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Flashcards in Gastrointestinal Deck (294)


The foregut structures include: Pharynx, 1st and 2nd parts of the duodenum, Esophagus, Stomach, Liver, Gallbladder, Respiratory system (e.g. trachea, lung buds), Pancreatic buds.


Foregut development

The foregut structures, except the intra-thoracic esophagus, are supplied by the celiac artery. The intra-thoracic esophagus is supplied by aortic branches.
During gestational week 4, the primitive stomach develops. The primitive stomach grows asymmetrically (the dorsal portion grows faster than the ventral aspect) resulting in the development of the greater and lesser curvatures. The stomach then rotates 90 degrees clockwise during its formation, which causes the dorsal mesentery (located posteriorly) to fold on itself, forming a pouch and subsequently lengthening, becoming the greater omentum. Because of the 90 degree clockwise rotation of the stomach, left vagus nerve ultimately innervates the ventral stomach whereas the right vagus nerve innervates the dorsal stomach.



The the following structures are derived from the midgut: 3rd and 4th parts of the duodenum, Jejunum, Ileum, Cecum, Appendix, Ascending colon, Hepatic flexure, Proximal 2/3 of transverse colon.


Midgut development

The midgut structures are supplied by the superior mesenteric artery. Between weeks 6 - 8 of embryogenesis, the midgut herniates through the primitive umbilical ring causing a physiological umbilical herniation. During the physiologic umbilical herniation, the midgut loop herniates through the umbilical ring and rotates 90 degrees counterclockwise around the superior mesenteric artery. Around weeks 10-11, the midgut undergoes an additional 180 degrees counterclockwise rotation, for a total of 270 degrees, before returning to the abdomen.



The following structures are derived from the hindgut: Distal 1/3 of the transverse colon, Splenic flexure, Descending colon, Rectum, Anal canal above the pectinate line (i.e. the portion closest to the rectum). The hindgut derivatives are supplied by the inferior mesenteric artery.



Omphalocele occurs when the midgut loop fails to return to the abdominal cavity during development. An omphalocele has the peritoneum and amnion of the umbilical cord surrounding the protrusion resulting in a shiny sac protruding from the midline base of the umbilical cord. (OmphaloCELE is sealed by the peritoneum).



Gastroschisis is an incomplete closure of the lateral folds, resulting in a defect of the ventral abdominal wall with protrusion of intestinal loops. A gastroschisis is usually lateral to the umbilicus and not covered with peritoneum (no shiny sac).


Duodenal atresia

Duodenal atresia is a condition where there is occlusion of the duodenal lumen secondary to failed recanalization.
Duodenal atresia is associated with Down syndrome. Key clinical features of duodenal atresia include: Polyhydramnios, Bile-containing vomitus (since the obstruction is distal to the point where bile enters the gut), Double bubble appearance with no distal gas on plain radiographs


VACTERL syndrome

VACTERL syndrome is a congenital syndrome caused by defective migration of mesoderm-derived cells: Vertebral defect (present in 70% of TEF cases), Anal atresia (imperforate anus) ± fistula (80%), Cardiac anomalies, such as VSD, single umbilical artery (53%), Tracheo-Esophageal fistula ± esophageal atresia (70%), Renal anomalies (53%), Limb anomalies such as radial dysplasia, pre-axial polydactyly, and syndactyly (65%). VATER syndrome is a more limited form of the VACTERL syndrome without cardiac or limb defects.


Anal atresia

Anal atresia is commonly associated with urogenital anomalies such as: Renal agenesis, Hypospadias, Epispadias, Bladder exstrophy


Abnormal midgut rostral fold closures

Abnormal midgut rostral fold closures may result in sternal defects.


Abnormal midgut caudal fold closures

Abnormal midgut caudal fold closures may result in bladder exstrophy.


Meconium ileus

Meconium ileus is a newborn bowel obstruction of the distal ileum due to an abnormally thick meconium. Meconium ileus is usually a complication in newborn cystic fibrosis. Due to the lack of NaCl, which limits the flow of water into intestinal lumen, the meconium can become abnormally thick and impacted. The thickened meconium obstructs distal-ileum, causing proximal dilatation, bowel wall thickening, and congestions.


Necrotizing enterocolitis (NEC)

Necrotizing enterocolitis (NEC) is characterized by intestinal necrosis and is one of the most common gastrointestinal emergencies in newborns. NEC is often seen in premature, formula-fed infants with immature immune systems. Newborns with NEC can present with abdominal distention/tenderness and rectal bleeding (hematochezia). Diagnosis is made via clinical symptoms along with abdominal radiograph showing pneumatosis intestinalis (presence of gas in the bowel wall).


Jejunal atresia

Jejunal atresia (aka apple peel atresia) occurs when the jejunum fails to vascularize during embryogenesis, resulting in a proximal blind pouch and a distal twirling (apple peel-like) distal ileum.


tracheoesophageal fistula

A tracheoesophageal fistula is an abnormal connection between the trachea and esophagus. Tracheoesophageal fistulas are commonly congenital and the result of mesodermal defects. A fistula is an abnormal connection between two epithelium-lined hollow organs or vessels. The most common tracheoesophageal anomaly is esophageal atresia with distal tracheoesophageal fistula (85% of cases). Infants with esophageal atresia with distal tracheoesophageal fistula present with drooling, choking, and vomiting with their first feeding. In infants with esophageal atresia with distal tracheoesophageal fistula, a connection between the trachea and stomach allows air to enter the stomach in newborns. Chest X-ray reveals an air bubble in stomach. In pure esophageal atresia, chest X-ray shows a gasless abdomen. Infants with esophageal atresia with distal tracheoesophageal fistula may develop cyanosis due to laryngospasm, a protective reflex that prevents aspiration into the trachea. Failure to pass nasogastric tube into an infant's stomach is indicative of esophageal atresia.


Infantile pyloric stenosis

Infantile pyloric stenosis is caused by hypertrophy of the pylorus, which connects the stomach to the duodenum. This condition may progress to near-complete obstruction of the gastric outlet. Infants present with postprandial forceful non-billious vomiting, usually 2 weeks after birth. The condition is more common in firstborn males. Patients may appear dehydrated and emaciated. Vomiting of gastric acid (HCl) causes a volume contraction that leads to a hypokalemic hypochloremic metabolic alkalosis. Physical exam may reveal a palpable "olive-like" mass at the lateral edge of the rectus abdominis muscle in the right upper quadrant of the abdomen, along with visible peristalsis in the abdomen. The treatment for infantile hypertrophic pyloric stenosis is pyloromyotomy.


Pancreatic development

The pancreas, a derivative of the embryonic foregut, develops from the ventral and dorsal pancreatic buds during week 8 of development. Accompanying duodenal clockwise rotation, the ventral pancreas will rotate and fuse with the dorsal pancreas, and will then be nestled in the curvature of the 2nd and 3rd parts of the duodenum. The main pancreatic duct and common bile duct will join to become the hepatopancreatic ampulla of Vater, which will empty into the duodenum at the major (hepatopancreatic) papillae. The endoderm in the pancreas is present in tubules that branch to become: Exocrine pancreas (e.g. ductal epithelium and acinar cells), Pancreatic islet cells (e.g. alpha cells, beta cells, delta cells, pancreatic polypeptide cells). The mesoderm present in the developing pancreas forms the adult connective tissue and vasculature.


ventral pancreatic bud

The ventral pancreatic bud gives rise to the: Uncinate process, Lower part of the head, Main pancreatic duct.


dorsal pancreatic bud

The dorsal pancreatic bud gives rise to the majority of the adult pancreas: Upper part of the head, Body, Tail, Accessory pancreatic duct


Pancreatic divisum

Pancreatic divisum occurs when the distal 2/3 of the dorsal pancreatic duct fails to anastomose with the entire ventral pancreatic duct, resulting in an unformed major pancreatic duct. Pancreatic divisum results in two separate ductal systems: Larger dorsal pancreas derivatives (e.g. part of head, body, and tail) feed into the minor papillae, Smaller ventral pancreatic derivatives (e.g. uncinate process, part of head) feed into the major papillae. Pancreatic divisum is usually asymptomatic, occurring in 5% of people, but may result in recurring pancreatitis due to inadequate drainage of the dorsal pancreas by the small minor papillae.


Annular pancreas

Annular pancreas occurs when the ventral and dorsal pancreatic buds form a band of pancreatic tissue around the 2nd part of the duodenum, which may be asymptomatic or it may cause duodenal obstruction. Early indicators of an annular pancreas may include: Polyhydramnios (impaired ability to recycle amniotic fluid by blocking the GI tract), Duodenal obstruction, Recurrent bilious vomiting, Low birth weight, Impaired feeding


Spleen development

It arises in the mesentery of the stomach (hence is mesoderm is origin) but is supplied by the foregut (celiac artery)


retroperitoneal structures

The retroperitoneal structures include GI structures that lack a mesentery and non-GI structures. The retroperitoneal structures can be remembered by the mnemonic SAD PUCKER: Suprarenal (adrenal) glands, Aorta and IVC, Duodenum (2nd through 4th parts), Pancreas (except tail), Ureters, Colon (descending and ascending), Kidneys, Esophagus (thoracic portion), Rectum


falciform ligament

The falciform ligament connects the liver to the anterior abdominal wall. The falciform ligament is a derivative of the embryonic ventral mesentery. The falciform ligament contains the round ligament of the liver (ligamentum teres hepatis), which represents the remnant of the fetal umbilical vein. The round ligament of the liver also divides the liver into an anatomical right and left lobe.


lesser omentum

The lesser omentum is derived from embryonic ventral mesentery and is a double layered peritoneum that extends from the liver to the lesser curvature of the stomach and the first part of the duodenum. The lesser omentum consists of two ligaments: hepatogastric ligament and hepatoduodenal ligament


hepatoduodenal ligament

The hepatoduodenal ligament connects the liver to the duodenum. It borders the omental foramen, which connects the greater and lesser sacs. The hepatoduodenal ligament contains the portal triad, which includes the: Proper hepatic artery, Portal vein, Common bile duct. The Pringle maneuver is where the hepatoduodenal ligament is compressed between the thumb and index finger to control bleeding from the liver.


hepatogastric ligament

The hepatogastric ligament connects the liver to the lesser curvature of the stomach. It contains gastric arteries. The hepatogastric ligament separates the greater and lesser sacs and may be cut during surgery to access the lesser sac.


greater omentum

The greater omentum is derived from embryonic dorsal mesentery and is a four layered peritoneum that extends from the greater curvature of the stomach and drapes over the abdomen to cover the small intestines. The greater omentum consists of three ligaments: Gastrocolic ligament, Gastrosplenic ligament, Splenorenal ligament. The sole blood supply to the greater omentum are the right and left gastroepiploic vessels, which anastomose along the greater curvature of the stomach. The main functions of the greater omentum are: Intraperitoneal infection and wound isolation, Immune contribution through "milky spots" which are collections of macrophages, Fat storage


gastrocolic ligament

The gastrocolic ligament is part of the greater omentum. It connects the greater curvature of the stomach and the transverse colon. The gastrocolic ligament contains gastroepiploic arteries. The gastrosplenic ligament connects the greater curvature of the stomach to the spleen, and acts to separate the greater and lesser sacs on the left. The gastrosplenic ligament contains the short gastric vessels and the left gastroepiploic vessels.


splenorenal ligament

The splenorenal ligament connects the spleen to the posterior abdominal wall. It contains the splenic artery and vein as well as the tail of the pancreas.


