Gastrointestinal

Gluten-sensitivity enteropathy, celiac sprue. Autoimmune-mediated intolerance of gliadin → malabsorption and steatorrhea.  - Associated with HLA-DQ2, HLA-DQ8, northern European descent, dermatitis herpetiformis, ↓ bone density. Findings:- IgA anti-tissue transglutaminase, anti-endomysial, anti-deamidated gliadin peptide antibodies- Villous atrophy- Crypt hyperplasia - Intraepithelial lymphocytosis- Moderatly ↑ risk of malignancy (eg, T-cell lymphoma) - ↓ mucosal absorption primarly affects distal duodenum and/or proximal jejunum.- D-xylose test: passively absorbed in proximal small intestine; blood and urine levels ↓ with mucosa defects or bacterial overgrowth, normal in pancreatic insufficiency.

Infection with Tropheryma whipplei (intracellular gram ⊕ actinomycete)- PAS ⊕ foamy macrophages in intestinal lamina propria, mesenteric nodes.- Diastase-resistance granules (which consist of lysosomes and partially digested bacteria). - Most common in middle-aged Caucasian males. - Cardiac symptoms (eg, valve insufficiencies)- Arthralgias (often presents as first symptom)- Neurologic symptoms (myoclonia, ataxia, impairement of oculomotor function)- Diarrhea/steatorrhea occur later in disease course Treatment: IV ceftriaxone for 2 weeks

Location: Any portion of the GI tract, usually the terminal ileum and colon. Skip lesions, rectal sparing.- Risk factors: Smoking, HLA-B27 association, mutation of NOD2 Morphology: - Transmural inflammation → fistulas- Cobblestone mucosa, creeping fat, bowel wall thickening ("string sign" on barium swallow x-ray), linear ulcers, fissures.- Noncaseating granulomas and lymphoid aggregates. Th1 mediated. Complications:- Malabsorption/malnutrition- Colorectal cancer - Fistulas (eg, enterovesical fistulae, which can cause recurrent UTI and pneumaturia), phlegmon/abcess, strictures (causing obstruction), perianal disease. Intestinal manifestation: Diarrhea that may or may not be bloody. Extraintestinal manifestation:- Rash (pyoderma grangrenosum, erythema nodosum)- Eye inflammation (episcleritis, uveitis)- Oral ulcerations (aphthous stomatitis)- Arthritis (peripheral, spondylitis)- Kidney stones (usually calcium oxalate), gallstones. - May be ⊕ for anti-Saccharomyces cerevisiae antibodies (ASCA). Treatment: Corticosteroids, azathioprine, antibiotics, infliximab, adalimumab (anti-TNFα)

Location: Ascending inflammation beginning in the rectum and spreading continuously.- HLA-B27 association, smoking is protective. Morphology: - Mucosal and submucosal inflammation only.- Friable mucosa with superficial and/or deep ulcerations. - Loss of haustra → "lead pipe" appearance on imaging- Crypt abcesses and ulcers, bleeding, no granulomas. Th2 mediated. Complications:- Malabsorption/malnutrition- Colorectal cancer - Fulminant colitis, toxic megacolon, perforation. Intestinal manifestation: Bloody diarrhea, tenesmus. Extraintestinal manifestation:- Rash (pyoderma grangrenosum, erythema nodosum)- Eye inflammation (episcleritis, uveitis)- Oral ulcerations (aphthous stomatitis)- Arthritis (peripheral, spondylitis)- 1° sclerosing cholangitis. Associated with p-ANCA. Treatment: 5-aminosalicylic preparations (eg, mesalamine), 6-mercaptopurine, infliximab, colectomy.

Twisting portion of bowel around its mesentery; can lead to obstruction and infarction. - Can occur throughout the GI tract. - Midgut volvulus more common in infants and children.- Sigmoid volvulus (coffee bean sign on x-ray) more common in elderly.

