GASTRO-1 Flashcards
Choanal Atresia
- Congenital condition characterized by a bony and/or membranous obstruction of the posterior nasal passage.
- Unilateral choanal atresia often presents late with chronic inflammation (e.g., rhinorrhea, congestion) of the affected nasal passage.
- Bilateral choanal atresia manifests as obstructed nasal breathing with intermittent cyanosis immediately after birth; breathing improves when crying, as it allows the infant to breathe through his or her mouth.
VACTERL Association
Mesodermal defects
A group of associated birth defects consisting of
- Vertebral anomaly
- Anal atresia
- Cardiac anomaly
- Tracheoesophageal fistula
- Esophageal atresia
- Renal anomaly
- Limb malformation
Duodenal Atresia
- ∼ 50% of cases are associated with further anomalies, e.g., bile duct and VACTERL association.
- 20–25% of cases are associated with chromosomal abnormalities, especially Down syndrome.
- Occurs when recanalization of the closed duodenum fails to occur or occurs only partially during the embryonic period (usually between the 8th–10th week of gestation).
- Because the development of the duodenum is connected to the growth of the pancreas and the hepatobiliary system, duodenal atresia is commonly associated with anomalies of these organs as well.
Clinical Presentation:
- Intrauterine → polyhydramnios
- Postpartum
- Vomiting, that is typically bilious if the stenosis is distal to the major duodenal papilla
- Atresia or high-grade stenosis → vomiting few hours after birth
- Mild stenosis → vomiting after a few days
- Distended upper abdomen and scaphoid lower abdomen (the lower abdomen is sucked inwards in a concave shape, as there is no gas present in the gastrointestinal tract distal to the obstruction, whereas gas builds up proximal to it)
- Delayed meconium passage (If stenosis (rather than atresia) is present, the newborn may be able to pass meconium; it will, however, take more time because of the obstruction)
X-ray of the abdomen
- Double bubble sign → air and fluid build up proximal to the obstruction and are separated by the pyloric sphincter, which resembles two bubbles on imaging → one in the stomach and one in the duodenum
- Gasless distal bowel
Preoperative management
- Parenteral nutrition via a central catheter shortly after birth
- Fluid replacement and restoration of the electrolyte balance
- Gastric decompression
Surgery → bypass the atresia or stenosis
- The exact procedure depends on the anatomic findings and associated anomalies
- Common procedure → duodenoduodenostomy or duodenojejunostomy with a proximal transverse-to-distal longitudinal (diamond-shaped) anastomosis
Duodenal Atresia
Double Bubble Sign on Ultrasound Seen in Duodenal Atresia
S → stomach
D → proximal duodenum
Shaded area → pyloric sphincter
Duodenal Atresia in a Newborn
(dilation of the pre-stenotic bowel segments (duodenum (D) and stomach (S)) with an air-fluid level in each dilated segment (double bubble sign). No air is visible in the post-stenotic bowel loops)
Ileal Atresia
- Absence of the jejunal lumen or ileal lumen
- Less common than duodenal atresia
- Vascular accident in utero (usually a disruption of superior mesenteric artery) → ischemic necrosis and reabsorption of the jejunum/ileum → discontinuous bowel
- Risk factors → vasoconstrictive drugs (e.g., cocaine, MDMA, or cigarettes) during pregnancy
- Clinical features → similar to duodenal atresia
- Polyhydramnios (intrauterine)
- Bilious vomiting and upper abdominal distension (postpartum)
- Diagnostics → abdominal x-ray shows a triple bubble sign (dilated small bowel loops and air-fluid levels) and gasless colon. Distal segment of the ileum assumes a spiral configuration around an ileocolic vessel (apple peel or christmas tree)
- Treatment → surgical correction with bypass of the occluded part of bowel is always required
Jejunal Atresia
- Absence of the jejunal lumen or ileal lumen
- Less common than duodenal atresia
- Vascular accident in utero (usually a disruption of superior mesenteric artery) → ischemic necrosis and reabsorption of the jejunum/ileum → discontinuous bowel
- Risk factors → vasoconstrictive drugs (e.g., cocaine, MDMA, or cigarettes) during pregnancy
- Clinical features → similar to duodenal atresia
- Polyhydramnios (intrauterine)
- Bilious vomiting and upper abdominal distension (postpartum)
- Diagnostics → abdominal x-ray shows a triple bubble sign (dilated small bowel loops and air-fluid levels) and gasless colon. Distal segment of the ileum assumes a spiral configuration around an ileocolic vessel (apple peel or christmas tree)
- Treatment → surgical correction with bypass of the occluded part of bowel is always required
Apple Peel or Christmas Tree Seen in Jejunal Atresia
Hypertrophic Pyloric Stenosis
Etiology:
- Environmental factors
- Exposure to nicotine during pregnancy
- Bottle feeding (bottle-fed infants drink more milk in less time, which may lead to pylorus muscle hypertrophy through overstimulation. Another hypothesis maintains that formula components make it harder to digest and gastric emptying is delayed, which may also burden the pylorus muscle)
- Genetic factors → patients with affected relatives have a higher risk of hypertrophic pyloric stenosis
- Macrolide antibiotics
- Erythromycin and azithromycin are associated with a higher risk of hypertrophic pyloric stenosis, especially when administered within 2 weeks after birth
Clinical Presentation:
- Symptoms usually develop between the 2nd and 7th week of age (rarely after the 12th week).
- Frequent regurgitation progressing to projectile, nonbilious vomiting immediately after feeding
- An enlarged, thickened, “olive-shaped”, non-tender pylorus (diameter of 1–2 cm) should be palpable in the epigastrium
- A peristaltic wave, moving from left to right, may be evident in the epigastrium
- “Hungry vomiter” → demands re-feeding after vomiting, demonstrates a strong rooting and sucking reflex, irritable
- If left untreated → dehydration, weight loss, failure to thrive
Findings:
- Initial imaging → abdominal ultrasound shows an elongated and thickened pylorus
- Barium studies
- Narrow pyloric orifice
- String sign → elongated, thickened pylorus
- Beak sign → The pylorus is only partially open to the stomach because of hypertrophy, resulting in two muscular layers adjacent to one another in an “open beak.”
- Hypochloremic, hypokalemic metabolic alkalosis, a classic result, is now uncommon because infants are typically diagnosed and treated early.
- The loss of gastric hydrochloric acid from emesis results in increased bicarbonate and decreased chloride concentrations in the blood.
- Hypokalemia usually occurs in infants that have been vomiting for many days or even weeks.
