform Ligament

-Connects liver to anterior abdominal wall
-Contains ligamentum teres hepatitis (derivative of fetal umbilical vein)
-Derivative of ventral mesentery


Hepatoduodenal Ligament

-Connects liver to duodenum
-Contains portal triad; hepatic artery, portal vein, common bile duct
-Pringle maneuver-ligament may be compressed b/w thumb & index finger placed in omental foramen to control bleeding
-Connects greater & lesser sacs


Gastrohepatic Ligament

-Connects liver to lesser curvature of stomach
-Contains gastric arteries
-Separates greater & lesser sacs on the right
-May be cut during surgery to access lesser sac


Gastrocolic Ligament

-Connects greater curvature & transverse colon
-Contains gastroepiploic arteries
-Part of greater omentum


Gastrosplenic Ligament

-Connects greater curvature and spleen
-Contais short gastrics, left gastroepiploic vesssls
-Separates greater & lesser sacs on the left


Splenorenal Ligament

-Connects spleen to posterior abdominal wall
-Contains splenic artery & vein, tail of pancreas


Layers of gut wall (in digestive tract)

-Mucosa-epithelial (absorption), lamina propria (support), muscularis mucosa (motility)
-Submucosa-includes submucosal nerve plexus (Meissner's)
-Muscularis externa-includes Myenteric nerve plexus (Auerbach's)
-Serosa (when intraperitoneal)/adventitia (when retroperitoneal)



-extends into submucosa, inner or outer muscular layer



-in the mucosa only


Digestive Tract: Frequencies of Basal Electric Rhythm (slow waves)

-Stomach (3 waves/min)
-Duodenum (12 waves/min)
-Ileum (8-9 waves/min)


Histology of Esophagus

-nonkeratinized stratified squamous epithelium


Histology of Stomach

-gastric glands


Histology of Duodenum

-villi & microvilli inc. absorptive surface
-Brunner's glands (submucosa) & crypts of Lieberkuhn


Histology of Jejunum

-Plicae circulares & crypts of Lieberkuhn


Histology of Ileum

-Peyer's patches (lamina propria, submucosa), plicae circulares (proximal ileum), and crypts of Lieberkuhn
-Largest # of goblet cells in the small intestine


Histology of Colon

-crypts but no vili, numerous globlet cells


Abdominal Aorta & Branches

-Arteries supplying GI structures branch anteriorly
-Arteries supplying non-GI structures branch laterally
-SUperior mesenteric artery syndrome occurs when the transverse portion (3rd segment) of the duodenum is entrapped b/w SMA & aorta, causing intestinal obstruction


Blood Supply/Innervation of Foregut

Artery: Celiac
Parasympathetic Innervation: Vagus
Vertebral Level: T12/L1
-supplies stomach to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)


Blood Supply/Innervation of Midgut

Artery: SMA
Parasympathetic Innervation: Vagus
Vertebral Level: L1
-supplies distal duodenum to proximal 2/3 of transverse colon


Blood Supply/Innervation of Hindgut

Artery: IMA
Parasympathetic Innervation: Pelvic
Vertebral Level: L3
-supplies distal 1/3 of transverse colon to upper portion of rectum; splenic flexure is a watershed region


Celiac Trunk

-Branches of celiac trunk; common hepatic, splenic, left gastric
-These constitute the main blood supply of the stomach
-Short gastrics have poor anastomoses if splenic artery is blocked
-Strong anastomoses exist between:
Left & right gastroepiploics
Left & right gastrics


Collateral Circulation of the Stomach

-If branches of abdominal aorta are blocked, these arterial anastomoses (origin) compensate:
-Superior epigastric (internal thoracic/mammary) with inferior epigastric (external iliac)
-Superior pancreaticoduodenal (celiac trunk) with inferior pancreaticoduodunal (SMA)
-Middle colic (SMA) with left colic (IMA)
-Superior rectal (IMA) with middle & inferior rectal (internal iliac)


Portosystemic Anastomosis: Esophagus

Clinical Sign: esophageal varices
- left gastric (portal) to esophageal (systemic)


Portosystemic Anastomosis: Umbilicus

Clinical Sign: Caput medusae
-paraumbilical (portal) to superficial & inferior epigastric below the umbilicus, & superior epigastric & lateral thoracic above the umbilicus (systemic)


Portosystemic Anastomosis: Rectum

Clinical Sign: Internal hemorrhoids
-Superior rectal (portal) to middle & inferior rectal (systemic)


Varices of gut, but & caput (medusae) are commonly seen with?

portal HTN


How to treat Portosystemic Anastomosis in the GI?