Telescoping of proximal bowel segment into a distal segment, commonly at ileocecal junction. - Compromised blood supply → intermittent abdominal pain often with "current jelly" stools.- Patient may draw legs to chest to ease pain.- Exam may reveal sausage-shaped mass. - Ultrasound shows "target sign." Often due to a lead point, but can be idiopathic. Most common pathologic lead point is Meckel diverticulum (children) or intraluminal mass/tumor (adults).- Majority of cases occur in children; unusual in adults. May be associated with rotavirus vaccine, Henoch-Schönlein purpura, and recent viral infection (eg, adenovirus; Peyer patch hypertrophy creates lead point).

Reduction in intestinal blood flow causes ischemia.  - Typically occurs in elderly >60 years. - Usually caused by transient hypoperfusion.- Commonly occurs at watershed areas (splenic flexure, distal colon). Presentation:- Crampy abdominal pain followed by hematochezia.- A classic case is a patient who presents with bloody diarrhea and severe abdominal pain after an abdominal aortic aneurysm repair. - Thumbprint sign on imaging due to mucosal edema/hemorrhage.

Necrosis of mucosa (primarily colonic) with possible perforation, which can lead to pneumatosis intestinalis, free air in abdomen, portal venous gas. - Seen in premature, formula-fed infants with immature immune system.- Most common cause of acute abdomen in premature infants.- Peak incidence 2nd-4th week after birth (not during the first week) Treatment: parenteral nutrition, gut decompression via nasogastric tube, IV antibiotics (eg, ampicillin, gentamycin, and metronidazole), surgery

Tortuous dilation of vessels → hematochezia. - Most often found in the right-sided colon (terminal ileum, cecum, ascending colon). - More common in older patients. - Confirmed by angiography. - Associated with aortic stenosis and von Willebrand disease.

Non-neoplastic:- Hamartomous polyps: Solitary lesions do not have significant risk of transforation. Growths of normal colonic tissue with distorted architecture. Associated with Peutz-Jeghers syndrome and juvenile polyposis.- Mucosal polyps: Small, usually <5 mm. Look similar to normal mucosa.- Inflammatory pseudopolyps: Due to mucosal erosion in inflammatory bowel disease.- Submucosal polyps: May include lipomas, leiomyomas, fibromas, and other lesions.- Hyperplastic polys: Most common; generally smaller and predominantly located in the rectosigmoid region. Occasionally evolves into serrated polyps and more advanced lesions. Malingnant potential:- Adenomatous polyps: Neoplastic, via chromosomal instability pathway with mutations in APC and KRAS. Tubular histology has less malignant potential than villous; tubulovillous has intermediate malignant potential. May present with occult bleeding.- Serrated polyps: Premalignant. Characterized by CpG island methylator phenotpye (CIMP; cytosine base followed by guanine, linked by a phosphodiester bond). Defect may silence MMR gene (DNA mismatch repair). Mutations lead to microsatellite instability and mutations in BRAF. "Saw-tooth" pattern of crypts on biopsy. Up to 20% of cases of sporadic CRC.

- Most patients are >50 years old- 25% have a family history Risk factors: Adenomatous and serrated polyps, familial cancer syndromes, IBD, smoking, diet of processed meat with low fiber, obesity, alcohol consumption.Protective factors: Physical activity, diet rich in fiber and lower in meat, long-term use of aspirin and NSAIDs - Rectosigmoid > ascending > descending- Ascending – exophytic mass, iron deficiency anemia, melena, weight loss- Descending – infiltrating mass, partial obstruction, colicky pain, hematochezia- Rarely, presents with S bovis bacteremia. Diagnosis:- Iron deficiency anemia (especially >50 years old) - Screen low-risk patients starting at age 50 with colonoscopy; alternatives include flexible sigmoidoscopy, fecal occult blood testing, fecal immunochemical testing, and CT colonography.- Patients with 1° relative who has colon cancer should be screened via colonoscopy at age 40, or starting 10 years prior to their relative's presentation. - "Apple core" lesion seen on barium enema x-ray.- CEA tumor marker: good for monitoring recurrence