Layers of gut wall

Layers of the gut wall (MSMS). Mucosa is the outer epithelium, lamina propria, and muscularis mucosa. Submucosa includes the submucosal nerve plexus (Meissner), and secretes fluid. Muscularis externa includes the myenteric nerve plexus (Auerbach), motility. Serosa (when intraperitoneal), adventitia (when retroperitoneal). Ulcers can extend into submucosa, inner or outer muscular layer.


Frequencies of the basal electric rhythm

Frequencies of the basal electric rhythm (slow waves) stomach (3 waves/min), duodenum 12 waves/min, ileum (8-9 waves/min).


Esophagus histology

Nonkeratinized stratified squamous epithelium


Stomach histology

Gastric glands


Duodenum histology

Villi and microvilli increases absorptive surface. Brunner glands (HCO3 secreting cells of submucosa) and crypts of Lieberkuhn.


Jejnum histology

Plicae circulares and crypts of Lieberkulhn.


Ileum histology

Peyer patches (lymphoid aggregates in lamina propria, submucosa), plicae circulares (proximal ileum), and crypts of Lieberkuhn.


Colon histology

Colon has cryptes of Lieberkuhn but no villi, abundant goblet goblet cells.


level of celiac trunk branch off the aorta

T12, the left inferior phrenic artery also branches at this level


level of superior mesenteric branch off the aorta

L1, the left middle suprarenal artery also branches at this level


level of renal branch off the aorta



level of inferior mesenteric branch off the aorta



level of bifurcation of abdominal aorta

L4 (bifourcation)


location of testicular/ ovarian branch off the aorta

In-between the renal artery and the inferior mesenteric artery


Abdominal aorta and branches

Arteries supplying GI structures branch anteriorly. Arteries suppluing non-GI structures branch laterally.


Superior mesenteric artery (SMA) syndrome

It occurs when the transverse portion (third part) of the duodenum is entrapped between SMA and aorta, causing intestinal obstructions.


Foregut blood supply and innervation

The celiac artery for blood supply, the vagus nerve for parasympathetic innervation. Vertebral level is T12/L1. Structures include the pharynx (vagus nerve only) and lower esophagus (celiac artery only) to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)


Midgut blood supply and innervation

The superior mesenteric artery for blood supply, the vagus nerve for parasympathetic innervation. Vertebral level is L1. Structures include the distal duodenum to proximal 2/3 of the transverse colon


Hindgut blood supply and innervation

The inferior mesenteric artery for blood supply, the pelvic nerve for parasympathetic innervation. Vertebral level is L3. Structures include the distal 1/3 of transverse colon to upper portion of rectum; splenic flexure is a watershed region between the superior mesenteric artery and the inferior mesenteric artery.


celiac trunk

The celiac trunk is the first large unpaired branch of the abdominal aorta. It arises at the level of T12 and travels anteriorly for ~1cm before branching into 3 arteries: Left gastric a, Splenic a, Common hepatic a.


Common hepatic artery

The common hepatic a. travels right along the duodenum and gives rise to the proper hepatic a. and the gastroduodenal a. The right gastric artery has variable origins and can arise from the common hepatic artery or the proper hepatic artery. Origin varies person to person and by source.


Proper hepatic a

The proper hepatic a. is an ascending branch which travels with the common bile duct and hepatic portal vein within the hepatoduodenal ligament. The proper hepatic a. gives has 3 main branches: Right hepatic a. (Gives rise to the cystic a.), Left hepatic a., Right gastric a. (Travels within the lesser curvature of the stomach and anastomoses with the left gastric a.). The right gastric artery has variable origins and can arise from the common hepatic artery or the proper hepatic artery. Origin of the artery varies person to person and by source.


Gastroduodenal a.

The gastroduodenal a. is a descending branch of the common hepatic a. and splits to form two arteries: Superior pancreaticoduodenal a. and the tight gastroepiploic a. Superior pancreaticoduodenal a. further divides into anterior-superior and posterior-superior branches that descend to supply the head of the pancreas and the proximal duodenum. Right gastroepiploic a. courses along the greater curvature of the stomach within the greater omentum and anastomoses with the left gastroepiploic a. (branch of the splenic a.)


Splenic a.

The splenic a. travels a tortuous path to the left along the superior border of the pancreas. The artery then passes within the splenorenal ligament to enter the hilum of the spleen. The splenic a. gives rise to the following major named branches: Left gastroepiploic a., Short gastric aa., Greater pancreatic a., and Dorsal pancreatic a. Left gastroepiploic a. courses to the right along the greater curvature of the stomach within the greater omentum and anastomoses with the right gastroepiploic a. Short gastric aa. supplies the fundus of the stomach. Greater pancreatic a. is the largest artery supplying the pancreas. Dorsal pancreatic a. forms an anastamosis with the superior pancreaticoduodenal artery. The splenic artery gives off many small branches that supply the pancreas.


Left gastric a.

The left gastric a. runs along the lesser curvature of the stomach and gives off the esophageal branches.


Celiac trunk anastomoses

There are 3 main anastomoses to the celiac vasculature. Two anastomoses involve the greater and lesser curvatures of the stomach, and the last anastomosis involves the celiac a. to the superior mesenteric artery (SMA). Anastomoses are made between the corresponding superior and inferior branches.


Anastomoses of the lesser curvature of the stomach

The lesser curvature of the stomach is supplied by the right gastric a. (branch of proper hepatic a.) and left gastric a.


Anastomoses of the greater curvature of the stomach

The greater curvature of the stomach is supplied by the right gastroepiploic a. (branch of gastroduodenal a.) and left gastroepiploic a. (branch of splenic a.)


Anastomosis between the superior and inferior pancreaticoduodenal aa.

The last anastomosis is between the superior and inferior pancreaticoduodenal aa. Superior pancreaticoduodenal a. is a branch of gastroduodenal a., which branches to form the anterior-superior pancreaticoduodenal and posterior-superior pancreaticoduodenal arteries, Inferior pancreaticoduodenal a. is a branch of the superior mesenteric a. and branches to form the anterior-inferior pancreaticoduodenal and posterior-inferior pancreaticoduodenal arteries


Blood supply of liver

The liver has a dual blood supply which includes the hepatic portal v. and the hepatic a.. The hepatic portal vein carries nutrients and drugs absorbed from the GI tract. The hepatic artery carries oxygen rich blood from the heart to supply the metabolic needs of the hepatocytes. These two blood supplies branch into the portal triads where they are taken to the hepatic sinusoids.


Anastomosis of the esophogus

This is an anastamosis between the portal and systemic venous circulation, connecting left gastric vein (portal) with azygous/ esophagus vein (systemic).


Anastomosis of the umbilics

The anastomosis is between the paraumbilical (portal) and small epigastric veins of the anterior abdominal call.


Portosystemic anastomoses

Varices of the gut, butt, and caput (medusae) are commonly seen with portal hypertension. The treatment includes a transjugular intrahepatic portosystemic shunt (TIPS) between the portal vein and the hepatic vein relieves portal hypertension by shunting blood to the systemic circulation, bypassing the liver.


The pectinate line

The pectinate line forms the junction between hindgut and embryonic ectoderm derivative. The innervation, arterial blood supply, venous drainage and mucosal lining are different superior and inferior to the line. The venous drainage and innervation of the anal canal helps explain internal vs. external hemorrhoids.


Superior to the pectinate line

Superior to the pectinate line the anal canal has a simple columnar epithelium. It is supplied by the superior rectal artery off of the inferior mesenteric artery (IMA) and drained via the superior rectal vein (which drains via the portal system). It is innervated by the sympathetic and parasympathetic branches of the inferior hypogastric plexus (pelvic plexus). Internal hemorrhoids (superior to the pectinate line) can form as a result of portal hypertension, constipation, increased intra-abdominal pressure, prolonged straining, and pregnancy. They are relatively painless because of its visceral innervation from the inferior hypogastric plexus. Structures proximal to the pectinate line drain into the inferior mesenteric vein (IMV) providing the connection to the portal system.


Inferior to the pectinate line

Inferior to the pectinate line, the anal canal is characterized by non-keratinized stratified squamous epithelium and receives blood supply from the inferior rectal vein/artery/nerve (VAN) off of the pudendal VAN. External hemorrhoids (inferior to the pectinate line) can form as a result of varicosities in the systemic venous system. They are relatively painful because the nerve supply inferior to the pectinate line is somatic branches of the pudendal nerve. Structures distal to the pectinate line drain into the internal iliac veins and do not directly enter the portal system.


Anal fissure

An anal fissure is tear in the anal mucosa below the Pectinate line. Patients appear to have Pain while Pooping, blood on toilet Paper, and is located Posteriorly because this area is Poorly Perfused.


Liver anatomy

The liver parenchyma consists of hepatocytes. The liver stroma consists of reticular fibers (type III collagen). It begins with the Glisson capsule, which surrounds the entire liver, and extends into the space of Disse. Bile manufactured in hepatocytes flows along bile canaliculi, opposite to the flow of blood, into bile ducts. Bile ducts combine to form the right and left bile ducts of the right and left lobes of the liver, which feed into the biliary tree. Bile ducts, portal veins, and hepatic arteries form portal triads.


Zones of the hepatic acinus

The hepatic acinus consists of a diamond-shaped mass of hepatocytes with corners at 2 hepatic arterioles and 2 portal venules. It is divided into three concentric metabolic zones spreading away from the portal triad. These zones follow the gradient of metabolites, nutrients, and hormones, which are highest in density closest to the portal triad (zone 1), and lowest at the central veins (zone 3). Injury to the liver causes predictable pathological patterns of the three zones (i.e., centrilobular necrosis indicates a lesion around the central vein, in zone 3; periportal fibrosis indicates fibrosis around the portal triad, in zone 1).


Zone 1

Zone 1 is closest to the portal triad, highly oxygenated, and carries out processes most dependent upon oxygen such as: Gluconeogenesis, Beta-oxidation of fatty acids, Cholesterol synthesis. Hepatotoxicity induced by viral hepatitis and cocaine first affects zone 1 (periportal zone) of the liver.


Zone 2

Zone 2 is the transition between zones 1 and 3 and is affected in yellow fever.


Zone 3

Zone 3 is poorly oxygenated and is the: First site affected by ischemia, Most sensitive to metabolic toxins, Site of alcoholic hepatitis, Site of detoxification (location of the highest concentration of cytochrome P450 enzymes), Glycolysis, Lipogenesis


Kupffer cells

Kupffer cells are the monocyte/macrophage cells of the liver. They are the first line against infection or toxins in the liver.


Biliary structures

The gallbladder is a pear-shaped sac that underlies the right lobe of the liver (between the right and quadrate lobes). The common hepatic duct descends from the liver where it is joined by the cystic duct from the gallbladder, forming the common bile duct. The bile duct continues to descend before joining with the pancreatic duct at the major duodenal papilla. Here, bile and pancreatic secretions enter the descending part of the duodenum. The Sphincter of Oddi controls secretions from the Ampulla of Vater into duodenum. Viewed from the duodenal lumen, the Sphincter of Oddi and Ampulla of Vater also mark the transition from embryologic foregut (supplied by celiac artery) to midgut (supplied by superior mesenteric artery). Gallstones that reach the confluence of the common bile and pacreatic duct at the ampulla of Vater can block both the common bile and pancreatic ducts (double duct sign), causing both cholangitis and pancreatis, respectively. Tumors that arise in the head of the pancreas can cause obstruction of common bile duct along causing painless jaundice.