-transjugular intrahepatic portosystemic shunt (TIPS) b/w the portal veins & hepatic vein percutaneously relieves portal HTN by shunting blood to the systemic circulation


Pectinate (dentate) Line

-formed where endoderm (hindgut) meets ectoderm


Above the Pectinate Line

-internal hemorrhoids, adenocarcinoma
-artery supply from superior rectal artery (branch of IMA)
-Venous drainage is to superior rectal vein to inferior mesenteric vein to portal system
-Internal hemorrhoids recessive visceral innervation & are NOT painful
-Lymphatic drainage to deep nodes


Below Pectinate Line

-external hemorrhoids, squamous cell carcinoma
-arterial supply from inferior rectal artery (branch of internal pudendal artery)
-Venous drainage to inferior rectal vein to internal pudendal vein to internal iliac vein to IVC
-External hemorrhoids receive somatic innervation (inferior rectal branch of pudendal nerve) and are therefore painful
-Lymphatic drainage to superficial inguinal nodes


Liver Anatomy

-Apical surface of hepatocytes faces bile canaliculi
-Basolateral surface faces sinusoids
ZONE I: periportal zone: affected 1st by viral hepatitis
ZONE II: intermediate zone
ZONE III: pericentral vein (centrilobular) zone: affected 1st by ischemia, contains P-450 system, most sensitive to toxic injury, site of alcoholic hepatitis


Biliary Structures

-Gallstones that reach the common channel at ampulla of Vater can block both the bile & pancreatic ducts
-Tumors that arise in the head of the pancreas (near the duodenum) can cause obstruction of the common bile duct


Organization of the Femoral Region

-Lateral to Medial: Nerve-Artery-Vein-Empty space-Lymphatics (NAVEL)


Femoral Triangle

-contains femoral vein, artery nerve


Femoral Sheath

-Fascial tube 3-4cm below inguinal ligament
-Contains femoral vein, artery, and canal (deep inguinal lymph nodes) but not nerve



-A protrusion of peritoneum through an opening, usually a site of weakness


Diaphragmatic Hernia

-abdominal structures enter the thorax; may occur in infants as a result of defective development of pleuroperitoneal membrane
-most commonly a hiatal hernia, in which stomach herniates upward through the esophageal hiatus of the diaphragm

-Sliding hiatal hernia = most common. GE junction is displaced up. "hourglass stomach"
-Paraesophageal hernia = GE junction is normal, Fundus protrudes into the thorax


Indirect inguinal hernia

-Goes through the internal (deep) inguinal ring, external (superficial) inguinal ring, & into the scrotum
-Enters internal inguinal ring lateral to inferior epigastric artery
-Occurs in infants owing to failure of processus vaginalis to close (can form hydrocele)
-Males more
-Follows the path of descent of the testes
-Covered by all 3 layers of spermatic fascia


Direct Inguinal Hernia

-Protrudes through the inguinal (Hesselbach's) triangle
-Bulges directly through abdominal wall medial to inferior epigastric artery
-Goes through the external (superficial) inguinal ring only, covered by external spermatic fascia
-older men
MDs don't LIe
-Medial to inferior epigastric artery = Direct hernia
-Lateral to inferior epigastric artery = Indirect hernia


Femoral Hernia

-Protrudes below inguinal ligament through femoral canal below & lateral to pubic tubercle
-more in women
-Leading cause of bowel incarceration


Hesselbach's Triangle

-inferior epigastric vessels
-lateral border of rectus abdominis
-inguinal ligament



Source: G cells (antrum of stomach)

Action: inc. gastric H+ secretion
inc. growth of gastric mucosa
inc. gastric motility

Regulation: inc. by stomch distention/alkalinization, aa, peptides, vagal stimulation, dec. my stomach pH <1.5