Chromosomal instability pathway: mutations in APC cause FAP and most sporadic CRC (via adenoma-carcinoma sequence). Loss APC (loss of intracellular adhesion and increased cellular proliferation) → Colon at risk → KRAS mutation (unregulated intracellular signalling) → Adenoma → Loss of p53/DCC (tumorigenesis) → Carcinoma Microsatellite instability pathway: mutations or methylation of mismatch repair genes (eg, MLH1) cause Lynch syndrome and some sporadic CRC (via serrated polyp pathway). - Overexpression of COX-2 has been linked to colorectal cancer, NSAIDs may be chemoprotective.

Cirrhosis – diffuse bridging fibrosis (via stellate cells) and regenerative nodules disrupt normal architecture of liver; ↑ risk for hepatocellular carcinoma (HCC).- Etiologies: alcohol (60-70% of cases), nonalcoholic steatohepatitis, chronic viral hepatitis, autoimmune hepatitis, biliary disease, genetic/metabolic disorders. Portal hypertension – ↑ pressure in portal venous system.- Etiologies include cirrhosis, vascular obstruction (eg, portal vein thrombosis, Budd-Chiari syndrome), schistosomiasis. Integumentary: Jaundice, spider angiomas, palmar erythema, purpura, petechiaeNeurologic: Hepatic encephalopathy, asterixisEffects of portal hypertension: Esophageal varices (→ hematemesis), gastric varices (→ melena), caput medusae, ascites, anorectal varicesHematologic: Thrombocytopenia, macrocytic anemia, coagulation disorders, splenomegalyRenal: Hepatorenal syndromeReproductive: Testicular atrophy, gynecomastia, amenorrheaMetabolic: Hyperbilirubinemia, hyponatremiaCardiovascular: Cardiomyopathy, peripheral edema

Enzymes released in liver damage:Aspartate and alanine aminotransferase:- ↑ in most liver disease: ALT > AST- ↑ in alcoholic liver disease: AST > ALT- AST > ALT in nonalcoholic liver disease suggests progression to cirrhosis.Alkaline phosphatase: ↑ in cholestasis (eg, biliary obstruction), infiltrative disorders, bone disease.γ-glutamyl-transpeptidase: ↑  in various liver and biliary diseases (just als ALP can be), but not in bone disease; associated with alcohol use. Functional liver markers:- Bilirubin: ↑ in various liver diseases (eg, biliary obstruction, alcoholic or viral hepatitis, cirrhosis), hemolysis- Albumin: ↓ in advanced liver disease (marker of liver's biosynthetic function)- Prothrombin time: ↑ in advanced liver disease (↓ production of clotting factors, thereby measuring the liver's biosynthetic function)- Platelets: ↓ in advanced liver disease (↓ thrombopoietin, liver sequestration) and portal hypertension (splenomegaly/splenic sequestration)

Rare, often fatal childhood hepatic encephalopathy in children <19 years who have been treated with aspirin.- Infection usually VZV or influenza Findings:- Mitochondral abnormalities- Fatty liver (microvesicular fatty change)- Hypoglycemia- Vomiting- Hepatomegaly- Coma Pathophysiology: Viruses alter the metabolism of salicylates → accumulation of salicylate metabolites → hepatic mitochondrial injury → ↓ β-oxidation and failure of hepatic ATP production → hepatic failure → hyperammonemia and metabolic acidosis.  - Avoid aspirin in children, except in those with Kawasaki disease.

Non-alcohol related accumulation of fat in the liver cells. Etiology: Metabolic syndrome (insulin resistance); obesity → fatty infiltration of hepatocytes → cellular "ballooning" and eventual necrosis.- Inflammatory infiltrates, with scattered lymphocytes, neutrophils, Kupffer cells. - May cause cirrhosis and HCC - AST/ALT ratio <1.0 (ALT>AST – Lipids)

Cirrhosis → portosystemic shunts → ↓ NH3 metabolism → neuropsychiatric dysfunction.Reversible neuropsychiatric dysfunction ranging from disorientation/asterixis (mild) to difficult arousal or coma (severe).  Triggers:- ↑ NH3 production and absorption (due to dietary protein, GI bleed, constipation, infection).- ↓ NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS). Treatment: Lactulose (↑ NH4+ generation) and rifaximin or neomycin (↓ NH3 producing gut bacteria).