- Hyponatremia or hypernatremia may be present (as a result of dehydration)
Conservative measures → before surgery
- Correct electrolyte imbalance (e.g., replace K+)
- IV rehydration
- Frequent administration of small meals (12–24 per day)
- Elevate head
Treatment of choice → pyloromyotomy (a longitudinal muscle-splitting incision of the hypertrophic sphincter)
Pancreas Location
- In the abdominal cavity, between the duodenal curvature and the splenic hilum
- Secondary retroperitoneal organ
- Caudal to the omental bursa
- At vertebral level L1/L2
- Head is located within the C-shaped duodenal curvature and contains the pancreatic duct and distal common bile duct
- Uncinate process of pancreas → an extension of the pancreatic head that is located posterior to the superior mesenteric vessels (the remainder of the pancreas is not)
- Neck → lies anterior to the portal vein
- Body → lies anterior to the aorta and extends to the left kidney
- Tail → lies in the splenorenal ligament and extends to the splenic hilum. The distal segment is intraperitoneal.
The uncinate process is _______ to the superior mesenteric vessels. The head, body, and tail of the pancreas lie ______ to the superior mesenteric vessels.
Posterior; anterior
Tumors in the pancreatic ____ often cause bile duct obstruction and can manifest with painless jaundice (Courvoisier sign).
Head
Innervation of the Pancreas
- Innervation → celiac ganglia
- Sympathetic fibers from T6–12
- Parasympathetic fibers from the vagus nerve
Lymphatics of the Pancreas
Celiac, superior mesenteric, and splenic lymph nodes → paraaortic lymph nodes
Vasculature of the Pancreas
Arteries
- Because the pancreas is embryologically derived from the foregut, it mainly receives arterial supply from the celiac trunk and its branches.
- Head and neck
- Inferior pancreaticoduodenal branches (from the superior mesenteric artery)
- Superior pancreaticoduodenal branches (from the gastroduodenal artery)
- Superior and inferior pancreaticoduodenal branches form anastomoses between the celiac trunk and superior mesenteric artery
- Body and tail branches of the splenic artery (itself a branch of the celiac trunk) (the branches of the splenic artery that supply the pancreas include the dorsal pancreatic artery, the great pancreatic artery, and the inferior pancreatic artery)
- Head and neck
Veins
- Head and neck:
- Pancreatic veins → superior mesenteric vein → portal vein
- Body and tail:
- Pancreatic veins → splenic vein → portal vein
Microstructure of the exocrine pancreas
The functional unit (acinus) of the exocrine pancreas is visible:
- Acinar cells (green overlay; example indicated by A, arrow)
- Centroacinar cells (white overlay; example indicated by C)
- Acinar lumen (pink overlay, L) with the intercalated duct (dashed line, D)
Exocrine Pancreas
- > 90% of the pancreas
- Produces digestive enzymes that are secreted into the gastrointestinal tract
- Composed of serous glandular tissue that is separated into lobules by collagenous septae (septae contain blood and lymphatic vessels, nerves, and excretory ducts)
- Pancreatic acini
- Units of secretory acinar cells surrounding a small lumen
- Secrete proenzymes (e.g., trypsinogen, chymotrypsinogen) into intercalated ducts → ducts eventually merge to form the pancreatic duct → duct carries the enzymes out of the pancreas and to the duodenum
- Centroacinar cells → pale cells in the center of the acini, which secrete bicarbonate ions into the pancreatic fluid
- Electron micrographs of acinar cells show:
- Basophilic rough endoplasmic reticulum at the basal pole
- Eosinophilic proenzyme granules at the apical pole
- Histologically, the exocrine pancreas closely resembles the salivary glands. However, unlike the salivary glands, the pancreatic exocrine glands lack myoepithelial cells in the acini and do not possess striated ducts. Additionally, centroacinar cells are unique to the pancreas.
Endocrine Pancreas
- Produces different hormones that are primarily involved in the regulation of blood glucose levels
- Composed of islets of Langerhans embedded within the exocrine pancreas
- Islet cell types are dispersed throughout the pancreas.
- Alpha cells produce glucagon.
- Beta cells produce insulin.
- Delta cells produce somatostatin.
- Epsilon cells produce ghrelin.
- Pancreatic polypeptide cells (formerly gamma cells) produce pancreatic polypeptide (PP).
- Islet cell types are dispersed throughout the pancreas.
Parenchyma of pancreas
Composed predominantly of deeply staining exocrine acinar cells (example indicated by white dashed outline) and a few scattered islets of Langerhans composed of pale-staining endocrine cells (red overlay). The acinar cells are pyramidal in shape. They have a basophilic base (because of an abundance of rough endoplasmic reticulum) and an eosinophilic apex (because of an abundance of zymogen granules). Centroacinar cells (green overlay; black arrows) are the epithelial cells of the pancreatic ducts and are identifiable as pale-staining cells located centrally within the acini. Centroacinar cells secrete bicarbonate. The Islets of Langerhans are composed of clusters of pale, round endocrine cells that produce insulin, glucagon, and somatostatin.
Pancreatic acini and islets of Langerhans
Pancreatic parenchyma is composed predominantly of deeply staining exocrine acinar cells among which are scattered islets of Langerhans composed of pale-staining endocrine cells. Acinar cells are pyramidal in shape. The base of acinar cells is basophilic (examples indicated by white arrows) because of an abundance of rough endoplasmic reticulum and basally located nuclei. The apex of acinar cells is brightly eosinophilic (examples indicated by white arrowheads) because these cells contain abundant zymogen granules. The endocrine cells of the islets of Langerhans (green overlay) are pale and round and produce insulin, glucagon, and somatostatin.
Parenchyma of the pancreas
The pancreas is encapsulated by a thin connective tissue capsule and surrounded by peripancreatic fat. The pancreatic parenchyma is divided into lobules by connective tissue septae in which lie blood vessels, nerves, and branches of the pancreatic ducts. Each lobule of the pancreas is composed of clusters of dark-staining exocrine acinar cells that contain pancreatic zymogens. Scattered amid the acinar cells are the islets of Langerhans composed of pale-staining endocrine cells that secrete pancreatic hormones. Centroacinar cells are the epithelial cells of the pancreatic ducts and are located at the center of the pancreatic acini. Centroacinar cells secrete bicarbonate.
Pancreatic Ducts
- Smaller ducts have cuboidal epithelium.
- Larger interlobular ducts have columnar epithelium.
- Most pancreatic malignancies are adenocarcinomas that originate in the ductal epithelium.
Exocrine Pancreatic Secretions
The pancreatic fluid is isotonic.
It contains the following:
- Digestive pancreatic enzymes
- Pancreatic proteases → digestion of proteins
- Secreted as inactive proenzymes (zymogens) by pancreatic acinar cells into the pancreatic duct (in their active form, proteolytic enzymes would cause autodigestion of the pancreatic tissue. This can occur in acute pancreatitis)
- Trypsin and chymotrypsin
- Proenzymes: trypsinogen and chymotrypsinogen
- Activated in the duodenum → trypsinogen is activated to trypsin by enterokinases, which are located at the brush border of the duodenal and jejunal mucosa.
- Once activated, trypsin activates chymotrypsinogen to form chymotrypsin and, furthermore, converts additional trypsinogen molecules to trypsin (positive feedback loop).