-inc. in Zollinger-Ellison syndrome
-inc. by chronic PPI use
-Phenylalanine & tryptophan are potent stimulators



Source: I cells (duodenum, jejunum)

Action: inc. pancreatic secretion
inc. gallbladder contraction
dec. gastric emptying
inc. sphincter of Oddi relaxation

Regulation: inc. by fatty acids, amino acids

-CCK acts on neural muscarinic pathways to cause pancreatic secretion



Source: S cells (duodenum)

Action: inc. pancreatic HCO3- secretion
dec. gastric acid secretion
inc. bile secretion

Regulation: inc. by acid, fatty acids in lumen of duodenum

-inc. HCO3- neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function



Source: D Cells (pancreatic islets, GI mucosa)

Action: dec. gastric acid & pepsinogen secretion
dec. pancreatic & s intestine fluid secretion
dec. gallbladder contraction
dec. insulin & glucagon release

Regulation: inc. by acid, dec. by vagal stimulation

-inhibitory hormone
-antigrowth hormone effects (inhibits digestion & absorption of substances needed for growth)


Glucose-Dependent Insulinotropic Peptide

Source: K cells (duodenum, jejunum)

Action: Exocrine: dec. gastric H+ secretion
Endocrine: inc. insulin release

Regulation: inc. by fatty acids, aa, oral glucose

-also known as gastric inhibitory peptide (GIP)
-An oral glucose load is used more rapidly than the equivalent given by IV due to GIP secretion


Vasoactive Intestinal Polypeptide (VIP)

Source: Parasympathetic ganglia in sphincters, gallbladder, small intestine

Action: inc. intestinal water & electrolyte secretion
inc. relaxation of intestinal smooth muscle & sphincters

Regulation: inc. by distention & vagal stimulation
dec. by adrenergic input

-VIPoma- non-alpha, non-beta, islet cell pancreatic tumor that secretes VIP
-Copious watery diarrea, hypokalemia, & achlorhydria (WDHA syndrome)


Nitric Oxide

Action: inc. smooth muscle relaxation, including lower esophageal sphincter

-loss of NO secretion is implicated in inc. lower esophageal tone of achalasia



Source: small intestine

Action: produces migrating motor complexes (MMCs)

Regulation: inc. fasting state

-motilin receptor agonists (such as erythromycin) are used to stimulate intestinal peristalsis


Intrinsic Factor

Source: parietal cells (stomach)

Action: vit. B12-binding protein (required for B12 uptaken in terminal ileum)

-Autoimmune destruction of parietal cells lead to chronic gastritis & pernicious anemia


Gastric Acid

Source: Parietal Cells (stomach)

Action: dec. stomach pH

Regulation: inc. by histamine, ACh, gastrin
dec. by somatostatin, GIP, prostaglandin, secretin

Gastrinoma: gastrin-secreting tumor that causes continuous high levels of acid secretion & ulcers



Source: Chief Cells (stomach)

Action: protein digestion

Regulation: inc. by vagal stimulation, local acid

-inactive pepsiongen to pepsin by H+



Source: Mucosal cells (stomach, duodenum, salivary glands, pancreas) & Brunner's gland (duodenum)

Action: Neutralizes acid

Regulation: inc. by pancreatic & biliary secretion with secretin

-HCO3- is trapped in mucus that covers the gastric epithelium



-secretion from parotid, submandibular, & sublingual glands is stimulated by sympathetic & parasympathetic activity
-amylase digests starch, HCO3- neutralizes bacterial acids, mucins lubricate food.
-Normally hypotonic b/c of absorption but more isotonic with higher flow rates (less time for absorption)


Brunner's Glands

-located in duodenal submucosal
-secrete alkaline mucus
-hypertrophy seen in peptic ulcer disease



Role: starch digestion
-secreted in active form


Lipase, Phospholipase A, Colipase

Role: fat digestion



Role: protein digestion
-Includes trypsin, chymotrypsin, elastase, carboxypeptidases
-Secreted as proenzymes also known as zymogens