Most common 1° malignant tumor of liver in adults. - Associated with HBV (+/- cirrhosis) and all other causes of cirrhosis (HCV, alcoholic and nonalcoholic fatty liver disease, autoimmune disease, hemochromatosis, α1-antitrypsin deficiency) and specific carcinogens (eg, aflatoxin from Aspergillus). - May lead to Budd-Chiari syndrome. Findings: Jaundice, tender hepatomegaly, ascites, anorexia. - Spreads hematogenously.- Paraneoplastic syndromes: erythrocytosis (EPO), hypercalcemia (PTHrP) Diagnosis: ↑ α-fetoprotein; ultrasound or contrast CT/MRI, biopsy.

Most common, benign liver tumor. - Typically occurs at age 30-50 years. - Biopsy contraindicated because of risk of hemorrhage. Macroscopic: Cystic lesions with a dark colorHistology: Cavernous vascular spaces of variable size, lined by flat endothelial cells.Ultrasound: Hyperechoic (pale)Contrast CT: Iris diaphragm phenomenon (centripetal enhancement during later phase central enrichment)

Misfolded gene product protein aggregates in hepatocellular ER → intracellular accumualtion → hepatocyte distruction → hepatitis and liver cirrhosis with PAS ⊕ globules in liver.In lungs, ↓ α1-antitrypsin → uninhibited elastase in alveoli → ↓ elastic tissue → panacinar emphysema.- Codominant trait. Presentation:- Severe form: prolonged neonatal jaundice, hepatitis, cirrhosis, panacinar emphysema- Mild form: Manifestation in adolescence with liver damage and dyspnea without a history of smoking.- Increased risk of HCC. Diagnostics: - Electrophoresis (↓ alpha-1 peak), serum antitrypsin level, liver biopsy- Panlobular emphysema seen on CXR in contrast to centrilobular emphysema in smokers.

Abnormal yellowing of the skin and/or sclera due to bilirubin deposition.- Sclera starting >2-3 mg/dL- Skin starting >4-5 mg/dL- Hyperbilirubinemia 2° to ↑ production or ↓ disposition (impaired hepatic uptake, conjugation, excretion). Unconjugated (indirect) hyperbilirubinemia: Hemolytic, physiologic (newborns), Crigler-Najjar, Gilbert syndrome. Conjugated (direct) hyperbilirubinemia: - Biliary tract obstruction: gallstones, cholangiocarcinoma, pancreatic or liver cancer, liver fluke (Fasciola hepatica).- Biliary tract disease: 1° sclerosing cholangitis, 1° biliary cholangitis- Excretion defect: Dubin-Johnson syndrome, Rotor syndrome Mixed (direct and indirect) hyperbilirubinemia: Hepatitis, cirrhosis

Extrahepatic biliary obstruction → ↑ pressure in intrahepatic ducts → injury/fibrosis and bile stasis. - Patients with known obstructive lesions (gallstones, biliary strictures, pancreatic carcinoma). - May be complicated by ascending cholangitis.

↑ cholesterol and/or bilirubin, ↓ bile salts, phosphatidylcholine, lecithin, and gallbladder stasis all cause stones. 2 types of stones:- Cholesterol stones (radiolucent with 10-20% opaque due to calcifications) – 80% of stones. Associated with obesity, Crohn disease, advanced age, estrogen therapy, multiparity, rapid weight loss, Native American origin.- Pigment stones→ Black = radiopaque. Associated with Crohn disease (↑ enterohepatic cycling of bilirubin), chronic hemolysis, alcoholic cirrhosis, advanced age, total parenteral nutrition (TPN)→ Brown = radiolucent, infection. Biliary tract infection (eg, E coli, Clonorchis sinensis) → release of β-glucuronidases → Both → ↑ unconjugated bilirubin → calcium bilirubinate precipitation Presentation:- Biliary colic, especially postprandial- Nausea, vomiting- Bloating, dyspepsia - Most common complication is cholecystitis.- Can also cause pancreatitis, ascending cholangitis. - Risk factors: Female, Fat, Fertile, Forty, Fair-skinned- Diagnose with ultrasound. - Treat with elective cholecystectomy if symptomatic.