- Elastase (activated by trypsin)
- Digestion of elastin fibers
- Activated by trypsin
- Carboxypeptidase → activated by trypsin
- Nucleases → digestion of RNA/DNA
- Phospholipase A → digestion of phospholipids
- Pancreatic amylase (secreted in active form) → digestion of carbohydrates
- Pancreatic lipase → digestion of lipids
- Pancreatic proteases → digestion of proteins
- Electrolytes (Na+, K+, Cl-, HCO3-) → concentration of Cl- and HCO3- increases with the rate of pancreatic juice secretion
- Water
Dorsal Pancreatic Bud
- Rest of pancreatic head, neck, body, tail, and accessory pancreatic duct
Ventral Pancreatic Bud
- Main pancreatic duct
- Uncinate process
- Lower part of pancreatic head
Dorsal pancreatic bud: rest of pancreatic head, neck, body, tail, and accessory pancreatic duct
Intraperitoneal Organs
- Organs covered by visceral peritoneum
- Connected by mesentery
Organs:
- Stomach
- Duodenum (first part)
- Jejunum
- Ileum
- Cecum/appendix
- Transverse colon
- Sigmoid colon
- Liver and gall bladder
- Spleen
- Pancreas (tail)
- Female reproductive organs (ovaries, uterus, and fallopian tubes)
Extraperitoneal Organs
Retroperitoneal organs
- Organs that are not covered by visceral peritoneum
- Not connected by mesentery
Organs:
- Esophagus
- Anal canal
- Kidneys
- Adrenal glands
- Ureters
- IVC
- Aorta
Secondary retroperitoneal organs
- Organs that were intraperitoneal in utero but became retroperitoneal after fusion of the mesenterywith posterior abdominal wall
Organs:
- Duodenum (second, third, and fourth parts)
- Ascending colon
- Descending colon
- Upper rectum
- Pancreas (head, neck, and body)
Subperitoneal organs
- Organs that lie inferior to the peritoneal cavity
Organs:
- Lower rectum
- Bladder (only the superior surface of the bladder is covered by peritoneum. A full bladder is a preperitoneal structure, as it lies anterior to the peritoneal cavity)
Retroperitoneal Organs
- Organs that are not covered by visceral peritoneum
- Not connected by mesentery
Organs:
- Esophagus
- Anal canal
- Kidneys
- Adrenal glands
- Ureters
- IVC
- Aorta
Secondary retroperitoneal organs
- Organs that were intraperitoneal in utero but became retroperitoneal after fusion of the mesenterywith posterior abdominal wall
Organs:
- Duodenum (second, third, and fourth parts)
- Ascending colon
- Descending colon
- Upper rectum
- Pancreas (head, neck, and body)
Secondary Retroperitoneal Organs
- Organs that were intraperitoneal in utero but became retroperitoneal after fusion of the mesenterywith posterior abdominal wall
Organs:
- Duodenum (second, third, and fourth parts)
- Ascending colon
- Descending colon
- Upper rectum
- Pancreas (head, neck, and body)
Subperitoneal Organs
- Organs that lie inferior to the peritoneal cavity
Organs:
- Lower rectum
- Bladder (only the superior surface of the bladder is covered by peritoneum. A full bladder is a preperitoneal structure, as it lies anterior to the peritoneal cavity)
Splenorenal Ligament
Attachment:
- Spleen ←→ Left pararenal space
Content:
- Splenic artery
- Splenic vein
- Tail of the pancreas
Clinical Significance:
- Forms the left lateral boundary of the lesser sac (along with the gastrosplenic ligament)
- Ligament is cut during splenectomy.
- Dissected during distal pancreatectomy
Gastrophrenic Ligament
Attachment:
- Stomach ←→ Diaphragm
Content:
- Left inferior phrenic artery
Clinical Significance:
- Anchors the stomach to the diaphragm
- Part of the grater omentum
Gastrosplenic Ligament
Attachment:
- Greater curvature of the stomach ←→ Spleen
Content:
- Short gastric arteries
- Left gastroepiploic artery
Clinical Significance:
- Separates greater and lesser sacs on left side (forms the left lateral boundary of the lesser sac (along with the splenorenal ligament))
Gastrocolic Ligament
Attachment:
- Greater curvature of the stomach ←→ Transverse colon
Content:
- Right gastroepiploic artery
- Left gastroepiploic artery
Clinical Significance:
- Forms the anterior wall of the lesser sac
- Part of greater omentum
- Can be divided to access the lesser sac during surgery
- Derivative of dorsal mesentery
Hepatogastric Ligament
Attachment:
- Lesser curvature of the stomach ←→ Fissure of ligamentum venosum of the liver
Content:
- Right gastric artery
- Left gastric artery
Clinical Significance:
- Separates greater and lesser sacs on the right side
- Cut to access lesser sac during surgery (eg, pancreatic surgery)
Ligamentum Venosum
Attachment:
- Left branch of portal vein ←→ IVC
Content:
- Does not contain any structures
Clinical Significance:
- Fetal remnant of ductus venosus
- Fissure for the ligamentum venosum separates the caudate lobe from the left lobe of the liver.
- Can be divided to expose the left hepatic veinduring surgery
Hepatoduodenal Ligament
Attachment:
- First part of duodenum ←→ Porta hepatis in the liver
Content:
- Portal triad:
- Proper hepatic artery
- Portal vein
- Common bile duct
Clinical Significance:
- Forms anterior border of the epiploic foramen
- Derivative of ventral mesentery
- Clamped in the Pringle maneuver → ligament is compressed manually or with a vascular clamp in omental foramen to control bleeding from hepatic inflow source
- Borders the omental foramen, which connects the greater and lesser sacs
- Part of lesser omentum
Falciform Ligament
Attachment:
- Liver ←→ Anterior abdominal wall
Content:
- Ligamentum teres (derivative of fetal umbilical vein)
Clinical Significance:
- Divides liver into right (larger) and left (smaller) lobes
- Remnant of fetal ventral mesentery
- Inferior aspect of the ligament serves as a landmark for locating the drainage of hepatic veins into the IVC.
- May become recanalized with blood vessels in patients with portal hypertension due to shunting of blood to the anterior abdominal wall
Greater Omentum
- Component of visceral peritoneum that extends from the greater curvature of the stomach to cover the intestines.
- Contains:
- Gastrosplenic ligament
- Gastrophrenic ligament
- Gastrocolic ligament
Lesser Omentum
- Fold of peritoneum that extends from the lesser curvature of the stomach to the liver.
- Contains
- Gastrohepatic ligament
- Hepatoduodenal ligament
Sigmoid Mesocolon
Attachment:
- Sigmoid colon ←→ Posterior abdominal wall
Contents:
- Sigmoid artery and sigmoid vein
- Superior rectal artery and superior rectal vein
Clinical Significance:
- Overlies the left common iliac artery
- The sigmoid mesocolon twists on itself in sigmoid volvulus.