Femoral triangle

The femoral triangle is an anatomical space inferior to the inguinal ligament which spans between the iliac crest and pubic tubercle, and is bounded laterally by the sartorius m. and medially by the adductor longus m. From lateral to medial, the contents of the femoral triangle are the: Femoral Nerve, Femoral Artery, Femoral Vein, Empty space filled by the femoral canal, and Lymphatics. Mnemonic: NAVEL, Venous near the penis. The lymphatics are found within the femoral canal. The "E" of the mnemonic stands as a reminder that the femoral canal is medial to the femoral nerve, artery, and vein.


The femoral sheath

The femoral sheath contains the femoral a., femoral v., and femoral canal. The femoral canal contains some inguinal lymphatics and nodes, and is a potential site for hernias. Femoral hernias occur when a loop of intestine passes through the femoral ring and into the femoral canal. It occurs more commonly in females. The vessels in the femoral triangle are superficial. The femoral vein can be used for venous access (for lab draws, drugs, nutrition) and is a route used for right coronary angiography. It is crucial to understand the location of the inguinal and femoral canal. The inguinal canal runs superior to the inguinal ligament in a superficial medial direction. The femoral vessels (and the canal) run deep to it at a right angle.


The inguinal canal

The inguinal canal is a fascial tunnel at the inferior border of the anterior abdominal wall mainly formed by the aponeurosis of the external oblique. The external oblique aponeurosis forms its anterior wall of the inguinal canal. The inguinal canal contains the spermatic cord (in males) or round ligament of the uterus (females) and the ilio-Inguinal nerve (both sexes). The path of the inguinal canal can be approximated by the inguinal ligament, which forms its floor. The inguinal canal is comprised of a superficial and a deep ring.


The superficial ring

The superficial ring marks the end of the inguinal canal at the anterior abdomen. It is formed by the aponeurosis of the external oblique muscle and resides lateral to the pubic tubercle and superior to the pubic crest.


Boundaries of the inguinal canal

Anterior wall: Aponeurosis of internal and external oblique. Posterior wall: Aponeurosis of transverse abdominal muscle and fascia. Superior wall: Muscle fibers from the transverse abdominal and internal oblique muscles. Inferior wall: Lacunar and inguinal lacunar ligaments. Some sources may refer to the superior wall as the roof and inferior wall as the floor. These terms are interchangeable.


The deep ring

The deep ring is the entrance to the inguinal canal and is formed by the evagination of the transversalis fascia. It is found lateral to the inferior epigastric a. at the midpoint along the inguinal ligament, which is midway between the anterior superior iliac spine (ASIS) and pubic tubercle. An indirect hernia is a hernia that goes through the deep ring and is the most common type of inguinal hernia.


The inguinal (Hesselbach’s) triangle

The inguinal (Hesselbach’s) triangle is the site of direct inguinal hernias. The borders of the inguinal triangle are: Lateral: Inferior epigastric a. Medial: Lateral portion of rectus abdominis m. (linea semilunaris). Inferior: Inguinal ligament.


Femoral hernias

Femoral hernias protrude through the femoral canal, below the inguinal ligament. Femoral hernias more common in females because of the wider pelvis shape. Femoral hernias have the highest rate of intestinal incarceration.


diaphragmatic hernias

In diaphragmatic hernias, intraabdominal contents enter the thorax. Specifically, hiatal hernia is protrusion of the stomach through the esophageal hiatus into the thorax. The majority of hiatal hernias are asymptomatic. The most common symptom is acid reflux. Congenital diaphragmatic hernias occur as a result of abnormal development of the pleuroperitoneal membrane. Abdominal contents will spill into the thorax, depending on the location of the defect. The defect in congenital diaphragmatic hernias is commonly on the left posterolateral part of the diaphragm. This defect allows abdominal viscera to herniate into the thorax. Discontinuity of diaphragm causes pulmonary hypoplasia and hypertension, which presents as neonatal respiratory distress. Possible abnormalities visualized include: Absence of the stomach below the diaphragm, Fluid-filled stomach behind left atrium, Abdominal contents (bowel, liver) in the thorax, Displacement of the lungs due to herniated bowel.


sliding hiatal hernia

Most common type of hiatal hernia is sliding hiatal hernia, where the gastroesophageal (GE) junction and the proximal part of the stomach are above the level of the diaphragm. These structures enter the thorax via the diaphragmatic esophageal hiatus, forming a bell-shaped dilation, commonly referred to as the "hourglass stomach."


paraesophageal hernia

In paraesophageal hernia, the GE junction is normal and remains intra-abdominal (at the level of the diaphragm). A part of stomach (commonly the fundus) enters the widened hiatus into the thorax.


Direct inguinal hernias

Direct hernias “punch through" the floor of the inguinal canal through the external superficial inguinal ring. Direct hernias lie medial to the inferior epigastric vessels. Direct inguinal hernias occur in Hesselbach’s triangle. Direct inguinal hernias occur in both males and females, but are 10 times more likely to occur in men. The "punch through" nature makes this more common in older men, as the abdominal wall weakens. A mnemonic to help you remember the relationship between the inguinal hernias is MDs don't LIe: Medial to inferior epigastric artery = Direct hernia. Lateral to inferior epigastric artery = Indirect hernia


indirect inguinal hernia

An indirect inguinal hernia enters the inguinal canal at the deep inguinal ring and passes inferomedially to emerge via the superficial ring. If it is large enough, it extends into the scrotum. Indirect hernias lie lateral to the inferior epigastric vessels. These are usually from the persistence of the processus vaginalis, which should normally close. Three types of indirect inguinal hernias exist, which are based on how far the herniation has reached. Bubonocele hernias are limited to inguinal canal. Funicular are a result of herniation down to the epididymis, but remain separate from it. Complete hernias result from a fully patent processus vaginalis, which allows herniation to be continuous with the tunica vaginalis of the testes. While this hernia can occur in females, it is much more common in males due to the descent pathway of the testes. Indirect inguinal hernias predispose male patients to hydrocele.



Gastrin acts to increase gastric acid secretion, increase growth of gastric mucosa, and increase gastric motility. Gastrin is produced by G cells in antrum of stomach. The stimuli for gastrin secretion include presence of protein-digestion products (i.e. small peptides, amino acids), mechanical distention of the stomach, vagal stimulation. Gastrin secretion is inhibited by gastric pH of 1.5 or less, somatostatin, secretin, gastrin may be increased outside of normal physiologic stimuli in Zollinger-Ellison syndrome, where there are a gastrin-secreting neuroendocrine tumors of the pancreas or small intestine. It also occurs in chronic atrophic gastritis from H. pylori and chronic proton pump inhibitor (PPI) use. Gastrin increases acid secretion primarily through its effects on enterochrommaffin-like (ECL) cells (leading to histamine release) rather than through its direct effect on parietal cells.



The general effect of somatostatin on the gastrointestinal (GI) system is a decrease in most GI secretions and hormone release. Mnemonic: SomatoSTOPin. Specific GI functions is to decrease gastric acid and pepsinogen secretion, decrease pancreatic and small intestine fluid secretion, decrease gallbladder contraction, decrease insulin and glucagon release, decreases GI hormones. Other effects of somatostatin, outside the GI system, include decreasing anterior pituitary release of growth hormone (GH), thyroid stimulating hormone (TSH), and prolactin. Somatostatin is produced by D cells of pancreatic islets and intestinal mucosa as well as neuroendocrine neurons in hypothalamus. Somatostatin secretion is stimulated by acid. Somatostatin secretion is decreased by vagal stimulation. Octreotide is a synthetic analogue of somatostatin use to treat acromegaly, insulinoma, carcinoid syndrome, variceal bleeding, and VIPoma



Secretin acts to increase pancreatic HCO3- secretion, allowing for neutralization of the gastric acid in the duodenum and function of pancreatic enzymes; decrease gastric acid secretion; increase bile secretion. Secretin is produced by S cells in the duodenum. Secretin secretion is stimulated by acid and fatty acids in the lumen of the duodenum.


Cholecystokinin (CCK)

Cholecystokinin (CCK) acts to increase pancreatic secretion, increase gallbladder contraction, decrease gastric emptying, increase relaxation of the sphincter of Oddi. CCK is produced by I cells in the duodenum and jejunum. CCK secretion is stimulated by fatty acids and amino acids. CCK acts on neural muscarinic pathways to cause pancreatic secretion.



The effect of histamine on the parietal cells of the stomach can cause increased gastric acid secretion. Histamine is produced by mucosal mast cells and enterochromaffin-like (ECL) cells. Histamine secretion is stimulated by gastrin and acetylcholine. Gastrin acts on ECL cell to cause histamine release.


Vasoactive intestinal peptide (VIP)

Vasoactive intestinal peptide (VIP) acts to increase the secretion of intestinal water and electrolytes, relax intestinal smooth muscle and sphincters, and inhibit gastric acid secretion. VIP is produced by the parasympathetic ganglia in sphincters, the gallbladder, and small intestine. VIP secretion is stimulated by intestinal distention and vagal stimulation. VIPomas are tumors of cells secreting VIP. The increased pancreatic secretions and increased GI relaxation result in severe diarrhea, which can in turn cause hypokalemia and achlorhydria. VIPoma is also termed “WDHA syndrome” for Watery, Diarrhea, Hypokalemia, Achlorhydria


Gastric inhibitory peptide (GIP)

Gastric inhibitory peptide (glucose-dependent insulinotropic peptide, GIP) has an endocrine function to stimulate insulin release and an exocrine function to decrease acid secretion. GIP is produced by K cells of the duodenum and jejunum. GIP secretion is stimulated by the presence of the following substances in the small intestine: fatty acids, amino acids, and orally ingested glucose. Oral glucose is more effective than intravenous glucose in causing insulin release due to GIP secretion.



Motilin is a hormone released cyclically from M cells in the small intestine (not the M cells in Peyer's patches). Motilin mediates the migrating motor complex (MMC) during the inter-digestive phase.


Nitric oxide

NO increase smooth muscle relaxation, including the lower esophageal sphincter (LES). The loss of NO secretion is implicated in increased LES tone.



Pepsinogen is secreted as a proenzyme by chief cells of the stomach. Pepsinogen is cleaved by HCl into active pepsin, which degrades proteins. Pepsin acts through a positive feedback mechanism in catalyzing more pepsinogen conversion to pepsin.


Gastric acid secretion

H+ is secreted by parietal cells of the stomach in an active process mediated by H+/K+-ATPase. Chloride is secreted through a separate channel to combine with H+ from the H+/K+-ATPase to form HCl. HCO3- produced in the parietal cells by carbonic anhydrase is transported across the basolateral membrane in exchange for Cl-. The rise in blood pH following reabsorption of HCO3- is known as the “alkaline tide." The H+/K+-ATPase pumps 1 K+ ion into the cell in exchange for 1 H+ ion that goes into the gastric lumen. Proton pump inhibitors (omeprazole, pantoprazole) target the H+/K+-ATPase. H+ secretion by parietal cells is increased by acetylcholine (neurocrine), gastrin (endocrine), histamine (paracrine), gastrin-releasing peptide (GRP), which acts to increase gastrin secretion


HCO3- secretion

It is secreted by mucosal cells (in the stomach, duodenum, salivary glands, and pancreas) and Brunner glands (in the duodenum). It neutralizes acid. Secretion is increased by pancreatic and biliary secretion with secretin. HCO3- is trapped in mucus that covers the gastric epithelium


Intrinsic Factor (IF)

Intrinsic Factor (IF) is important for absorption of Vitamin B12 in the terminal ileum. Lack of gastric parietal cells, which produce intrinsic factor, results in pernicious anemia.