-Converted to active enzyme trypsin leads to activation of other proenzymes and creation of more trypsinogen (+ feedback loop)
-Converted to trypsin by enterokinase/enteropeptidase, an enzyme secreted from duodenal mucosa


Salivary Amylase

Carbohydrate Digestion
-starts digestion, hydrolyzes alpha 1,4, linkages to yield disaccharides (maltose & alpha-limit dextrins)


Pancreatic Amylase

-Highest conc. in duodenal lumen, hydrolyzes starch to oligosaccharides & disaccharides


Oligosaccharide Hydrolases

-At brush border of intestine, the rate-limiting step in carbohydrate digestion, produce monosaccharides from oligo- and disaccharides


Carbohydrate Absorption

-only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes
-Glucose & galactose are taken up by SGLTI (Na+ dependent)
-Fructose is taken up by facilitated diffusion by GLUT-5
-All are transported to blood by GLUT-2
-D-xylose absorption test: distinguishes GI mucosal damage from other causes of malabsorption


Iron Absorption

-absorbed as Fe2+ in duodenum


Folate Absorption

-absorbed in jejunum


B12 Absorption

-absorbed in terminal ileum along with bile acids, requires intrinsic factor


Peyer's Patches

-unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum
-Contain specialized M cells that take up antigen
-B cells stimulated in germinal centers of Peyer's patches differentiate into IgA-secreting plasma cells, which ultimately reside in lamina propria
-IgA receives protective secretory component & is then transported across the epithelium to the gut to deal with intraluminal antigen



-composed of bile salts (bile acids conjugated to glycine or taurine, making them water soluble), phospholipids, cholesterol, bilirubin, water, & ions
-Cholesterol 7 alpha-hydroxylase catalyzes rate-limiting step

1) digestion & absorption of lipids & fat-soluble vit
2) cholesterol excretion (body's only means of eliminating cholesterol)
3) Antimicrobial activity (via membrane disruption)



-product of heme metabolism, bilirubin is removed from blood by liver, conjugated with glucuronate, & excreted in bile
-Direct bilirubin: conjugated with glucuronic acid, water soluble
-Indirect bilirubin: unconjugated; water insoluble


Pleomorphic Adenoma

Salivary gland tumors (parotid gland)
-benign mixed tumor
-most common salivary gland tumor
-presents as a painless, mobile mass
-it is composed of cartilage & epithelium and recurs frequently


Warthin's Tumor

Salivary gland tumors
-papillary cystadenoma lymphomatosum
-a benign cystic tumor with germinal centers


Mucoepidermoid Carcinoma

Salivary gland tumors
-most common malignant tumor & has mucinous & squamous components
-presents as a painful mass b/c of common involvement of the facial nerve



-Failure of relaxation of LES due to loss of myenteric (Auerbach's) plexus
-High LES opening pressure & uncoordinated peristalsis leads to progressive dysphagia to solids & liquids (vs. obstruction-solids only)
-Barium swallow shows dilated esophagus with an area of distal stenosis "birds beak"
-Associated with inc. risk of esophageal squamous cell carcinoma
-Secondary may arise from Chagas' disease
-Scleroderma (CREST) is associated with esophageal dysmotility involving low pressure proximal to LES


Gastroesophageal Reflux Disease (GERD)

-commonly presents as heartburn & regurg upon lying down
-may also present with nocturnal cough & dyspnea, adult-onset asthma
-Dec. in LES tone


Esophageal Varices

-Painless bleeding of dilated submucosal veins in lower 1/3 of esophagus secondary to portal HTN



-Associated with reflux, infection (candidia: white pseudomembrane; HSV-1: punched-out ulvers, CMV: linear ulcers) or chemical ingestion


Mallory-Weiss Syndrome

-Mucosal lacerations at the gastroesophageal junction due to severe vomiting
-Leads to hematemesis
-Usually found in alcoholics & bulimics


BoerHaave Syndrome

-Transmural esophageal rupture due to violent retching "Been-Heaving Syndrome"


esophageal Strictures

-Associated with lye ingestion & acid reflux


Plummer-Vinson Syndrome

-Triad of: Dysphagia (due to esophageal webs)
glossitis, iron deficiency anemia


Barrett's Esophagus

-Glandular Metaplasia - replacement of nonkeratinized (stratified) squamous epithelium with intestinal (nonciliated columnar) epithelium in the distal esophagus
-Due to chronic acid reflux
-Associated with esophagitis, esophageal ulcers, & increased risk of esophageal adenocarcinoma