Transverse Mesocolon
Attachment:
- Transverse colon ←→ Posterior abdominal wall
Contents:
- Middle colic artery
- Middle colic vein
Clinical Significance:
- Runs from the second part of the duodenum to the splenic flexure
- Divides the abdominal cavity into supracolic and infracolic compartments
Phrenoesophageal ligament (PEL)
Attachment:
- Peritoneal fold that encircles the distal portion of the esophagus and gastroesophageal junction ←→ Peritoneal surface of the diaphragm
Clinical Significance:
- Closes the esophageal hiatus and helps maintain the intra-abdominal position of the GEJ
- Typically cut in procedures that require mobilization of the distal esophagus or the fundus of the stomach (eg, esophagectomy, fundoplication)
Phrenicocolic Ligament
Attachment:
- Diaphragm ←→ Splenic flexure
Contents:
- Does not contain any structures
Clinical Significance:
- Provides ligament support to the spleen
- Limits communication between the left paracolic gutter and the left subphrenic space, making left subphrenic collections less common after abdominal surgery
Ileum Histology
Mucosa
- Similar to duodenal mucosa, with thinning out of plicae circulares
- Simple columnar epithelium
- Structures that increase the absorptive surface area
- Thin plicae circulares → transverse folds of the mucosa and submucosa (visible to the naked eye)
- Intestinal villi
- Finger-like projections of mucosa
- Tallest in the jejunum (shortest in the duodenum)
- Lined by simple columnar epithelium and the specialized cells of the small intestine
- Each villus has an arteriole, venule, and lymphatic channel at its core.
- Microvilli
- Have a superficial layer of glycocalyx that enables binding of nutrients and enzymes
- Give the small intestinal mucosal surface a “brush border” appearance
- Minute projections from the epithelial cells of the villi
- Crypts of Lieberkuhn
- Intestinal glands
- Lie within the lamina propria
- Flanked by two adjacent villi
- Lined by specialized cells of the small intestine
- Contain stem cells that replace enterocytes/goblet cells and Paneth cells that secrete defensins, lysozyme, and TNF
- Peyer patches
- Aggregates of nonencapsulated lymphoid tissue within the lamina propria and submucosa (GALT of the ileum)
- Contain specialized cells:
- Microfold cells (M cells) → endocytose antigens and deliver them to antigen-presenting cells
- B lymphocytes in germinal centers become plasma cells and secrete IgA, which prevents pathogens from binding to and invading the intestinal mucosa.
Submucosa
- No glands
- Meissner plexus
Muscularis propia
- Inner circular smooth muscle and outer longitudinal smooth muscle layers
- Auerbach plexus lies between the two layers of smooth muscle.
Serosa
- Mesothelium of the visceral peritoneum
Jejunum Histology
Mucosa
- Similar to duodenal mucosa
- Plicae circulares are most prominent in the jejunum.
- Simple columnar epithelium
- Structures that increase the absorptive surface area
- Plicae circulares → transverse folds of the mucosa and submucosa (visible to the naked eye)
- Intestinal villi
- Finger-like projections of mucosa
- Tallest in the jejunum (shortest in the duodenum)
- Lined by simple columnar epithelium and the specialized cells of the small intestine
- Each villus has an arteriole, venule, and lymphatic channel at its core.
- Microvilli
- Have a superficial layer of glycocalyx that enables binding of nutrients and enzymes
- Give the small intestinal mucosal surface a “brush border” appearance
- Minute projections from the epithelial cells of the villi
- Crypts of Lieberkuhn
- Intestinal glands
- Lie within the lamina propria
- Flanked by two adjacent villi
- Lined by specialized cells of the small intestine
- Contain stem cells that replace enterocytes/goblet cells and Paneth cells that secrete defensins, lysozyme, and TNF
Submucosa
- No glands
- Meissner plexus
Muscularis propia
- Inner circular smooth muscle and outer longitudinal smooth muscle layers
- Auerbach plexus lies between the two layers of smooth muscle.
Serosa
- Mesothelium of the visceral peritoneum
Rectum & Anal Canal Below the Pectinate Line Histology
Mucosa
- Stratified squamous epithelial lining (accordingly, carcinomas arising below the pectinate line are squamous cell carcinomas)
- Transitions to keratinized stratified squamous epithelium toward the anal orifice
- No crypts of Lieberkuhn
Submucosa
- Contain the external hemorrhoidal plexus of veins
Muscularis propia
- The inner circular layer of smooth muscle forms the internal anal sphincter.
- No teniae coli
Adventitia
- Adventitial tissue; no serosa (the rectum and anal canal are retroperitoneal organs)
Rectum & Anal Canal Above the Pectinate Line Histology
Mucosa
- Columnar epithelial lining (accordingly, carcinomas arising above the pectinate line are adenocarcinomas)
Submucosa
- Collagen, elastic fibers
- Contain blood vessels and the Meissner plexus
- Contain the internal hemorrhoidal plexus of veins
Muscularis propia
- Inner circular and outer longitudinal smooth muscle layers separated by the Auerbach plexus
- No teniae coli
Adventitia
- Adventitial tissue; no serosa (the rectum and anal canal are retroperitoneal organs)
Appendix Histology
Mucosa
- Columnar epithelial lining
Submucosa
- Contains numerous lymphoid follicles that distort the mucosal crypts
- Contains blood vessels and the Meissner plexus
Muscularis propia
- Inner circular and outer longitudinal smooth muscle layers separated by the Auerbach plexus
- No teniae coli
Serosa
- Mesothelium of the visceral peritoneum
Cecum & Colon Histology
Mucosa
- Columnar epithelial lining
- Contains intestinal glands (crypts of Lieberkuhn) lined with goblet cells
- Lamina propriacontaining mucosa-associated lymphoid tissue (MALT) (the lamina propria lies between adjacent crypts of Lieberkuhn)
- No villi
Submucosa
- Collagen, elastic fibers
- Contains blood vessels and the Meissner plexus
Muscularis propia
- Inner circular smooth muscle and bands of longitudinal smooth muscle (teniae coli) separated by the Auerbach plexus
- Teniae coli with haustra
Serosa
- Mesothelium of the visceral peritoneum
Duodenum Histology
Mucosa
- Simple columnar epithelium
- Structures that increase the absorptive surface area
- Plicae circulares → transverse folds of the mucosa and submucosa (visible to the naked eye) and most prominent in the jejunum
- Intestinal villi
- Finger-like projections of mucosa
- Shortest in the duodenum
- Tallest in the jejunum
- Lined by simple columnar epithelium and the specialized cells of the small intestine
- Each villus has an arteriole, venule, and lymphatic channel at its core.