Parietal (oxyntic) cells

Larger eosinophilic cells that secrete hydrochloric acid (HCl) and intrinsic factor (IF). Receptor include M3 (Gq, binds ACh), CCKb receptor (Gq, binds gastrin), H2 receptors (Gs, histamine), prostaglandins receptors (Gi), and somatostatin receptors (Gi).


Pancreatic secretions

All pancreatic secretions, like all digestive secretions below the stomach, are isotonic. Pancreatic secretions are high volume, have much higher [HCO3-], much lower [Cl-] and equal [Na+] and [K+] relative to plasma. They also contain digestive enzymes (amylase, lipase, protease). Flow rate alters the composition of pancreatic secretions. At a low flow rate, isotonic fluid is composed mostly of Na+ and Cl-. At a high flow rate, isotonic fluid is composed mostly of Na+ and HCO3-. Cl- and HCO3- content are inversely related, but total Cl- and HCO3- are constant. Pancreatic acinar cells produce initial secretions. Ductal cells modify these secretions by secreting HCO3- and absorbing Cl-.



α-Amylase hydrolyzes the internal α-1,4 glycosidic bonds in the polysaccharide chain of starch, forming disaccharides and trisaccharides.



Lipases aid in the digestion of fat.



Proteases are secreted as zymogens, and are activated by trypsin. Proteases that are secreted as zymogens include trypsin, chymotrypsin, elastase, carboxypeptidases



It is converted to active enzyme trypsin causing activation of other proenzymes and cleaving of additional trypsinogen molecules into active trypsin (positive feedback loop). It is converted to trypsin by enterokinase/ enteropeptidase, a brush border enzyme on duodenal and jejunal mucosa.


Carbohydrate absorption

Only monosaccharides (glucose, galactase, fructose) are absorbed by enterocytes. Glucose and galgactose are taken up by SGLT1 (Na dependent). Fructose is taken up by facilitated diffusion by GLUT-5. All are transported by GLUT-2. D-xylose absorption test distinguishes GI mucosal damage from other causes of malabsorption.


Iron absorption

Absorbed as Fe in duodenum.


Folate absorption

Absorbed in small bowel


B12 absorption

Absorbed in terminal ileum along with bile salts, requires intrinsic factor.


Peyer patches

Unencapsulated lymphoid tissue is found in the lamina propria and submucosa of ileum. It contains specialized M cells that sample and present antigens to immune cells. C cells stimulated in germinal centers of Peyer patches, differentiate into IgA-secreting plasma cells, which ultimately reside in lamina propria. IgA receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen.



It is composed of bile salts (bile acids conjugated to glycine or taurine, making them water soluble), phospholipids, cholesterol, bilirubin, water, and ions. Cholesterol 7 alpha-hydroxylase catalyzes rate-limiting step of bile synthesis. Functions include digestion and absorption of lipids and fat-soluble vitamins, cholesterol excretion (its the body's only means of eliminating cholesterol), and antimicrobial activity (via membrane disruption).


Unconjugated bilirubin

Heme is metabolized by heme oxygenase to biliverdin, which is subsequently reduced to bilirubin. Unconjugated bilirubin is removed from the blood by the liver, conjugated with glucuronate, and excreted in bile. Bilirubin is taken up by the liver and conjugated with glucuronic acid by uridine diphosphate glucuronyl transferase (UDP-glucuronosyltransferase) in the endoplasmic reticulum (forming conjugated bilirubin).


Conjugated bilirubin

Conjugated bilirubin is released from the liver, where it travels relatively undisturbed to the colon. Once in contact with the enteric flora of the colon, it is rapidly deconjugated and released for metabolism by anaerobic bacteria. Some of the important by-products of this metabolism include urobilinogens and stercobilinogens (which are in turn metabolized to urobilins and stercobilins and excreted in feces (80%), which give color to stool). 20% is reabsorbed; 10% of that is excreted as urobilin in the kidney, which gives it its yellow color, the other 90% reenter the enterohepatic circulation.


Pleomorphic salivary gland adenoma

It is a benign mixed tumor, the most common salivary tumor. It presents as a painless, mobile mass. It is composed of chondromyxoid stroma and epithelium and recurs if incompletely excised or ruptured intraoperatively.


Mucoepidermoid salivary gland

It is the most common malignant salivary gland tumor. It has mucinous and squamous components. It typically presents as a painless, slow growing mass.


Warthin tumor

Also called papillary cystadenoma lymphomatosum. It is a benign cystic tumor of the salivary gland. It has germinal centers.



Failure of relaxation of LES due to loss of myenteric (Auerbach) plexus. High LES resting pressure and uncoordinated peristalsis causing progressive dysphagia to solids and liquids (vs obstruction, which is solids only). Barium swallow shows dilated esophagus with an area of distal stenosis. It is associated with an increase risk of esophageal squamous cell carcinoma. Birds beak is seen on barium swallow. Secondary achalasia may arise from Chagas disease (T. cruzi infection) or malignancies (mass effect or paraneoplastic).


Boerhaave syndrome

Boerhaave syndrome is characterized by a transmural rupture of the distal esophagus that is most commonly caused by vomiting. Pneumomediastinum is a complication due to violent retching. This is a surgical emergency


Eosinophilic esophagitis

This is infiltration of eosinophils in the esophagus in atopic patients. Food allergens causes dysphagia, heartburn, strictures. It is unresponsive to GERD therapy.


Esophageal stricutres

It is associated with lye ingestion and acid reflex.


Esophageal varices

Dilated submucosal veins in the lower 1/3 of the esophagus secondary to portal hypertension. Common in alcoholics, may be a source of upper GI bleeding.



It is associated with reflux, infection in immunocompromised (candida: white pseudomembrane; HSV-1: punched out ulcers; CMV: linear ulcers), or chemical ingestion.


Gastroesophageal reflux disease

It commonly presents as heartburn and regurgitation upon lying down. It may also present with nocturnal cough and dyspnea, adult-onset, asthma. There is a decrease in LES tone.


Mallory-Weiss syndrome

Mucosal lacerations at the gastroesophageal junction due to severe vomiting. It leads to hematemesis, It usually found in alcoholics and bulimics.


Plummer-Vison syndrome

It has a triad Dysphagia, Iron deficiency anemia, and Esophageal webs. It may be associated with glossitis. There is an increased risk esophageal squamous cell carcinoma (Plumbers DIE)


Sclerodermal esophageal dysmotility

Esophageal smooth muscle atrophy causes a decrease in LES pressure and dysmotility. This leads to acid reflux and dysphagia, which causes stricture, Barrett esophagus, and aspiration. It is apart CREST syndrome.


Barrett esophagus

This is glandular metaplasia. Replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (nonciliated columnar with goblet cells) in distal esophagus. It occurs due to chronic acid reflux (GERD). It is associated with esophagitis, esophageal ulcers, and an increase in esophageal adenocarcinoma.


Squamous cell esophageal carcinoma

Squamous cell carcinoma is a malignant proliferation of squamous cells that usually arises in the upper 2/3 of the esophagus. The most common form worldwide is squamous cell carcinoma.


Risk factors of esophageal carcinoma

Major risk factors of esophageal carcinoma include: Achalasia- squamous; Alcohol- squamous; Barret Esophagus- adeno; Cigarettes- both; Diverticula (e.g., Zenker)- squamous; Esophageal web (including Plummer-Vinson)- squamous; Familial- squamous; Fat (obesity)- adeno; GERD- adeno; Hot liquids (and other esophageal injury)- squamous


Adenocarcinoma esophageal carcinoma

Adenocarcinoma is most common in the United States. Adenocarcinoma is a malignant proliferation of glands that arises from preexisting Barrett esophagus and usually involves the lower 1/3 of the esophagus.


Erosive (acute) gastritis

Erosive (acute) gastritis occurs due to an imbalance between mucosal barrier and the acidic environment. Damage can include an ulcer (loss of mucosal layer, erosion (loss of superficial epithelium), or superficial inflammation. Risk factors for developing erosive gastritis include some of the following: NSAID use, which decreases PGE2 synthesis (most common); Alcohol, which causes direct mucosal damage; Burns (Curling ulcer), which causes ischemia due to hypovolemia; Brain injury (Cushing ulcer), where increased intracranial pressure causes increased vagal stimulation that leads to increased acid production; Chemotherapy; Bile reflux


Chronic gastritis

Nonerosive (chronic) gastritis is divided into two types, an autoimmune gastritis ("type A") and a Helicobacter pylori gastritis ("type B"). H. pylori gastritis is much more common.


Type A chronic gastritis

Type A, or chronic autoimmune gastritis, is characterized by an autoimmune destruction of gastric parietal cells and is associated with serum anti-parietal cell and anti-intrinsic factor antibodies. Type A chronic gastritis comes before Type B, so it occurs in the first part of the stomach (fundus/body). It is an Autoimmune disorder, Autoantibodies to parietal cells, Pernicious Anemia, and Achlorhydria


Type B chronic gastritis

Type B, or chronic H. pylori gastritis, is the most common form of chronic gastritis and is due to H. pylori induced inflammation. H. pylori commonly colonize the antrum and utilize proteases/ureases along with inflammation to weaken mucosal defenses. H. pylori does not invade. Individuals with chronic H. pylori gastritis present with epigastric pain and are at an increased risk for Peptic ulcer disease, Gastric adenocarcinoma (intestinal type), MALT lymphoma


Menetrier disease

Gastric hyerplasia of the mucosa causes hypertrophied rugae, excess mucus production with resultant protein loss and parietal cell atrophy with a decrease acid production. It is precancerous. Rugae of the stomach are so hypertrophied that they look like brain gyri.


Stomach cancer

It is most commonly gastric adenocarcinoma. There is also lymphoma and carcinoid (rare). There is early aggressive local spread with node/liver metastases. It often presents with weight loss early satiety, and in some cases acanthosis nigricans.


Intestinal gastric cancer

Intestinal gastric cancer is the most common subtype of stomach adenocarcinoma. It is frequently found on the lesser curvature of the pyloric antrum and appears as a large, irregular ulcer with raised mucosal margins. The most significant risk factor for the intestinal form of gastric cancer is intestinal metaplasia from chronic inflammation caused by H. pylori (major cause) and autoimmune gastritis. Other risk factors for intestinal gastric cancer include: Dietary nitrosamines, Smoking, Ulcers, Achlorhydria (low or absent gastric acid production), Type A blood


Diffuse gastric cancer

Diffuse subtype of gastric cancer is less common of stomach adenocarcinoma. In this subtype, signet ring cells diffusely penetrate the gastric wall. Signet ring cells contain large mucin vacuoles that displace the nucleus to the periphery. The signet ring cells cause the gastric wall to thicken, leading to what is called “leather bottle stomach” or "linitis plastica" because as food digests, the stomach does not stretch out. Diffuse gastric cancer has no association with H. pylori, nitrosamines, or intestinal metaplasia.


Virchow node

There is involvement of the left supraclavicular node by metastasis from the stomach.


Krukenberg tumor

Bilateral metastases from the stomach to the ovaries. There are abundant mucin-secreting, signet ring cells.


Sister Mary Joseph nodule

Subcutaneous periumbilical metastasis from the stomach.


Gastric Ulcer

The pain can be greater with meals. There can also be weight loss. There is an H pylori in 70% of cases. It occurs due to a decrease in mucosal protection against gastric acid. Other causes include NSAIDs. There is an increase risk of carcinoma. Biopsy margins can rule out malignancy.