Esophageal Cancer

-Squamous or adenocarcinoma
-typically presents with progressive dysphagia (first solids, then liquids) & weight loss; poor prognosis
Risk Factors: Achalasia, Alcohol (squamous), Barrett's esophagus (adeno), Cigarettes (both), Diverticula (Zenker's squ), Esophageal web (squ), Familial, Fat (obesity, adeno), GERD (adeno), Hot liquids (squamous)


Malabsorption Syndromes

-can cause diarrhea, steatorrhea, weight loss, weakness, & vit & mineral deficiencies


Tropical Sprue

Malabsorption Syndromes
-unknown cause, but responds to abs
-similar to celiac sprue, can affect entire small bowel


Whipple's Disease

Malabsorption Syndromes
-infection with Tropheryma whipplei (gram +),
PAS + foamy macrophages in intestinal lamina propria, mesenteric nodes
-Cardiac symptoms, arthralgias, & neurological symptoms are common
-most often in older men


Celiac Sprue

Malabsorption Syndromes
-autoantibodies to gluten (gliadin) in wheat and other grains
-Primarily affects distal duodenum or proximal jejunum
-Histology shows loss of villi


Disaccharidase Deficiency

Malabsorption Syndromes
-most common is lactase deficiency (milk intolerance)
-normal appearing villi
-osmotic diarrhea
-since lactase is located at tips of intestinal villi, self-limited lastase deficiency can occur following injury (viral diarrhea)
+ for lactase deficiency if:
-admin. of lactose produces symptoms & glucose rises < 20mg/dL



Malabsorption Syndromes
-dec. synthesis of appoliproprotein B, inability to generate chylomicrons, dec, secretion of cholesterol, VLDL into bloodstream, fat accumulation in enteroctes
-presents in early childhood with malabsorption & neurologic manifestations


Pancreatic Insufficiency

Malabsorption Syndromes
-due to cystic fibrosis, obstructing cancer, & chronic pancreatitis
-causes malabsorption of fat & fat-soluble vit (A, D, E,K)
-inc. neutral fat in stool


Celiac Sprue

-autoimmune-mediated intolerance of gliadin (wheat) leading to steatorrhea
-associated with HLA-DQ2, HLA-DQ8, & people of northern European descent
-Findings include anti-endomysial, anti-tissue transglutaminase, & anti-gliadin abs; blunting of villi; & lymphocytes in the lamina propria.
-Dec. mucosal absorption that primarily affects jejunum
-Serum levels of tissue transglutaminase abs are used for screening
-Associated with dermatitis herpetiformis
-moderately inc. risk of malignancy (T-cell lymphoma)


Acute Gastritis (erosive)

-Disruption of mucosal barrier leads to inflammation, can be caused by stress, NSAIDs (dec. PGE1, dec. gastric mucosa protection), alcohol, uremia, burns (curling's ulcer, dec. plasma volume, sloughing of gastric mucosa) and brain injury (Cushing's ulcer, inc. vagal stimulation, inc. ACh, inc. H+ production)

-Especially common with alcoholics & NSAIDs (patients with RA)


Chronic Gastritis (nonerosive)
Type A

-autoimmune disorder characterized by autoantibodies to parietal cells, pernicious anemia, & achlorhydria
-associated with other autoimmune disorders

-Anemia affects gastric body


Chronic Gastritis (nonerosive)
Type B

-most common type
-caused by H. pylori infection
-inc. risk of MALT lymphoma
-H. pylori bacterium affects antrum


Menetrier's Disease

-Gastric hypertrophy with protein loss, pariteal cell atrophy, & inc, mucous cells
-Rugae of stomach are so hypertrophied that they look like brain gyri


Stomach Cancer

-mostly adenocarcinoma, early aggressive local spread & node/liver metastases
-often presents with acanthosis nigricans