- Microvilli
- Minute projections from the epithelial cells of the villi
- Give the small intestinal mucosal surface a “brush border” appearance
- Have a superficial layer of glycocalyx that enables binding of nutrients and enzymes
- Crypts of Lieberkuhn
- Intestinal glands
- Lie within the lamina propria
- Flanked by two adjacent villi
- Lined by specialized cells of the small intestine
- Contain stem cells that replace enterocytes/goblet cells and Paneth cells that secrete defensins, lysozyme, and TNF
Submucosa
- Brunner glands
- Lined by columnar cells that secrete mucus and HCO3-
- Secretions neutralize acidic chymefrom the stomach.
- Meissner plexus
Muscularis propia
- Inner circular smooth muscle and outer longitudinal smooth muscle layers
- Auerbach plexus lies between the two layers of smooth muscle.
Serosa
- Mesothelium of the visceral peritoneum
Duodenum
The duodenal epithelium consists of single-layered columnar epithelium (enterocytes) with interspersed goblet cells (green overlay). In contrast to other parts of the intestine, the duodenum contains villi (V, black dashed lines) as well as crypts (C, white dashed lines) and submucosal glands (Brunner glands, red overlay). Brunner glands are usually located in the submucosa, but their ducts may extend past the muscularis mucosae (white arrows) into the mucosa of the lamina propria.
Plicae circulares
The mucosa of the small intestine contains circumferential folds known as plicae circulares (Kerckring folds; valvulae conniventes), which increase the absorptive surface area. Plicae circulares are most prominent in the jejunum. The ileum contains aggregates of lymphoid tissue within its lamina propria, which are known as Peyer patches.
Plicae Circulares (Valves of Kerckring)
(Endoscopic view of the duodenum)
The transverse folds of mucosa are the plicae circulares. The smaller mucosal folds are intestinal villi. Bile is visible as an accumulation of golden yellow fluid between the plicae circulares.
Brush border in enterocyte
(electron micrograph of the apex of an intestinal mucosal cell (enterocyte))
The finger-like extensions of the cell membrane are microvilli that increase the absorptive surface area of the cell, giving it a “brush border” appearance.
Each microvillus is made up of a support framework of actin filaments that are attached to the terminal web (white arrowhead) of the cell membrane.
The apices of the microvilli are covered by glycocalyx (the light gray substance that the white arrow is pointing to), which enables binding of nutrients before absorption.
Cytoplasmic organelles are visible in the upper left.
Intestinal villi and crypts of Lieberkuhn
(photomicrograph of jejunal tissue)
Small intestinal mucosa is composed of finger-like projections, known as villi (example outlined in black). Villi are lined by columnar epithelium interspersed by goblet cells (examples indicated by green overlay). Crypts of Lieberkuhn (examples outlined in white) are mucosal invaginations between two adjacent villi (the white arrowhead indicates a transversely-cut crypt). The muscularis mucosa (between the black arrows) lies between the lamina propria and the submucosa (red overlay).
Brunner Glands
(photomicrograph of duodenal tissue)
Tissues (from top left to bottom right and from inside out):
– Brunner glands (dark red) surrounded by submucosal connective tissue (light blue)
– Lamina muscularis mucosa (light purple)
– Villous and cryptic mucosa (purple) with the lamina propria (pale purple with dark purple nuclei) on the inside and the lamina epithelialis (purple) with goblet cells (dark blue, large) and enterocytes (dark purple, small) on the outside
Jejunum
- Mucosa → composed of villi (finger-like projections; examples indicated by green overlay) and crypts of Lieberkuhn (between two adjacent villi)
- Plicae circulares → a fold of submucosa (white overlay) and mucosa that protrudes into the lumen
- Lymphatics and blood vessels within the submucosa
- Muscularis propria → composed of an inner circular (dotted white bracket) and outer longitudinal (solid white bracket) layer of smooth muscles
- Subserosa (yellow overlay) and serosa (dotted green line)
Jejunum
Tissue layers (from bottom left to top right):
- Serosa (pink)
- Muscularis propria, outer layer (dark pink)
- Muscularis propria, inner layer (dark pink)
- Plicae circulares → folds of submucosa (pink) and mucosa with villi (purple).
Peyer Patches
Peyer patches (example indicated by green overlay) are large secondary lymphoid follicles within the ileal lamina propria and submucosa that sometimes reach the simple columnar epithelium. The epithelium lines the characteristic villi and crypts of the ileum.
Posterior to the Stomach
- Spleen
- Tail of the pancreas
- Left kidney
- Left adrenal gland
- Transverse colon
- Transverse mesocolon and lesser sac
Stomach Histology
- The stomach’s four histological layers are the same as the layers of the gastrointestinal tract.
- The mucosa of the stomach is specialized in the following ways:
- It contains millions of gastric pits that are lined by mucus-secreting cells (foveolar cells) and open into one or more gastric glands (the mucus layer contains bicarbonates, which neutralize gastric acid)
- Gastric glands in the lamina propria contain various specialized cells and vary in composition and thickness depending on their location in the stomach.
- Stem cells located at the necks of the gastric glands proliferate and differentiate to replace gastric cells.
- Enteroendocrine cells are located throughout the gastric mucosa and secrete various secretory and regulatory products of the gastrointestinal tract.
Fundus and body
- Chief cell (basophilic)
- Parietal cell (eosinophilic; pink)
- Enterochromaffin-like cell (ECL cell)
- P/D1 cell
Pylorus and antrum
- D cell
- G cell
Gastric mucosa
Large eosinophilic parietal cells (circled) with a central circular nucleus, giving them a fried-egg appearance, can be seen. Chief cells are visible as pyramidal basophilic cells with basal nuclei (white arrowheads). The lamina propria is visible on the right side of the image and is composed of cells with flattened, irregular nuclei.
This is the typical appearance of the physiological gastric mucosa of the gastric fundus.
Parietal cells and chief cells
(photomicrograph of a section of a fundic gastric gland)
A typical gastric gland is lined by parietal cells (example indicated by arrow), chief cells, and mucous neck cells.
- Parietal cells are visible as large eosinophilic cells with a circular nucleus, giving them a fried-egg appearance (green overlay).
- Chief cells (white dashed outline) are visible as pyramidal cells with basally located nuclei and basophilic cytoplasm that contains zymogen granules.
- Mucous neck cells (not visible here) are located at the distal end of the gastric gland.
This is the typical histological appearance of the base of a fundic gastric gland.
Pyloric glands
(lamina propria of the gastric antrum)
The pyloric glands open into the gastric pits. They secrete mucous that protects the mucous membrane against the acid and pepsin contained in the secretions of the fundic glands.
Greater Omentum
(white star)
Colonic mucosa
The colonic mucosa is composed of the following layers:
- Simple columnar epithelium (visible as tall, pale-staining cells with basal basophilic nuclei)
- Numerous straight glands, known as crypts of Lieberkuhn (white overlay), which are predominantly lined by goblet cells (stained deep pink)
- Lamina propria (red overlay) located between the crypts of Lieberkuhn
- Muscularis mucosa (between green arrows)
Part of the submucosa (green overlay) containing blood vessels (example indicated by black arrow) and lymphatics is visible.