Duodenal ulcer

The pain decreases with meals and there is weight gain. H. pylori is present in almost 100% of cases. It occurs due to a decrease in mucosal protection or an increase of gastric secretion. Other causes include Zollinger-Ellison syndrome. It is generally benign and there is no increase in carcinoma. Histology will show hypertrophy of Brunner glands.


Ulcer complications

Hemorrhage can occur due to gastric or duodenal ulcers (posterior ulcers more commonly than anterior). Ruptured gastric ulcer on the lesser curvature of the stomach causes bleeding from the left gastric artery. An ulcer on the posterior wall of duodenum causes bleeding from the gastroduodenal. A duodenal (anterior more than posterior) ulcer can also cause perforation. It may be seen from from free air under diaphragm with referred pain to the shoulder via phrenic nerve.


Malabsorption syndromes

They can cause diarrhea, steatorrhea, weight loss, vitamin and mineral deficiencies.


Celiac disease

This is an autoimmune-mediated intolerance of gliadin (gluten protein found in wheat) causes malabsorption and steatorrhea. It is associated with HLA-DQ2, HLA-DQ8, northern European descent, dermatitis herpetiformis, and a decrease in bone density. Findings include anti-endomysial, anti-tissue transglutaminase, and anti-gliadin antibodies. There is blunting of villi and lymphocytes in the lamina propria. There is a moderate increase in risk of malignancy (eg T cell lymphoma). A decrease in mucosal absorption primarily affects the distal duodenum and/or proximal jejunum. Treatment is a gluten free diet.


Diasccharidase deficiency

The most common type is lactase deficiency, which causes milk intolerance. There are normal appearing villi and osmotic diarrhea. Since lactose is located the the tips of intestinal villi, self limited lactase deficiency can occur following injury (viral enteritis). Lactose tolerance test is positive for lactose deficiency if administration of lactose produces symptoms and serum glucose rises less than 20 mg/dL.


Pancreatic insufficiency

It can occur due to cystic fibrosis, obstructing cancer, chronic pancreatitis. It can causes malabsorption of fat and fat soluble vitamins as well as vitamin B12. It increase neutral fat in stool. D-xylose absorption test will show normal urinary excretion in pancreatic insufficiency. There is a decrease in excretion with intestinal mucosa defects ow with bacterial overgrowth.


Tropical sprue

It has similar findings as celiac sprue (affects small bowel), but it responds to antibiotics. The cause is unknown but is seen in residents of or recent visitors to the tropics.


Whipple disease

It occurs due to infection with Tropheryma whipplei (gram positive). PAS positive with foamy macrophages in intestinal lamina propria and mesenteric nodes. There are cardiac symptoms, arthalgias, and neurologic symptoms. It most commonly occurs in older men. FOAMY WHIPPed cream in a CAN (cardiac, arthalgias, and neurologic).


Location of Crohn disease

It can affect any portion of the GI tract, usually occuring in the terminal ileum and colon. There are skip lesions and rectal sparing.


Location of ulcerative colitis

Colon inflammation. Continuous colonic lesions, the rectum is always involved


Gross morphology of Crohn disease

There is transmural inflammation that can cause fistula. Cobblestone mucosa, creeping fat, bowel wall thickening (string sign on barium swallow xray), linear ulcers, and fissures.


Gross morphology of ulcerative colitis

Colonoscopy will typically show a friable erythematous mucosa, with or without ulcerations, and pseudopolyps, that extends continuously from the rectum to part of or the entire colon. Inflammation of the mucosa and submucosa only. The loss of haustra gives the lead pipe appearance on imaging.


Microscopic morphology of ulcerative colitis

Biopsy typically reveals inflammation limited to the submucosa and crypt abscesses. No granulomas (Th2 mediated).


Complications of ulcerative colitis

Complications of ulcerative colitis include: Increased risk of colorectal cancer. The risk begins 8-10 years after the initial diagnosis of panocolitis, and 12-15 years after the onset of left-sided colitis. At this time point, colonoscopies every 1-2 years with biopsies for dysplasia are recommended. Severe bleeding. Strictures. Colonic perforation. Toxic megacolon (colonic diameter ≥6 cm or cecum diameter >9 cm plus the presence of systemic toxicity). Malnutrition. Sclerosing cholangitis.


Manifestation of ulcerative colitis

Patients with ulcerative colitis classically present with symptoms of: Diarrhea, Abdominal cramping, Rectal bleeding, Rectal mucus discharge, Occasional tenesmus (feeling of incomplete evacuation of stools, despite an empty colon).


Extraintestinal manifestations of ulcerative colitis

Various extraintestinal symptoms have also been associated with ulcerative colitis, such as: Uveitis (inflammation of the middle layer of eye), Pyoderma gangrenosum (necrotic ulcerations of legs), Ankylosing spondylitis (chronic inflammation of the spine), Primary sclerosing cholangitis (sclerosis of both intrahepatic and extrahepatic bile ducts), Aphthous ulcers (small, shallow sore inside the mouth or at the base of the gums).


Treatment of ulcerative colitis

oral 5-aminosalicylic acid (5-ASA) medications (mesalazine, sulfasalazine), 6-mercaptopurine, infliximab, colectomy


Microscopic morphology of Crohn disease

Biopsy will also reveal transmural inflammation and granulomas (Th1 mediated), which are not seen with ulcerative colitis. There are also lymphoid aggregates.


Complications of Crohn disease

The major complications seen with CD are intestinal perforation, strictures (narrowing of lumen that leads to bowel obstruction), fistulas (including enterovesical fistulae, which can cause recurrent polymicrobial UTIs), sinus tracts, perineal disease, malabsoprtion, nutritional depletion, gallstones and the development of cancer in areas of inflammation such as the colon (if involved).


Manifestation of Crohn disease

Patients with CD typically present with “crampy” abdominal pain, diarrhea, fatigue, weight loss, and growth failure. Specific to children, growth failure is a particularly important presenting feature of Crohn’s disease; growth failure specifically refers to a vertical growth rate below the appropriate velocity for age.


Extraintestinal manifestations of Crohn disease

CD also can present with the same extraintestinal manifestations seen with ulcerative colitis, such as: Ankylosing spondylitis (arthritis of spine), Uveitis, Pyoderma gangrenosum, Erythema nodosum (flat, firm, hot, red, and painful lumps that usually appear on the shins), Calcium oxalate kidney stones due to increased absorption of oxalate, Gallstones with terminal ileum involvement due to decreased absorption of bile acids, Aphthous ulcers (small, shallow sore inside the mouth or at the base of the gums), migratory polyarthritis.


Treatment of Crohn disease

Severe CD is treated with steroids and DNA synthesis inhibitors (azathioprine or 6-mercaptopurine) and methotrexate. Biologic therapies are becoming more widely used. Infliximab (Remicade) and Adalimumab (Humira) are monoclonal antibodies against TNF-alpha, which is involved in systemic inflammation and stimulation of the acute phase reaction.


nemonic for Crohn disease

For Crohn, thick of a fat (creeping fat morphology) granny (granulomas) and an old crone skinning (skin lesions) down a cobblestone (mucosa) road away from the wreck (rectal sparing).


nemonic for ulcerative colitis

Causes ULCCCERS: ulcers, large intestine, continuous, colorectal carcinoma, crypt abscesses, extends proximally, red diarrhea, sclerosing cholangitis.


Irritable bowel syndrome (IBS)

Irritable bowel syndrome (IBS) is a syndrome characterized by chronic abdominal pain and altered bowel habits in the absence of any known physiological cause. IBS occurs more commonly in middle-aged women. IBS most commonly presents with no structural or histological findings. IBS is diagnosed based on the presence of recurrent abdominal pain or discomfort associated with 2 or more of the following: Pain improves upon defecation, Onset associated with a change in frequency of stool, Onset associated with a change in appearance of stool. IBS can be treated non-pharmacologically by an increased intake in fiber and avoidance of aggravating foods.



Acute inflammation of the appendix due to obstruction by a fecalith (in adults) or lymphoid hyperplasia (in children). There is initial diffuse periumbilical pain migrates to McBurney point (1/3 the distance from right anterior superior iliac spine to umbilicus). Nausea and fever. It may perforate, which can cause peritonitis. There are three common clinical signs that help identify acute appendicitis: Psoas sign (severe RLQ pain during right thigh extension due to the inflamed appendix irritating the peritoneum adjacent to the iliopsoas muscle group). Rovsing's sign (severe RLQ pain when pressure is applied to the left lower quadrant). McBurney's sign (severe RLQ pain with rebound tenderness when pressure is applied at McBurney's point).
Mnemonic: Please Remove My appendix. Treatment for appendicitis includes an appendectomy. Differential diagnosis includes diverticulitis (elderly), ectopic pregnancy (use beta hCG).



A blind pouch protruding from the alimentary tract that communicates with the lumen of the gut. Most (esophagus, stomach, duodenum, and colon) are acquired and are termed false in that they lack or have an attenuated muscularis externa. Most occur in the sigmoid colon.


True diverticulum

A true diverticulum involves all four layers of the wall, including the muscularis propria and adventitia. An example is a Meckel diverticulum.


False diverticulum (pseudodiverticulum)

A false diverticulum involves only the mucosa and submucosa. Diverticula occur where the vasa recta enters muscularis externa, which are areas of intrinsic weakness.



Diverticulosis is the presence of multiple colonic diverticula. It is common in people greater than 60 years of age. 70% of these patients are asymptomatic. These are false diverticula, as they don't involve all bowel wall layers. Diverticula formation is due to chronic increased intraluminal pressure from low-fiber diet (Western diet), hence the age-dependent prevalence. Diverticulosis most commonly occurs in the sigmoid colon. Complications include painless rectal bleeding, which typically resolves spontaneously, or progression to diverticulitis.



Diverticulitis is the acute inflammation of a diverticulum (mucosal outpouching of the bowel wall) of diverticulosis. This may be due to obstruction (fecal matter, undigested food particles), vascular compromise and perforation, or increased intraluminal pressure leading to erosion of the diverticular wall. Patients typically present with the triad of: Left lower quadrant or diffuse abdominal pain; Fever; Leukocytosis. Additional symptoms that patients may have are: Nausea, Vomiting, Constipation, Diarrhea. Rectal mass may be palpable if foci of inflammation are near the rectum. Complications of diverticulitis occur when persistent inflammation results in colonic obstruction, perforation, or abscess formation. It may also cause a colovesical fistual which can cause phenumaturia. Treat with antibiotics. It is sometimes called left sided appendicitis due to overlapping clinical presentation


Zenker diverticulum

Zenker diverticulum is an outpouching of the upper, posterior esophagus in a natural area of weakness known as Killian's triangle that is caused by increased intrabolus pressures during swallowing. The classic presentation is the regurgitation of food that was eaten days before because the food gets caught in the diverticulum itself, and remains there until regurgitated. Other symptoms of Zenker diverticulum include: Bad breath, Problems initiating swallowing, Neck mass that increases with size during eating and drinking (from contents filling the diverticulum), Feelings of aspiration, Dysphagia. Zenker diverticulum is diagnosed with a barium swallow, which will show the outpouching of the esophagus. Treatment is surgery.


Meckel diverticulum

It is a true diverticulum due to persistence of the vitelline duct. It may contain ectopic acid secreting gastric mucosa and/or pancreatic tissue. It is the most common congenital anomaly of the GI tract. It can cause melena, RLQ pain, intussusception, volvulus, or obstruction near the terminal ileum. In contrast with omphalomesenteric cyst, this is not cystic dilation of the vitelline duct. Diagnosis is based on a pertechnetate study for uptake by ectopic gastric mucosa. The five 2's: 2 inches long, 2 feet from the ileocecal valve, 2% of the population. It commonly presents in the first 2 years of life, it may have two types for epithelia (gastric/pancreatic).



