Gastrointestinal Flashcards
Foregut
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.
Midgut
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.
Hindgut
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
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
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
L1
level of inferior mesenteric branch off the aorta
L3
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
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.
somatostatin
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
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.
Histamine
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
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
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
α-Amylase hydrolyzes the internal α-1,4 glycosidic bonds in the polysaccharide chain of starch, forming disaccharides and trisaccharides.
Lipases
Lipases aid in the digestion of fat.
Proteases
Proteases are secreted as zymogens, and are activated by trypsin. Proteases that are secreted as zymogens include trypsin, chymotrypsin, elastase, carboxypeptidases
Trypsinogen
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.
Bile
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.