Layers of the Colonic Wall
Colonic layers from top to bottom and outside to inside:
- The mucosa (purple) is lined with columnar epithelium and contains numerous intestinal glands (crypts of Lieberkuhn).
- The submucosa contains MALT (white and pink), identifiable as the circular aggregates of basophilic cells.
- The muscularis propria (light pink) is composed of an inner circular and outer longitudinal layer.
- The serosa (dark pink) is composed of mesothelial tissue.
Transverse Section of the Appendix
Tissue layers (from the outside in):
- Muscularis propria (purple)
- Submucosa (dark purple)
- Mucosa (red) with secondary lymphoid follicles (light red, round, bordering the submucosa)
Normal Appendix
- Mucosa → simple columnar epithelium with multiple crypts
- Submucosa → Numerous lymphoid follicles (green overlay) distorting the crypts are a characteristic histological feature of the appendix, esp. in children and young adults.
- Muscular layer
- Subserosa
- Serosa
Peyer Patches
- Located in the mucosa of the ileum
- Aggregates of nonencapsulated lymphoid tissue within the lamina propria and submucosa (GALT of the ileum)
- Contain specialized cells:
- Microfold cells (M cells) → endocytose antigens and deliver them to antigen-presenting cells
- B lymphocytes in germinal centers become plasma cells and secrete IgA, which prevents pathogens from binding to and invading the intestinal mucosa.
Crypts of Lieberkuhn
- Intestinal glands
- Lie within the lamina propria
- Flanked by two adjacent villi
- Lined by specialized cells of the small intestine
- Contain stem cells that replace enterocytes/goblet cells and Paneth cells that secrete defensins, lysozyme, and TNF
Celiac Trunk Vertebral Level
T12
Superior Mesenteric Artery Vertebral Level
L1
Inferior Mesenteric Artery Vertebral Level
L3
Middle Suprarenal Artery Vertebral Level
L1
Renal Artery Vertebral Level
L1–L2
Gonadal Artery Vertebral Level
L2
Inferior Phrenic Artery Vertebral Level
T12
Lumbar Artery (set of four) Vertebral Level
L1–L4
The right middle suprarenal artery runs ______ to the inferior vena cava.
Posterior
Lumbar arteries
(four on each side)
- Run posterolaterally over the L1–L4 vertebrae and pass posterior to the sympathetic trunk and muscular attachments of psoas major
- Anastomose with arteries of the anterior abdominal wall (these include the superior and inferior epigastric arteries, iliolumbar artery, and deep circumflex iliac artery)
- Branches:
- Spinal branches
- Spinal canal
- Terminal branches
- Posterior abdominal wall
- Muscles of the back
- Spinal branches
Gonadal Arteries
- Source → arises from the anterior aspect of aorta and inferior to the renal arteries (below L2)
- Runs along the psoas major muscle, anterior to the ureters and external iliac arteries to enter the suspensory ligament of the ovary (ovarian arteries) or deep inguinal ring of the inguinal canal to supply the testis (testicular arteries)
- Branches:
- Ovarian artery
- Ovaries
- Lateral third of the fallopian tubes
- Testicular artery
- Testes
- Epididymis (via epididymal branches)
- Ovarian artery
Renal Arteries
- Source → approximately at the level of L1–L2
- Right renal artery → runs posterior to the IVC and head of pancreas to right kidney
- Left renal artery → runs posterior to the body of pancreas to the left kidney
- Enters the renal pelvis posterior to the renal veins
- Branches:
- Inferior suprarenal artery
- Adrenal glands
- Terminal branches
- Kidney
- Renal capsule
- Ureters
- Inferior suprarenal artery
Splenic Artery
- Runs along the superior margin of the pancreas and enters the splenorenal ligament to supply the spleen
- Branches
- Pancreatic branches → run dorsal to the pancreas to supply the organ
- Supply → pancreas
- Dorsal pancreatic artery → arises from the first part of the splenic artery and runs posterior to the pancreas
- Right branch → anastomoses with pancreaticoduodenal arteries
- Left branch → continues as the inferior pancreatic artery (transverse pancreatic artery) and anastomoses with other pancreatic branches of the splenic artery
- Greater pancreatic artery → arises from the middle part of the splenic artery and runs posterior to the pancreas alongside the pancreatic duct (anastomoses with branches of the inferior pancreatic artery)
- Posterior gastric artery → runs superiorly within the gastrophrenic ligament to the fundus of the stomach
- Supply → Posterior gastric wall and fundus region
- Short gastric arteries → run within the gastrosplenic ligament to the fundus of the stomach
- Supply → Stomach (fundus and greater curvature)
- Left gastroepiploic artery → runs within the gastrosplenic ligament to supply the fundus and then within the gastrocolic ligament to run along the greater curvature and anastomoses with the right gastroepiploic artery
- Supply → Stomach (fundus and greater curvature)
- Pancreatic branches → run dorsal to the pancreas to supply the organ
Common Hepatic Artery
- Greater branch of the celiac trunk
- Runs towards the porta hepatis on the right and divides into two major branches (proper hepatic artery and gastroduodenal artery)
- Branches
- Proper hepatic artery
- Continuation of the common hepatic artery after giving rise to the gastroduodenal artery
- Runs within the hepatoduodenal ligament to the porta hepatis (the portal vein and the bile duct run within the ligament as well. The hepatic artery proper lies anterior to the portal vein and left lateral to the bile duct)
- Braches:
- Right gastric artery → runs within the lesser omentum along the lesser curvature of the stomach and anastomoses with the left gastric artery
- Stomach (lesser curvature)
- Right hepatic artery
- Liver (right portion)
- Gall bladder (via cystic artery)
- Caudate lobe
- Left hepatic artery
- Liver (left portion)
- Caudate lobe
- Gastroduodenal artery → runs posterior to the first part of the duodenum and divides into two branches
- Right gastroepiploic artery → runs along the greater curvature of the stomach and anastomoses with left gastroepiploic artery
- Supply:
- Stomach
- Duodenum
- Pancreas
- Supply:
- Anterior and posterior superior pancreaticoduodenal artery → anastomose with anterior and posterior branches of the inferior pancreaticoduodenal artery around the head of the pancreas
- Supply:
- Stomach
- Duodenum
- Pancreas
- Supply:
- Proper hepatic artery
The hepatic artery proper lies _______ to the portal vein and ______ to the bile duct within the hepatoduodenal ligament.
Anterior; left lateral
Superior Rectal Artery
- Reaches rectum dorsally
- Anastomoses with middle rectal artery (from internal iliac artery) and inferior rectal artery (from internal pudendal artery)
- Multiple small branches
- Supply → Upper two-thirds of rectum
Abdominal Anastomoses
- All unpaired branches of the abdominal aorta form an anastomosis to ensure continued perfusion of organs in the event of vascular occlusion.