Anomaly of midgut rotation during fetal development causing improper positioning of bowel, formation of fibrous bands (Ladd bands). It can lead to volvulus, duodenal obstruction.



Twisting of a postion of the bowel around its mesentery. It can lead to obstruction and infarction. It can occur throughout the GI tract. Midgut volvulus is more common in infants and children. Sigmoid volvulus are more common in the elderly.



Intussusception is the telescoping of a proximal part of the intestine into a distal portion. Intussusception at the ileocecal junction is the most common cause of small bowel obstruction in children between 6 and 36 months. The majority of cases of intussusception are idiopathic, but there is increasing evidence that viral or enteric infections may play a role in children. In adults, the most common cause is tumor within the intestinal tract. Children with intussusception classically present "red currant jelly" stools. Note that red currant jelly stools are also seen in acute mesenteric ischemia, which most commonly presents in adults, rather than children.


Hirschsprung disease

Hirschsprung disease is a megacolon due to local aperistalsis from the absence of ganglion cells in the Meissner submucosal plexus and Auerbach myenteric plexus usually due to a failure of migration of parasympathetic ganglion cells from the neural crest, most often in the distal sigmoid and rectum. It is also associated with RET gene mutations. The normal portion of the colon proximal to the aganglionic segment is dilated, resulting in a "transition zone." Hirschsprung disease is associated with Down syndrome and mutations in the RET gene. Patients with Hirschsprung disease present with: Bilious vomit, Abdominal distention, Empty rectal vault upon digital exam, Chronic constipation from failure to pass meconium. Diagnosis of Hirschsprung disease is made via rectal suction biopsy. Treatment surgical resection of affected segment.


Acute mesenteric ischemia

Acute mesenteric ischemia is a blockage of intestinal blood flow that can lead to small bowel necrosis. Emboli most commonly travel to the superior mesenteric artery (SMA).
The main symptoms of acute mesenteric ischemia are pain disproportionate to physical findings and red "currant jelly" stools.



Adhesions are fibrous bands that form between tissues and organs, and are most commonly a result of injury during surgery. Adhesions can also occur with any intraabdominal process such as fistula's related to Crohns and diverticulitis with perforation.



Angiodysplasia is characterized by tortuous, deformed mucosal and submucosal blood vessels seen in the GI tract. Angiodysplasia most commonly presents as hematochezia in an elderly individual. Angiodysplasia is most often found in the: Terminal ileum, Cecum, Ascending colon. Diagnosis of angiodysplasia is confirmed by colonoscopy or angiography.


Duodenal atresia

Duodenal atresia is a condition where there is occlusion of the duodenal lumen secondary to failed recanalization. Duodenal atresia is associated with Down syndrome. Key clinical features of duodenal atresia include: Polyhydramnios, Bile-containing vomitus (since the obstruction is distal to the point where bile enters the gut), Double bubble appearance with no distal gas on plain radiographs


Necrotizing enterocolitis (NEC)

Necrotizing enterocolitis (NEC) is characterized by intestinal necrosis and is one of the most common gastrointestinal emergencies in newborns. NEC is often seen in premature, formula-fed infants with immature immune systems. Newborns with NEC can present with abdominal distention/tenderness and rectal bleeding (hematochezia). Diagnosis is made via clinical symptoms along with abdominal radiograph showing pneumatosis intestinalis (presence of gas in the bowel wall).



Intestinal hypomotility without obstruction, which causes constipation and a decrease in flatus. Findings include distended/tympanic abdomen with a decrease in bowel sounds. It is associated with abdominal surgeries, opiates, hypokalemia, sepsis. Treatment includes bowel rest, electrolyte correction, cholinergic drugs (stimulate intestinal motility).


Meconium ileus

Meconium ileus is a newborn bowel obstruction of the distal ileum due to an abnormally thick meconium. Meconium ileus is usually a complication in newborn cystic fibrosis. Due to the lack of NaCl, which limits the flow of water into intestinal lumen, the meconium can become abnormally thick and impacted. The thickened meconium obstructs distal-ileum, causing proximal dilatation, bowel wall thickening, and congestions.


Ischemic colitis

Ischemic colitis is an infarction of the bowel resulting from occlusion of blood flow in these arteries. Infarctions commonly occurs at "watershed areas" where the regions of different arteries overlap, including, near the splenic flexure and at the rectosigmoid junction.


Colonic polyps

Colonic polyps are abnormal, fleshy growths in the large intestine. 90% of colonic polyps are benign. They are divided into non-neoplastic and neoplastic polyps.


Hyperplastic colonic polyps

Non-neoplastic. Generally smaller and majority are located in the rectosigmoid area.


Hamartomatous polyps

Hamartomatous polyps are solitary non-neoplastic lesions that do not have a significant risk for malignant transformation. Hamartomatous polyps are composed of normal colonic tissue with distorted architecture. Hamartomatous polyps are associated with Peutz-Jeghers syndrome and juvenile polyposis.


Adenomatous colorectal polyps

Adenomatous polyps contain neoplastic proliferation of glands. The adenoma-carcinoma sequence describes the molecular progression from normal colonic mucosa to adenomatous polyp, and to carcinoma: APC mutations decrease intercellular adhesion and increases proliferation. This ultimately acts to increase the risk of an adenoma. KRAS mutation allows for unregulated intracellular signal transduction. This ultimately leads to the formation of an adenoma. p53 mutation (tumor suppressor gene) and increased expression of COX allows for increased tumorigenesis. This leads to a carcinoma. Aspirin can impede the progression from adenoma to carcinoma.


Serrated polyps

Serrated polyps are premalignant via the CpG hypermethylation phenotype pathway with microsatellite instability and mutations in BRAF. Biopsy of serrated polyps reveal "saw-tooth" pattern of crypts. Up to 20% of cases of sporadic colorectal cancer are due to serrated polyps.


Peutz-Jeghers syndrome (PJS)

Peutz-Jeghers syndrome (PJS) is an autosomal dominant disease that often involves mutations in a gene encoding a serine threonine kinase (STK11). Polyps are commonly found in the small intestine. PJS is characterized by multiple hamartomatous polyps and mucocutaneous hyper pigmentation, classically in the buccal mucosa. Peutz-Jeghers syndrome carries an increased risk of several malignancies: colon, pancreas, breast, lung, ovarian, uterine and testicular cancers. Thus, vigilant surveillance is recommended.


Familial adenomatous polyposis (PAP)

Autosomal dominant mutation of APC tumor suppressor gene on chromosome 5q. 2-hit hypothesis. 100% progress to CRC unless the colon is resected. Thousands of polyps arise starting after puberty. It is pancolonic and always involves the rectum.


Gardner syndrome

Gardner syndrome is similar to familial adenomatous polyposis, with large amounts of polyps in the colon. Bone and soft tissue tumors (osteomas of the mandible and skull, epidermal cysts, desmoid tumors) are also seen.


Turcot syndrome

In Turcot syndrome, an autosomal recessive disorder, colonic adenomas with high malignant potential are seen. These frequently become malignant in those below the age of 30. Malignant CNS tumors such as glioblastoma multiforme and medulloblastoma are also seen.


Juvenile polyposis

Juvenile polyposis consists of polyps in the colon, small bowel, and stomach. It is associated with painless rectal bleeding, rectal prolapse, and failure to thrive. Risk of malignancy is slightly increased later in life.


Lynch syndrome

Lynch syndrome, previously known as hereditary nonpolyposis colorectal cancer (HNPCC), is an autosomal dominant disorder that is caused by a germline mutation in one of several DNA mismatch repair (MMR) genes that causes microsatellite instability. The proximal colon is always involved in Lynch syndrome. In addition to colorectal cancer, patients with Lynch syndrome have an increased risk of the following malignancies: Endometrial, Ovarian, Skin. Lynch syndrome can be identified in families using the 3-2-1 rule: 3 relatives with Lynch syndrome, Associated cancers across 2 generations, 1 must be diagnosed before age 50.


Epidemiology of colorectal cancer

Most patients are over the age of 50 years old. About 25% have a family history.


Risk factors of colorectal cancer

Adenomatous and serrated polyps, familial cancer syndromes, IBD, tobacco use, diet of processed meat with low fiber.


Presentation of colorectal cancer

It occurs in the rectosigmoid more than the ascending colon and in the descending colon least frequently. Cancer in the ascending can cause an exophytic (tends to grow outward beyond the surface epithelium from which it originates) mass, iron deficiency anemia, and weight loss. Cancer in the descending cancer tends to be an infiltrating mass, partial obstruction, colicky pain, and hematochezia. Rarely it presents with Streptococcus bovis bacteria.


Diagnosis of colorectal cancer

Iron deficiency anemia in males (especially over the age of 50) and postmenopausal females raises suspicion. Screen patients over the age of 50 with colonoscopy, flexible sigmoidoscopy, or stool occult blood test. Apple core lesion is seen on barium enema xray. Carcinogenic embryonic antigen (CEA) can be used to monitor disease progression and recurrence, but is a poor screening test.


Molecular pathogenesis of colorectal cancer

There are 2 molecular pathways that lead to CRC: Microsatellite instability pathway (15%) involves DNA mismatch repair gene mutations (either sporadic or Lynch syndrome). Mutations accumulate, but no defined morphologic correlates. The APC/beta-catenin (chromosomal instability) pathway (85%), leading to sporadic cancer. The progression of mutations is as follows: Loss of the APC gene causes decreased intercellular adhesion and increased proliferation and puts the colon at risk. KRAS mutation causes unregulated intracellular signal transduction leading to adenoma. Loss of tumor supressor genes (p53, DCC) causes increased tumorgenesis leading to carcinoma.



Cirrhosis is a condition characterized by diffuse transformation of the hepatic architecture into regenerative parenchymal nodules surrounded by fibrous bands and varying degrees of vascular shunting. The three major features responsible for the signs and symptoms of cirrhosis are portal hypertension, impaired hepatic protein synthesis, and impaired hepatic detoxification.


Portal hypertension

Portal hypertension may result in some of the following complications: Ascites (fluid accumulation in the peritoneal cavity), Formation of portosystemic venous shunts (esophageal varices, caput medusae, and rectal varices), Congestive splenomegaly. Variceal hemorrhage (especially esophageal) is a major cause of mortality in portal hypertension. Patients typically present with hematemesis (vomiting of blood) and/or melena (blood in the stool).


Impaired hepatic protein synthesis

Impaired hepatic protein synthesis may result in some of the following complications: Hypoalbuminemia, Coagulopathies (due to decreased clotting factor synthesis), the degree of which can be measured clinically with a prothombin time (PT/INR).


Impaired hepatic detoxification

Impaired hepatic detoxification may result in some of the following complications: Hyperammonemia (NH3), leading to hepatic encephalopathy and asterixis, Hyperestrogenemia due to impaired estrogen metabolism, which in male patients who have progressed to chronic liver failure may lead to the development of palmar erythema (due to local vasodilation), spider angiomas, and gynecomastia. Hyperestrogenemia also leads to hypogonadism in both male and female patients.


Alkaline phosphatase (ALP)

A diagnostic marker for cholestatic and obstructive hepatobiliary disease, HCC, infiltrative disorders, and bone disease.


Aminotransferases (AST and ALT)

Often called liver enzymes. It is a diagnostic marker for viral hepatitis (ALT is greater than AST) and alcoholic hepatitis (AST is greater than ALT).



A marker for acute pancreatitis and mumps



It is decreased in Wilson disease.