- Associated with nausea/vomiting and dull RUQ pain. - Neurohormonal activation (eg, by CCK after a fatty meal) triggers contraction of gallbladder, forcing stone into cystic duct. - Labs are normal, ultrasound shows cholelithiasis.

Autodigestion of pancreas by pancreatic enzymes. Causes: Idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune disease, scorpion sting, hypercalcemia/hypertriglyceridemia (>1000 mg/dL), ERCP, drugs (eg, NRTIs, protease inhibitors, sulfa drugs). Diagnosis by 2 of 3 criteria:- Acute epigastric pain often radiating to the back- ↑ serum amylase or lipase (more specific) to 3x upper limit of normal- Characteristic imaging findings Complications: pseudocyst (lined by granulation tissue, not epithelium), abscess, necrosis, hemorrhage, infection, organ failure (ARDS, shock, renal failure), hypocalcemia (precipitation of Ca2+ soaps).

Chronic inflammation, atrophy, calcification of the pancreas.- Major causes include alcohol abuse and genetisc predisposition (ie, cystic fibrosis); can be idiopathic. - Complications include pancreatic insufficiency and pseudocysts.- Pancreatic insufficiency (typically when <10% pancreatic function) may manifest with steatorrhea, fat-soluble vitamin deficiency, diabetes mellitus. - Amylase and lipase may or may not be elevated (almost always elevated in acute pancreatitis).- ↓ Fecal elastase activity (pancreatic function test)

Very aggressive tumor arising from pancreatic ducts (disorganized glandular structure with cellular infiltration); often metastatic at presentation, with average survival ~1 year after diagnosis. - Tumors more common in pancreatic head (→ obstructive jaundice).  - Associated with CA 19-9 tumor marker (also CEA, less specific) Risk factors:- Tobacco use- Chronic pancreatitis (especially >20 years)- Diabetes- Age >50 years- Jewish and African-American males Presentation:- Abdominal pain radiating to back- Weight loss (due to malabsorption and anorexia)- Migratory thrombophlebitis – redness and tenderness on palpation of extremities (Trousseau syndrome)- Obstructive jaundice with palpable, nontender gallbladder (Courvoisier sign) Treatment: Whipple procedure, chemotherapy, radiation therapy

Source: G cells (antrum of stomach, duodenum) Action:↑ gastric H+ secretion↑ growth of gastric mucosa↑ gastric motility Regulation:↑ by stomach distention/alkalinization, amino acids, peptides, vagal stimulation via gastrin-releasing peptide (GRP)↓ by pH <1.5 - ↑ by chronic PPI use- ↑ in chronic atrophic gastritis (eg, H pylori)- ↑↑ in Zollinger-Ellison syndrome (gastrinoma)

Source: D cells (pancreatic islets, GI mucosa) Action:- ↓ gastric acid and pepsinogen secretion- ↓ pancreatic and small intestine fluid secretion- ↓ gallbladder contraction- ↓ insulin and glucagon release Regulation:- ↑ by acid- ↓ by vagal stimulation - Inhibits secretion of various hormones. - Ocreotide is an anolog used to treat acromegaly, carcinoid syndrome, and variceal bleeding.