- Sites of anastomosis
- Duodenum
- Celiac artery → superior pancreaticoduodenal artery
- Superior mesenteric artery → inferior pancreaticoduodenal artery
- Distal third of transverse colon
- Superior mesenteric artery → middle colic artery
- Inferior mesenteric artery → left colic artery
- Rectum
- Inferior mesenteric artery → superior rectal artery
- Internal iliac artery → middle rectal artery
- Duodenum
- Examples
- Marginal artery of Drummond
- Anastomosis between the terminal branches of the superior and inferior mesenteric artery
- Runs along the inner mesenteric border of the colon
- Extends from ileocecal junction to the rectosigmoid junction
- Poorly developed in the splenic flexure and rectosigmoid region (watershed areas)
- Riolan anastomosis (part of the marginal artery of Drummond)
- Anastomosis between branches of middle colic artery and left colic artery
- Provides collateral blood supply to the splenic flexure
- Marginal artery of Drummond
Marginal Artery of Drummond
- Anastomosis between the terminal branches of the superior and inferior mesenteric artery
- Runs along the inner mesenteric border of the colon
- Extends from ileocecal junction to the rectosigmoid junction
- Poorly developed in the splenic flexure and rectosigmoid region (watershed areas)
Riolan Anastomosis
- Part of the marginal artery of Drummond
- Anastomosis between branches of middle colic artery and left colic artery
- Provides collateral blood supply to the splenic flexure
Nutcracker Syndrome
- Compression of left renal vein between the aorta and superior mesenteric artery
- Clinical Features
- Hematuria (rupture of thin-walled varices due to elevated venous pressure)
- Abdominal/flank pain that may radiate to the thigh or buttock
- Left-sided varicocele in men
- In female individuals → chronic pelvic pain, dyspareunia, dysuria, and dysmenorrhea
- Diagnosis
- Urinalysis → microscopic/macroscopic hematuria and orthostatic proteinuria (renal vein compression alters glomerular hemodynamics, possibly enhancing the effects of endogenous angiotensin II)
- Doppler ultrasonography
- Treatment
- Conservative management with ACE inhibitors for mild cases (angiotensin II predominantly causes vasoconstriction of the postglomerular capillaries. This increases the glomerular hydrostatic pressure and induces proteinuria)
- Endovascular stenting in severe cases of hematuria
Splenic Artery Aneurysm
- Abnormal dilatation of the vessel wall of the splenic artery
- Risk factors
- Pregnancy and history of multiple pregnancies in women (hyperdynamic circulation exerts increased force against the wall and high levels of relaxin increase the elasticity of the vessel wall. In addition, the hormonal shifts in pregnancy lead to degenerative changes in the vessel wall)
- Hypertension
- Atherosclerosis
- Fibromuscular dysplasia
- Connective tissue disease
- Vasculitis (e.g., granulomatosis with polyangiitis)
- Pancreatitis
- Portal hypertension with splenomegaly
- Clinical features
- Asymptomatic
- Abdominal and flank pain
- Hematemesis
- Hematochezia
- Diagnosis
- Doppler ultrasonography
- CT/MR angiography
- Treatment
- If dilation < 3 cm → annual surveillance using CT or ultrasound
- If dilation > 3 cm or presence of risk factors → surgical ligation or endovascular therapy due to high risk of rupture
- Splenectomy → in case of rupture and hemodynamic instability
Celiac Artery Compression Syndrome
(Median Arcuate Ligament Compression Syndrome)
- Compression of the celiac trunk by the median arcuate ligament of the diaphragm (the diaphragm moves upwards during expiration, causing stretching of the crura and increased celiac trunk compression)
- Clinical features
- Postprandial epigastric pain (celiac trunk compression leads to ischemia of the foregut or ischemia of the midgut (due to shunting of blood from the superior mesenteric artery via the collateral circulation))
- Weight loss (Individuals avoid eating due to the pain)
- Abdominal bruit
- Diagnosis
- Doppler ultrasonography
- CT/MR angiography
- Treatment
- Surgery → median arcuate ligament release and celiac trunk reconstruction
- Endovascular stenting of celiac trunk
Inferior Vena Cava Area of Drainage
- Lower extremities
- Abdominal wall
- Pelvic wall
- Pelvic organs (except for the proximal rectum)
- Kidneys and ureters
- Adrenal glands
The ascending lumbar vein joins the subcostal vein to form the ____ vein on the right and ______ vein on the left, both of which drain into the superior vena cava.
Azygos; Hemiazygos
The ascending lumbar vein joins the subcostal vein to form the azygos vein on the ____ and hemiazygos vein on the ____, both of which drain into the _______.
Right; Left; Superior vena cava
The ________, _________, and ________ veins empty into the left renal vein.
Left suprarenal, left gonadal, and left inferior phrenic veins
The portal vein drains the structures of ________ and empties indirectly into the ______ via the ________.
Gastrointestinal tract; hepatic veins; hepatic sinusoids
The _______ drains the structures of the gastrointestinal tract and empties indirectly into the hepatic veins via the hepatic sinusoids.
Portal vein
In Budd-Chiari syndrome, the main hepatic veins are occluded, but the ____ lobe continues to drain via the ______ and may even undergo compensatory hypertrophy.
Caudate; minor hepatic veins
Hepatic Capsule
Two layers:
- Outer serous layer derived from peritoneum, which covers the entire liver (except the bare area of the liver) (the bare area of the liver is in direct contact with the diaphragm and not covered by peritoneum. Due to this, this area is susceptible to spread infections from the abdominal to the thoracic cavity)
- Fibrous inner layer (the Glisson capsule) that covers the entire liver (including the bare area of the liver), the hepatic artery, portal vein, and bile ducts
Porta Hepatis Structures
- Fissure between the caudate and quadrate lobes that contains several veins, arteries, and nerves:
- Common hepatic duct (leaving)
- Hepatic artery proper (entering)
- Hepatic portal vein (entering)
- Hepatic nerve plexus and lymphatic vessels
Liver Location
- Under the diaphragm in the right upper abdomen.
- Extends from the fifth intercostal space to the right costal margin in the midclavicular line
- Percussed at the fifth intercostal space
Hepatic Lobules
- Small hexagonal units in the liver divided by sheets of connective tissue
- These consist of:
- Central vein in the middle (drain into collecting veins that become hepatic veins, which leave the liver and empty into the vena cava)
- Portal triads at the vertices
- A portal triad consists of:
- Branch of hepatic artery proper (supplies liver with oxygen)
- Branch of portal vein (contains deoxygenated blood that is rich in nutrients)
- Bile ductule
- Each portal triad is accompanied by the following structures:
- Lymphatic vessels
- Branch of the vagus nerve
- A portal triad consists of:
Portal triad
The portal triad consists of three structures that run parallel to one another. These are a branch of the hepatic portal vein (large vessel), branch of the hepatic artery proper (pink, small vessel, left), and an interlobular bile duct (purple, small vessel, right).