Gamma-glutamyl transpeptidase (GGT)

It is increased in various liver and biliary diseases (just as ALP), but not in bone disease. It is associated with alcohol use.



It is a marker for acute pancreatitis (most specific).


Reye syndrome

Rare, often fatal childhood hepatic encephalopathy. Findings include mitochondiral abnormalities, fatty liver (microvesicular fatty change), hypoglycemia, vomiting, hepatomegaly, coma. It is associated with viral infection (especially VZV and influenza B) that has been treated with aspirin. Aspirin metabolites decrease beta oxidation by reversible inhibition of mitochondrial enzymes. Avoid aspirin in children, except in those with Kawaski disease.


Alcoholic liver disease

Marked by hepatic steatosis, alcoholic hepatitis, alcoholic cirrhosis


Hepatic steatosis

Seen in alcoholic liver disease. Macrovesicular fatty change that may be reversible with alcohol cessation.


Alcoholic hepatitis

Seen in alcoholic liver disease. Requires sustained, long- term consumption. There are swollen and necrotic hepatocytes with neutrophilic infiltration. Mallory bodies have intracytoplasmic eosinophilic inclusions of damaged keratin filaments. AST is usually 1.5 of ALT. (make a toAST with alcohol.)


Alcoholic cirrhosis

Final and irreversible form. Micronodular, irregularly shrunken liver with "hobnail" appearance appearance. Sclerosis around central vein (zone III). There is also manifestations of chronic liver disease (eg jaundice, hypoalbuninemia)


Non-alcoholic fatty liver disease

Metabolic syndrome (insulin resistance) causes fatty infiltration of hepatocytes leading to cellular ballooning and eventual necrosis. It is independent of alcohol use. ALT is greater than AST (Lipids).


Hepatic encephalopathy

Cirrhosis leads to portosystemic shunts, which decreases NH3 metabolism leading to neuropsychiatric dysfunction. The spectrum ranges from disorientation/ asterixis (mild) to difficult arousal or coma (severe). Triggers include an increase in NH3 production and absorption (due to dietary protein, GI bleed, constipation and infection) or a decrease in NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS). Treatment includes lactulose (increases NH4 generation leading to excretion) and rifaximin.


Hepatocellular carcinoma/hepatoma

It is the most common primary malignant tumor of liver in adults. It is associated with HBV (with or without cirrhosis) and all other causes of cirrhosis (including HCV, alcoholic and non-alcoholic fatty liver disease, autoimmune disease, hemochromatosis, alpha 1-antitrypsin deficiency, Wilson disease) and specific carcinogens (eg alfatoxin from Aspergillus). It may lead to Budd-Chiari syndrome. Findings includes jaundice, tender hepatomegaly, ascites, polycythemia, anorexia. It spread hematogenously. Diagnosis is based on increased alpha fetoprotein, ultrasound or contrast CT/MRI, biopsy.


Hepatic cavernous hemangioma

Common, benign liver tumor; typically occurs at age 30-50 years. Biopsy is contraindicated because of the risk of hemorrhage.


Hepatic adenoma

Rare, benign liver tumor, often related to oral contraceptive or anabolic steroid use. It may regress spontaneously or rupture (abdominal pain and shock).


Hepatic angiosarcoma

malignant tumor of endothelial origin. It is associated with exposure to arsenic, vinyl chloride.


Hepatic metastases

GI malignancies, breast and lung cancer. It is the most common site overall.


Budd-Chiari syndrome

Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis causes congestive liver disease (hepatomegaly, varices, abdominal pain, eventual liver failure). There is absence of JVD. It is associated with hypercoagulable states, polycythemia vera, postpartum state, HCC. It may cause nutmeg liver (mottled appearance).


Alpha 1-antitrypsin deficiency

Misfolded gene product protein aggregates in hepatocellular ER causes cirrhosis with PAS positive globules in the liver. Codominant trait. In lungs, a decrease in alpha 1 antitrypsin causes uninhibited elastase in alveoli, causing a decrease in elastic tissue, which leads to panacinar emphysema.



Abnormal yellowing of the skin and/or sclera due to bilirubin deposition. It occurs at high bilirubin levels (over 2.5 mg/dL) in blood secondary to an increase production or defective metabolism.


Unconjugated (indirect) hyperbilirubinemia

Hemolytic, physiologic (newborns), Crigler-Najjar, Gilbert syndrome.


Conjugated (direct) hyperbilirubinemia

Biliary tract obstruction due to gallstones, chalangiocarcinoma, pancreatic or liver cancer, liver fluke. Biliary tract disease includes primary sclerosing cholangitis and primary biliary cirrhosis. Excretion defect includes Dubin-Johnson syndrome and Rotor syndrome.


Mixed (direct and indirect) hyperbilirubinemia

Includes hepatitis and cirrhosis


Physiologic neonatal jaundice

At birth, immature UDP-glucuronosyltransferae causes unconjugated hyperbilirubinemia, which leads to jaundice/ kernicterus (bilirubin deposition in brain, particularly basal ganglia). Treatment includes phototherapy )converts unconjuageted bilirubin to water-soluble form).


Gilbert syndrome

There is mildly decreased UDP-glucuronosyltransferae conjugation and impaired bilirubin uptake. It is asymptomatic or presents with mild jaundice. There is an increase with unconjugated bilirubin without overt hemolysis. Bilirubin increases with fasting and stress. It is very common and there are no clinical consequences.


Crigler-Najjar syndrome, type 1

UDP-glucuronosyltransferae is absent. It presents early in life and patients die within a few years. Findings include jaundice, kernicterus (bilirubin deposition in the brain), increased unconjugated bilirubin. Treatment includes plasmapheresis and phototherapy. Types II is less severe and responds to phenobarbital, which increases liver enzyme synthesis.


Dubin-Johnson syndrome

Conjugated hyperbilirubinemia due to defective liver excretion. There is a grossly black liver. It is benign. Rotor syndrome is similar but is even milder and does not cause black liver.


Wilson disease (hepatolenticular degeneration)

Inadequate hepatic copper excretion and failure of copper to enter circulations as ceruloplasmin. It leads to copper accumulation, especially in the liver, brain, cornea, kidneys (leading to Falconi syndrome), and joints. It is autosomal recessive inheritance (chromosome 13). Copper is normally excreted into bile by hepatocyte copper transporting ATPase (ATP7B gene). Treatment includes chelation with penicillamine or trientine, oral zinc. It is characterized by a decrease in Ceruloplasmin, Cirrhosis, Corneal deposits (Kayser-Fleischer rings), Copper accumulation, Carcinoma (hepatocellular); Hemolytic anemia, Basal ganglia Degeneration (parkinsonian symptoms); Asterixis; Dementia, Dyskinesia, Dysarthria (Copper is Hella BAD).



Hemosiderosine in the deposition of hemosiderin (iron), which stains blue. Hemochromatosis is the disease caused by this iron deposition. The classic triad of micronodular Cirrhosis, Diabetes mellitus, and skin pigmentation causing bronze diabetes. It results in HF, testicular atrophy, and increased risk of HCC. The disease may be primary (autosommal recessive) or secondary to chronic transfusion therapy (eg beta-thalasemia major). Lab findings include increased ferritin, increased iron, decreased TIBC causing an increase of transferrin saturation. It can be identified on biopsy with a Prussian blue stain. The total body iron may reach 50g, enough to set off metal detectors at airports. Primary hemochromatosis is due to a C282Y or H63D mutation on HFE gene. It is associated with HLA-A3. Iron loss through menstruation slows progression in women. Treatment of hereditary hemochromatosis includes repeated phlebotomy, chelation with deferasirox, deferoxamine, deferipron (oral).


Biliary tract disease

It may present with pruritus, jaundice, dark urine, light colored stool, hepatosplenomegaly. It typically with cholestatic pattern of LFTs (increased conjugated bilirubin, increased cholesterol, and increased ALP).


Secondary biliary cirrhosis

Extrahepatic biliary obstruction causes an increase in pressure in intrahepatic ducts causes injury/fibrosis and bile stasis. Patients with known obstructive lesions (gallstones, biliary strictures, pancreatic carcinoma. It may be complicated by ascending cholangitis.


Primary biliary cirrhosis

An autoimmune reaction causes lymphocytic infiltrate with granulomas, leading to the destruction of intralobular bile ducts. It classically presents in middle-aged women. Anti-mitochondrial antibody positive, including IgM. It is associated with other autoimmune conditions (eg CREST, Sjogren syndrome, rheumatoid arthritis, celiac disease).


Primary sclerosing cholangitis

An unknown cause of concentric onion skin bile duct fibrosis causing alternating strictures and dilation with beading of intra and extrahepatic bile ducts on ERCP, magnetic resonance cholangiopancreatography (MRCP). It is classically in young men with IBD. Other findings include hypergammaglobulinemia (IgM), MPO-ANCA/P-ANCA positive. It is also associated with ulcerative colitis. It can lead to secondary biliary cirrhosis, and cholangiocarcinoma.


Cholelithiasis (gallstones)

Cholelithiasis (gallstones) occurs when cholesterol or bilirubin precipitate within bile. Cholesterol stones are most common (75%). There are two types: cholesterol stones and pigment stones. Cholelithiasis can lead to biliary colic, which presents with episodic post-prandial right upper quadrant pain. Biliary colic most often presents after a fatty meal. Diabetics with ​cholelithiasis may not experience biliary colic due to diabetic neuropathy.


Risk factors for cholelithiasis

Risk factors for the development of cholesterol stones include: (4 F's) Female gender, Fat, Fertile (pre-menopausal) and Over Forty years old. Others: Crohn's disease, cystic fibrosis, fibrates, estrogen therapy, rapid weight loss, cirrhosis, Native American origin, total parenteral nutrition, ileal resection


Cholesterol stones

Cholesterol stones are typically radiolucent (except the 10-20% with calcifications that are radiopaque).


Pigment stones

Pigment stones contain excess bilirubin. Black pigmented stones are caused by chronic extravascular hemolysis. Black pigmented stones are radiopaque. Risk factors for pigmented gallstones include: Infection of the biliary tree, Chronic hemolysis, Alcoholic cirrhosis, Advanced age, Total parenteral nutrition (TPN). Brown pigmented stones are radiolucent.


Symptoms of cholelithiasis

The vast majority of stones are asymptomatic. Symptoms occur when stones obstruct the biliary tract or pancreatic duct. Obstruction causes right upper quadrant inflammation, which affects the phrenic nerve of the diaphragm, eliciting referred pain radiating to the right shoulder and/or suprascapular region. Symptomatic cases are treated with cholecystectomy. Charcot’s triad of cholangitis: fever, jaundice, right upper quadrant pain (often colicky). Reynold’s pentad: addition of hypotension and mental status changes, indicating sepsis. Diabetic patients may present without pain.


Complications of cholelithiasis

Pancreatic duct obstruction may lead to pancreatitis. Remember that pancreatic duct joins common bile duct near the ampulla. If a fistula develops between the gallbladder and duodenum, gallstones may obstruct the ileocecal valve, resulting in gallstone ileus. Diagnosis is made by ultrasound. Air in the biliary tree is pathognomonic. Other complications include cholecystitis (most common), ascending cholangitis, and bile stasis. It is highly associated with gallbladder cancer.



Cholecystitis is acute or chronic inflammation of the gallbladder usually due to cholelithiasis. In cholecystitis, obstruction of bile flow may lead to infections associated with the following agents: E. coli (most common), Klebsiella, Enterococcus. It is highly associated with gallbladder cancer. Treatment is cholecystectomy. Diagnosis of cholelithiasis is made with ultrasound. Cholecystitis is diagnosed with ultrasound or cholescintigraphy (also known as hepatobiliary iminodiacetic acid (HIDA) scan).