Source: I cells (duodenum, jejunum) Action:- ↑ pancreatic secretion- ↑ gallbladder contraction- ↓ gastric emptying- ↑ sphincter of Oddi relaxation Regulation:- ↑ by fatty acids, amino acids - Acts on neural muscarinic pathways to cause pancreatic secretion

Source: S cells (duodenum) Action:- ↑ pancreatic HCO3- secretion- ↓ gastric acid secretion- ↑ bile secretion Regulation:- ↑ by acid, fatty acids in lumen of duodenum - ↑ HCO3- neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function

Source: K cells (duodenum, jejunum) Action:- Exocrine: ↓ gastric H+ secretion- Endocrine: ↑ insulin release Regulation:- ↑ by fatty acids, amino acids, oral glucose - Also known as gastric inhibitory peptide (GIP).- Oral glucose load leads to ↑ insulin compared to IV equivalent due to GIP secretion.

Source: Small intestine Action: Produces migrating motor complexes (MMCs) Regulation: ↑ in fasting state - Motilin receptor agonists (eg, erythromycin) are used to stimulate intestinal peristalsis.

Source: Parasympathetic ganglia in sphincters, gallbladder, small intestine Action:- ↑ intestinal water and electrolyte secretion- ↑ relaxation of intestinal smooth muscle and sphincters Regulation:- ↑ by distention and vagal stimulation- ↓ by adrenergic input - VIPoma – non-α, non-β islet cell pancreatic tumor that secretes VIP.Watery Diarrhea, Hypokalemia and Achlorhydria (WDHA syndrome)

Source: Stomach Action: ↑ appetite Regulation:- ↑ in fasting state- ↓ by food - ↑ in Prader-Willi syndrome- ↓ after gastric bypass surgery

Source: Parietal cells (stomach) Action: Vitamin B12-binding protein (required for B12 uptake in terminal ileum) Autoimmune destruction of parietal cells → chronic gastritis and pernicious anemia.

Source: Parietal cells (stomach) Action: ↓ stomach pH Regulation:- ↑ by histamine (H2), ACh (M3), gastrin (CCKB)- ↓ by somatostatin, secretin, GIP, prostaglandin

Source: Chief cells (stomach) Action: Protein digestion Regulation: ↑ by vagal stimulation (ACh), local acid - Pepsinogen (inactive) is converted to pepsin (active) in the presence of H+.

Source: Mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner glands (duodenum). Action: Neutralizes acid. Regulation: ↑ by pancreatic and biliary secretion with secretin. - Trapped in mucus that covers the gastric epithelium.

Isotonic fluid; low flow → high Cl-, high flow → high HCO3-. α-amylase: Starch digestion. Secreted in active form. Lipase: Fat digestion Proteases: Protein digestion- Includes trypsin, chymotrypsin, elastase, carboxypeptidases.- Secreted as proenzymes also known as zymogens. Trypsinogen: Converted to active enzyme trypsin → activation of other proenzymes and cleaving of additional trypsinogen molecules (positive feedback loop).- Converted to trypsin by enterokinase/enteropeptidase, a brush-border enzyme on duodenal and jejunal mucosa.

Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes. - Glucose and galactose are taken up by SGLT1 (Na+ dependent).- Fructose is taken up by facilitated diffusion by GLUT5 (passive).- All are transported to blood by GLUT2. - D-xylose absorption test: distinguishes GI mucosal damage from other causes of malabsorption.

Iron: Absorbed as Fe2+ in duodenum. Folate: Absorbed in small bowel. Vitamin B12: Absorbed in terminal ileum along with bile salts, requires intrinsic factor.

- Suprarenal (adrenal) glands- Aorta and IVC- Esophagus (thoracic portion)- Duodenum (2nd through 4th parts- Pancreas (except tail)- Colon (ascending and descending)- Rectum (partially)- Ureters- Kidneys