Intestinal: associated with H. pylori infection, dietary nitrosamines (smoked food), achlorhydria, chronic gastritis, type A blood, commonly on lesser curvature; looks like ulcer with raised margins

Diffuse: not associated with H. pylori, signet ring cells; stomach wall grossly thickened & leathery (linitis plastica)

-Virchow's node, Krukenberg's tumor, Sister Mary Joseph's Nodule


Virchow's Node

-involvement of left supraclavicular node by metastasis from stomach


Krukenberg's tumor

-bilateral metastases to ovaries
-abundant mucus, signet ring cells


Sister Mary Joseph's nodule

-subcutaneous periumbilical metastasis


Gastic Ulcer

-pain greater with food (weightloss)
-70% h. pylori infection
-dec. mucosal protection against gastric acid, NSAID use also implicated
-inc. risk of carcinoma
-often occurs in older patients


Duodenal Ulcer

-dec. with meals (weight gain)
-H. pylori in 100%
-dec. mucosal protection or inc. gastric acid secretion (Zollinger-Ellison syndrome)
-generally benign
-hypertrophy of Brunner's glands


Ulcer Complications: Hemorrhage

-gastric, duodenal (posterior > anterior)
-ruptured gastric ulcer on the lesser curvature of the stomach, bleeding from left gastric artery
-an ulcer on the posterior wall of the duodenum leads to bleeding from gastroduodenal artery


Ulcer Complications: Perforations

-duodenal (anterior > posterior)


Chron's Disease

-Disordered response to intestinal bacteria
-any portion of GI tract, usually terminal ileum & colon, skip lesions, rectal sparing
-transmural inflammation, cobblestone mucosa, creeping fat, bowel wall thickening "string sign on barium swallow", linear ulcers, fissures, fistulas
-Noncaseating granulomas & lymphoid aggregates (Th1 mediated)
Complications: Strictures, fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer
- Diarrhea may or may not be bloody
-Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, kidney stones


Treatment of Chron's Disease

-corticosteroids, azathioprine, methotrexate, infliximab, adalimumab


Ulcerative Colitis

-colitis = colon inflammation, continuous colonic lesions, always with rectal involvement
-mucosal & submucosal inflammation only, friable mucosal pseudopolyps with freely hanging mesentery
-loss of haustra "lead pipe" appearance on imaging
-crypt abscesses & ulcers, bleeding, no granulomas (Th2 mediated)
Complications: malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (worse with right-sided colitis or pancolitis)
-bloody diarrhea
-pyodermal gangrenosum, primary sclerosing cholangitis, ankylosing spondylitis, uveitis


Treatment of Ulcerative Colitis

-ASA preparations (sulfasalazine), 6-mercaptopurine, infliximab, colectomy


Irritable Bowel Syndrome

-recurrent abdominal pain associated with >2 of the following:
-pain improves with defecation
-change in stool frequency
-change in appearance of stool

-no structural abnormalities, most common in middle-aged women, chronic symptoms, may present with diarrhea, constipation, or alternating symptoms
-pathophysiology is multifaceted, treat symptoms



-acute inflammation of the appendix due to obstruction by fecalith (in adults) or lymphoid hyperplasia in children
-initial diffuse periumbilical pain migrates to McBurney's point (1/3 the distance from anterior superior iliac spine to umbilicus)
-Nausea, fever, may perforate (peritonitis)
-Differential: diverticulitis, (elderly), ectopic pregnancy (use beta-HCG to rule out)
-Treatment: appendectomy



-blind pouch protruding from the alimentary tract that communicates with the lumen of the gut
-most diverticula (esophagus, stomach, duodenum, colon) are acquired and are termed "false" in that they lack or have on attenuated muscularis externa
-most often in sigmoid colon
-"true" diverticulum - all 3 gut wall layers outpouch (Mechel's)
-"false" diverticulum or pseudodiverticulum - only mucosa & submucosa outpouch
-occur especially where vasa recta perforate muscularis external



-many false diverticula
-common (in 50% of people >60) caused by inc. intraluminal pressure & focal weakness in colonic wall
-associated with low-fiber diets, most often in sigmoid colon
-often asymptomatic or associated with vague discomfort, a common cause of hematochezia
-complications: diverticulitis, fistulas