Diagnosis and treatment of cholelithiasis

Treatment is cholecystectomy. Diagnosis of cholelithiasis is made with ultrasound. Cholecystitis is diagnosed with ultrasound or cholescintigraphy (also known as hepatobiliary iminodiacetic acid (HIDA) scan).


Acute calculous cholecystitis

Acute calculous cholecystitis is characterized by stone impaction in the cystic duct, leading to dilatation with pressure ischemia, bacterial overgrowth and inflammation. If left untreated, it may lead to rupture.


Acute acalculous cholecystitis

Acute acalculous cholecystitis occurs in the absence of stone impaction. It may be due to sepsis, immunosuppression, total parenteral nutrition, major trauma, diabetes, mechanical ventilation, coronary artery disease, multiple transfusions, etc.


Acute cholecystitis

Both acute and chronic cholecystitis present with right upper quadrant pain and Murphy's sign (sudden stop in inspiration upon RUQ palpation due to pain). In acute cholecystitis, other clinical and laboratory findings may include: Fever, Nausea and vomiting, Increased WBC count, Increased serum alkaline phosphatase (if bile duct is involved).


Chronic cholecystitis

Chronic cholecystitis is characterized by herniation of gallbladder mucosa into the muscular layer, causing diverticula known as Rokitansky-Aschoff sinuses. Both acute and chronic cholecystitis present with right upper quadrant pain and Murphy's sign (sudden stop in inspiration upon RUQ palpation due to pain).


Porcelain gallbladder

Calcified gallbladder due to chronic cholecystitis. It is usually found incidentally on imaging. Treatment includes prophylactic cholecystectomy due to high rates of gallbladder carcinoma.


Acute pancreatitis

Autodigestion of the pancreas by pancreatic enzymes occurs. Causes include idiopathic, Gallstones, Ethanoal, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/hypertriglyceridemia (over 1000mg/dL) ERCP, Drugs (eg sulfa drugs, NRTIs, protease inhibitors). GET SMASHED. Clinical presentation includes epigastric abdominal pain radiating to back, anorexia, nausea. Labs include an increase in amylase, lipase (higher specificity). It can lead to DIC, ARDS, diffuse fat necrosis, hypocalcemia (Ca collects in pancreatic Ca soap deposits), pseudocyst formation, hemorrhage, infection, multiorgan failure. Complications include pancreatic pseudocyst (lined by granulation tissue, not epithelium so it can rupture and hemorrhage).


Chronic pancreatitis

Chronic inflammation, atrophy, calcification of the pancreas. Major causes include alcohol abuse and idiopathic. Mutations in CFTR (cystic fibrosis) can cause chronic pancreatic insufficiency. It can lead to pancreatic insufficiency, which causes seatorrhea, fat soluble vitamin deficiency, and diabetes mellitus. Amylase and lipase may or may not be elevated (they are almost always elevated in acute pancreatitis). Coarse calcifications and atrophy can sometimes be seen on imaging.


Pancreatic adenocarcinoma

Average survival is about one year after diagnosis. It is a very aggressive tumor arising from pancreatic ducts (disorganized glandular structure with cellular infiltration). It mostly already metastasized at presentation. Tumors are more common in the pancreatic head (which can causes obstructive jaundice). It is associated with CA 19-9 tumor marker (also CEA, less specific). Treatment is a Whipple procedure, chemotherapy, and radiation therapy.


Risk factors for pancreatic adenocarcinoma

Risk factors include tobacco use, chronic pancreatitis (especially over 20 years), diabetes, age over 50, jewish and african american males.


Presentation of pancreatic adenocarcinoma

It often present with 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).


Trousseau's Syndrome

Trousseau's Syndrome is classically associated with pancreatic carcinoma. It is a superficial migratory thrombophlebitis that presents as recurrent pain, tenderness, and erythema along the course of a superficial vein of the limbs.


H2 blockers

Cimetidine, rantidine, famotidine, nizatidine. Take H2 blockers beofre you dine. Thick table for 2 to remember H2.


Mechanism of H2 blockers

Reversible block of histamine H2 receptors causes a decrease in H secretion by parietal cells.


Clinical use of H2 blockers

Peptic ulcer, gastritis, mild esophageal reflux.


Toxicity of H2 blockers

Cimitidine is a potent inhibitor of cytochrome P 450 (multiple drug interactions). It also has antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males). It can also cross the blood brain barrier (causing confusion, dizziness, headache) and placenta. Both cimetidine and rantidine decrease renal excretion of cretinine. Other H2 blockers are relatively free of these effects.


Proton pump inhibitors (PPI)

Proton pump inhibitors (PPI) include omeprazole, lansoprazole, esomeprazole, and other –prazole drugs. They all have equal efficacy at equal doses.


Mechanism of PPI's

Proton pump inhibitors irreversibly inhibit active H+/K+-ATPases in gastric parietal cells. Decreased H+ transport results in decreased stomach acidity.


Proton pump inhibitors clinical use

Proton pump inhibitors are used to treat: Gastroesophageal reflux disease (GERD), Gastritis, Peptic ulcers, Zollinger-Ellison syndrome, Erosive esophagitis


Side effects of PPIs

Proton pump inhibitors are relatively well tolerated. The most common side effects are gastrointestinal (nausea, vomiting, abdominal pain). Less common side effects are seen with chronic PPI use: Hypomagnesemia (due to disruption of intestinal Mg2+ absorption), Increased risk of fractures, Rebound hypersecretion of gastric acid upon discontinuation, Infection (i.e. Clostridium difficile, pneumonia). Omeprazole is a notable inhibitor of the cytochrome P450 system. Inhibition of CYP2C19 by omeprazole can block the activation of clopidogrel (anti-platelet drug).


Mechanism of bismuth

Bind to ulcer base, providing a physical protection and allowing HCO3 secretion to reestablish pH gradient un the mucous layer.


Clinical use of bismuth

Increases ulcer healing, travelers diarrhea.


Mechanism of sucralfate

Bind to ulcer base, providing a physical protection and allowing HCO3 secretion to reestablish pH gradient un the mucous layer.


Clinical use of sucralfate

Increases ulcer healing, travelers diarrhea.


Clinical use of misoprostol

Commonly used for prevention of peptic ulcers (especially those caused by NSAIDs). Misoprostol is also used for: Post-partum hemorrhage treatment, Patent ductus arteriosus (PDA) maintenance, Cervical ripening (used off label for labor induction), Termination of pregnancy (with mifepristone)


Mechanism of misoprostol

Misoprostol is a synthetic prostaglandin E1 (PGE1) analog that replaces the protective prostaglandins depleted with prostaglandin-inhibiting therapies (i.e. NSAIDs). It has also been shown to induce uterine contractions. Misoprostol decreases gastric acid secretion via G-protein coupled receptor inhibition of adenylate cyclase, which decreases proton pumping activity at the apical surface of parietal cells.


Side effects of misoprostol

Diarrhea is a side effect. Potential adverse events associated with the use of misoprostol include: Abortion, Premature birth, Birth defects. For this reason, women of childbearing age must be advised of its abortifacient properties when used for reducing the risk of NSAID-induced ulcers.


Mechanism of octreotide

Octreotide is a long acting somatostatin analogue. It inhibits actions of many splenchnic vasocontriction hormines.


Clinical use of octreotide

It is used to block diarrhea associated with VIPomas, or high levels of GH or TSH from pituitary adenomas associated with acromegaly. Note that octreotide is also indicated in the treatment of carcinoid syndrome, gastrinomas, glucagonomas and esophageal varices.


Toxicity of octreotide

Nausea, cramps, steatorrhea.



Antacids neutralize gastric acid and raise gastric pH. Common antacids include: Aluminum hydroxide, Magnesium hydroxide, Calcium carbonate. All antacids can alter the pharmacokinetics of other drugs by changing gastric and urinary pH, delaying gastric emptying, and/or chelation. All antacids can also cause hypokalemia by inducing metabolic alkalosis, which causes K+ entry into cells and excessive renal K+ loss.


Aluminum hydroxide

Aluminum hydroxide overuse may lead to these additional symptoms: Constipation, Decreased serum phosphate, Proximal muscle weakness, Osteodystrophy, Seizures


Magnesium hydroxide

Magnesium hydroxide (milk of magnesia) overuse may cause these additional symptoms: Diarrhea (osmotic laxative), Hyporeflexia (loss of K+ and Na+ through diarrhea), Hypotension, Cardiac arrest


Calcium carbonate

Calcium carbonate overuse can lead to these additional consequences: Hypercalcemia, Rebound increase in acid, Chelate other drugs (tetracycline)


Osmotic laxatives

Magnesium hydroxide, magnesium citrate, polyethylene, glycol, lactulose. They provide osmotic load to draw water into the GI lumen. It is used to treat constipation. Lactulose is also used to treat hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4. Toxicities include diarrhea, dehydration. They may be abuse by bulimics.



Sulfasalazine is a combination of two drugs: 5-aminosalicylic acid - modulates local chemical mediators of the inflammatory response, especially leukotrienes. It is thought to be a free radical scavenger or an inhibitor of tumor necrosis factor. Sulfapyridine - antibacterial agent Sulfasalazine is activated by colonic bacteria.


Sulfasalazine clinical use

Sulfasalazine is used to treat some of the following conditions: Juvenile rheumatoid arthritis, Rheumatoid arthritis, Ulcerative colitis Crohn disease


Toxicity of sulfasalazine

Toxicity: Anorexia, nausea, vomiting, Sulfa toxicity (porphyria, Stevens Johnson syndrome, kidney failure, kernicterus), Oligospermia (reversible)


Selective 5-HT3-receptor antagonists

Selective 5-HT3-receptor antagonists work mainly by blocking 5-HT3 receptors on vagal and spinal afferent nerves in the GI tract. Selective 5-HT3-receptor antagonists used in treatment include: Ondansetron, Granisetron, Dolasetron, Palonosetron


Clinical uses of selective 5-HT3-receptor antagonists

These agents are used to treat some of the following disorders: Chemotherapy-induced emesis, Radiation-induced emesis, Postoperative nausea and vomiting


Side effects of selective 5-HT3-receptor antagonists

Notable side effects/adverse events associated with the use of these agents include some of the following: Headache, Mild constipation, QT interval prolongation. Notable contraindications associated with the use of these agents include some of the following: Long QT interval (congenital or acquired)



Metoclopramide works as a dopamine (D2) receptor antagonist, a 5-HT3 receptor antagonist, and a 5-HT4 receptor agonist. It inhibits dopamine (D2) and 5-HT3 receptors in the chemoreceptor trigger zone of the CNS in order to prevent nausea and vomiting. It sensitizes GI muscarinic receptors to acetylcholine, leading to: Increased GI tone, Increased lower esophageal sphincter tone, Increased gastric emptying, Increased GI motility


Side effects and contraindications of metoclopramide

Notable side effects/adverse events associated with the use of metoclopramide includes some of the following: Extrapyramidal symptoms (akathisia, parkinsonism, and dystonias), Seizures, Drowsiness. Notable contraindications in the use of metoclopramide includes some of the following disorders: Parkinson’s disease, Small bowel obstruction, Seizure disorders



Reversible lipase inhibitors (Orlistat) prevent gastric and pancreatic lipase function, thus decreasing the absorption of dietary fats. Side effects of orlistat include steatorrhea and decreased absorption of fat-soluble vitamins.