Falciform ligament: Connects liver anterior abdominal wall- Contains ligamentum teres hepatis (derivative of fetal umbilical vein), patent paraumbilical veins- Derivative of ventral mesentery Hepatoduodenal ligmant: Connects liver to duodenum- Portal triad: proper hepatic artery, portal vein, common bile duct- Pringle maneuver – ligament may be compressed between thumb and index finger placed in omental foramen to control bleeding- Borders the omental foramen, which connects the greater and lesser sacs- Part of lesser omentum Gastrohepatic ligament: Connects liver to lesser curvature of stomach- Conatins gastric vessels- Separates greater and lesser sacs on the right- May be cut during to surgery to access lesser sac- Part of lesser omentum  Gastrocolic ligament: Connects greater curvature and transverse colon- Contains gastroepiploic arteries- Part of greater omentum Gastrosplenic ligament: Connects greater curvature to spleen- Contains short gastrics, left gastroepiploic vessels- Separates greater and lesser sacs on the left- Part of greater omentum Splenorenal ligament: Connects spleen to posterior abdominal wall- Contains splenic artery and vein, tail of pancreas

Layers of gut wall:- Mucosa – epithelium, lamina propria, muscularis mucosa- Submucosa – submucosal nerve plexus (Meissner), secretes fluid- Muscularis externa – Myenteric nerve plexus (Auerbach), motility- Serosa (when intraperitoneal), adventitia (when retroperitoneal) - Ulcers can extend into submucosa, inner or outer muscular layer. Erosions are in the mucosa only. Frequencies of basal electric rhythm (slow waves):- Stomach – 3 waves/min- Duodenum – 12 waves/min- Ileum – 8-9 waves/min

T12 – Inferior phrenic (branches superior suprarenal), middle suprarenal, celiac artery L1 – Superior mesenteric artery, renal (branches inferior suprarenal) L2 – Gonadal L3 – Inferior mesenteric artery L4 – Bifurcation  "Watershed regions": Splenic flexure (SMA and IMA), rectosigmoid (IMA and superior rectal artery) Superior mesenteric artery syndome – characterized by intermittent intestinal obstruction symptoms (primarily postprandial pain) when SMA and aorta compress transverse (third) portion of duodenum. Typically occurs in conditions associated with diminished mesenteric fat (eg, low body weight/malnutrition).

Foregut:- Artery: Celiac- Parasympathetic innervation: Vagus- T12, L1- Pharynx (vagus nerve only) and lower esophagus (celiac artery only) to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm) Midgut:- Artery: SMA- Parasympathetic innervation: Vagus- L1- Distal duodenum to proximal 2/3 of transverse colon Hindgut: - Artery: IMA- Parasympathetic innervation: Pelvic- L3- Distal 1/3 of transverse colon to upper portion of rectum

Branches of celiac trunk: Left gastric, common hepatic, splenic. Anastomoses between left and right gastroepiploics, left and right gastrics. Posterior duodenal ulcers penetrate gastroduodenal artery causing hemorrhage.Anterior duodenal ulcers perforate into the anterior abdominal cavity, potentially leading to pneumoperitoneum.

Esophageal varices: Left gastric ↔ azygos Umbilicus (Caput medusa): Paraumbilical ↔ small epigastric veins of the abdominal wall Anorectal varices: Superior rectal ↔ middle and inferior rectal - Treatment with a transjugular intrahepatic portosystemic shunt (TIPS) between the portal vein and hepatic vein relieves portal hypertension by shunting blood to the systemic circulation, bypassing the liver. Can precipitate hepatic encephalopathy.

Formed where endoderm (hindgut) meets ectoderm). Above pectinate line – internal hemorrhoids, adenocarcinoma- Visceral innervation- Superior rectal artery (branch of IMA)- Superior rectal vein → inferior mesenteric vein → splenic vein → portal vein- Drain to internal iliac lymph nodes- Internal hemorrhoids receive visceral innervation and are therefore not painful. Below pectinate line – external hemorrhoids, anal fissures, squamous cell carcinoma- Somatic innervation- Inferior rectal artery (branch of internal pudendal artery)- Inferior rectal vein → internal pudendal vein → internal iliac vein → common iliac vein → IVC- Drain to superficial inguinal lymph nodes- External hemorrhoids receive somatic innervaiton and are thereful painful if thrombosed.