-Inflammation of diverticula classically causing LLQ pain, fever, leukocytosis
-may perforate peritonitis, abscess formation, or bowel stenosis, give antibiotics
-stool occult blood is common +/- hematochezia, may also cause colovesical fistula (fistula with bladder) (pneumaturia)
-Sometimes called "left-sided" appendicitis due to overlapping clinical presentation


Zenker's Diverticulum

-false diverticulum, herniation of mucosal tissue at Killian's triangle b/w the thyropharyngeal & cricopharyngeal parts of the inferior pharyngeal constrictor
-Presenting symptoms: halitosis (due to trapped food particles), dysphagia, obstruction


Meckel's Diverticulum

-true diverticulum
-persistence of the vitelline duct, may contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue
-most common congenital anomaly of the GI tract
-can cause melena, RLQ pain, intussusception, volvulus, or obstruction near the terminal ileum
-contrast with omphalomesenteric cyst = cystic dilation of vitelline duct
Diagnosis: pertechnetate study for ectopic uptake
-2 in long, 2 feet from ileocecal valve, 2% of population, commonly presents in first 2 years of life, may have 2 types of epithelia (gastric/pancreatic)



-"telescoping" of 1 bowel segment into distal segment, commonly at ileocecal junction; can cause "currant jelly" stools & compromise blood supply
-Unusual in adults (associated with intraluminal mass or tumor)
-Majority of cases occur in children (usually idiopathic; may be viral (adenovirus)
-Abdominal emergency in early childhood



-Twisting of portion of bowel around its mesentery, can lead to obstruction and infarction
-may occur at cecum & sigmoid colon, where there is redundant mesentery


Hisrschsprung's Disease

-congential megacolon characterized by lack of ganglioin cells/enteric nervous plexuses (Auerbach's & Meissner's plexuses) in segment on intestinal biobsy
-due to failure of neural crest cell migration
-Presents as chronic constipation early in life
-Dilated portion of the colon proximal to the aganglionic segment, resulting in a "transitional zone"
-involves rectum, usually failure to pass meconium
-Risk inc. with down syndrome
Diagnosed: rectal suction biopsy
Treatment: resection


Duodenal Atresia

-causes early bilious vomiting with proximal stomach distention "double bubble" on x-ray b/c of failure of recanalization of small bowel
-associated by Down syndrome


Meconium Ileus

-in cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth


Necrotizing Enterocolitis

-necrosis of intestinal mucosa & possible perforation
-colon is usually involved, but can involve entire GI tract
-in neonates, more common in preemies (dec. immunity)


Ischemic Colitis

-reduction in intestinal blood flow causes ischemia (pain out of proportion with physical findings)
-pain after eating (weight loss), commonly occurs at splenic flexure & distal colon



-fibrous band of scar tissue; commonly forms after surgery; most common cause of small bowel obstruction
-can have well-demarcated necrotic zones



-tortuous dilation of vessels (hematochezia), most often in cecum, terminal ileum, & ascending colon
-more common in older patients
-confirmed by angiography


Colonic Polyps

-masses protruding into gut lumen (sawtooth appearance)
90% are non-neoplastic
-often rectosigmoid
-tubular or villous


Tubular Adenoma

smaller, more rounded, and more likely to be benigh


Villous Adenoma

long, finger-like projections


Adenomatous Polyp

-malignant risk is associated with inc. size, villous histology, inc. epithelial dysplasia
-precursor to colorectal cancer, the more villous the polyp, the more likely it is to be malignant
-polyp symptoms: often asymptomatic, lower GI bleed, partial obstruction, secretory diarrhea


Hyperplastic Polyp

-most common non-neoplastic polyp in colon
- >50% found in rectosigmoid colon


Juvenile Polyp

-mostly sporadic lesions in children < 5 yrs. of age
-80% in rectum
-if single, no malignant potential
-juvenile polyposis syndrome - multiple juvenile polyps in GI tract, inc. risk of adenocarcinoma



-single polyps are not malignant
-syndrome: autosomal dominant syndrome featuring multiple nonmalignant hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands, genitalia
-associated with inc. risk of CRC & other visceral malignancies