Periportal Zone and Portal Triad of Liver
The section shows a periportal zone containing the structures of the portal triad → a branch of the proper hepatic artery (white overlay), a branch of the portal vein (white outline), and an interlobular bile duct (arrow). Next to the periportal zone, there are several hepatic lobules with plates of hepatocytes (trabeculae; example in green overlay). Between the trabeculae, sinusoids can be seen (red overlay).
The basolateral surface of hepatocytes faces the ________.
Sinusoids
The apical surface of hepatocytes faces the ________.
Lumen of the bile canaliculi
Hepatic Sinusoids
- Large capillaries lined with highly fenestrated endothelial cells
- Blood flows through the sinusoids and empties into the central vein of each lobule.
Perisinusoidal Space (of Disse)
- Plasma-filled space between the sinusoids and hepatocytes
- Contains hepatic stellate cells (Ito cells), which store vitamin A and are the main source of extracellular matrix production in liver injury (formation of scar tissue → fibrosis)
Consequences of Heavy Ethanol Consumption
- When ethanol is metabolized, there is an increase in the NADH/NAD+ ratio in the liver.
- Heavy ethanol consumption and consequently excess NADH result in:
- Anion gap metabolic acidosis
- Lactic acidosis → increased conversion of pyruvate to lactate by lactate dehydrogenase → ↑ lactate
- Ketoacidosis → Acetyl-CoA is shunted into the ketogenesis pathway instead of the TCA cycle (increased NADH/NAD+ ratio inhibits the TCA cycle, leading to a buildup of acetyl-CoA) → ↑ ketone bodies
- Fasting hypoglycemia
- ↑ NADH/NAD+ ratio → inhibition of conversion of cytosolic malate to oxaloacetic acid (OAA), increased conversion of OAA to malate → impaired gluconeogenesis, inhibition of TCA cycle
- In TCA, malate is normally converted to OAA via reduction of NAD+ to NADH. OAA is then converted to phosphoenolpyruvate, which is used in gluconeogenesis. Ethanol consumption leads to an elevated NADH/NAD+ ratio, causing the reaction equilibrium to favor the reverse reaction of OAA to malate. As a result, less OAA is converted to PEP, leaving less substrate for gluconeogenesis, which results in hypoglycemia. The buildup of malate also inhibits the TCA cycle.
- Hepatosteatosis
- In the glycolysis pathway, ↑ NADH/NAD+ ratio leads to increased conversion of DHAP to glycerol-3-phosphate
- ↑ NADH/NAD+ratio → inhibition of TCA → ↑ acetyl-CoA → ↑ fatty acid synthesis (due to the increased concentration of NADH, malate is converted to pyruvate by malic enzyme. This reaction generates one NADPH molecule. Excess acetyl-CoA and NADPH favors the synthesis of saturated fatty acids)
- ↑ Fatty acids and ↑ glycerol-3-phosphate → ↑ triglycerides → hepatic steatosis
Gallbladder Composition/Structure
- Fundus
- Body
- Infundibulum → the narrow portion of the body that is continuous with the neck of the gallbladder
- Neck
- Connects to the cystic duct → common hepatic duct → common bile duct
- Most common site of gallstone impaction
Layers of the Gallbladder Wall
- The gallbladder has no submucosa or muscularis mucosae.
- Serosa (on the inferior peritoneal surface) and adventitia (on the superior hepatic surface)
- Muscularis externa
- Lamina propria
- Mucosa
- Simple columnar epithelium with microvilli
- Secretes mucin
Layers of the Gallbladder Wall
Tissue layers (from top to bottom and from the outside in):
- Mucosa (dark purple)
- Lamina propria (purple)
- Tunica muscularis (pink
- Tunica subserosa (mottled pink/white; part facing the abdominal cavity pictured here) or adventitia (part facing the liver, not pictured)
Ampulla of Vater
(where the common bile duct and the pancreatic duct come together into the 2nd part of the duodenum)
Liver cirrhosis in chronic hepatitis B
Green overlay → confluent periportal liver cell necrosis (piecemeal necrosis)
Blue overlay → potential presence of ground glass hepatocytes (accurate assessment is not possible here due to insufficient magnification)
Hepatocyte
Hepatocytes are polygonal in shape, with a central round nucleus and prominent nucleoli (central, well-demarcated circular structure). They are highly metabolically active and therefore contain numerous mitochondria (green overlay) and endoplasmic reticulum (red lines). They store glycogen, which can be seen here as numerous electron-dense cytoplasmic granules (white arrows). Biliary canaliculi (yellow overlay; black arrow) are seen at the anastomotic junction of two adjacent hepatocytes. Tight junctions (white arrowheads) prevent the admixing of bile and sinusoidal blood. Hepatic sinusoids (blue overlay) are lined by a single permeable layer of liver sinusoidal endothelial cells (LSECs). The perisinusoidal space (red overlay) lies between the sinusoidal endothelial cells and the hepatocyte. Microvilli on the surface of the hepatocyte project into this space to increase the absorptive surface area.
Femoral Triangle
- Triangular intermuscular space in the superomedial aspect of the anterior thigh through which the major neurovascular structures of the lower limb pass
- Boundaries
- Superior → inguinal ligament
- Lateral → medial border of the sartorius
- Medial → medial border of the adductor longus
- Floor → adductor longus, iliopsoas, and pectineus muscles
- Roof → fascia lata
- Contents (lateral to medial) [NAVeL]
- Femoral nerve
- Femoral branch of the genitofemoral nerve
- Femoral artery
- Femoral vein
- Femoral canal
- Lymphatics
- Easy access into the arterial system via the femoral artery (e.g., coronary angiography)
- Easy access into the central venous system via the femoral vein (puncture should be made immediately medial to the palpable femoral pulse)
- Femoral hernia → herniation of intra-abdominal contents through the femoral canal
Inguinal Canal
- Extends between the deep (internal) and superficial (external) ring
- Contains the ilioinguinal nerve and in:
- Males → spermatic cord
- Females → round ligament of the uterus
- Roof (superior) → internal oblique and transversus abdominis muscles
- Floor (inferior) → inguinal ligament (shelving edge of external oblique) and lacunar ligament (medially)
- Posterior wall → transversalis fascia laterally; conjoint tendon medially
- Anterior wall → external oblique aponeurosis and internal oblique muscle laterally
Rectus Sheath
- Sheath formed by the fusion of aponeuroses (broad tendons) of the flat muscles (external oblique, internal oblique, and transversus abdominis muscles), which encloses the vertical muscles (rectus abdominis and pyramidalis muscles)
- Above the arcuate line
- Anterior layer → composed of the external oblique aponeurosis and the anterior lamina of the internal oblique aponeurosis
- Posterior layer → composed of the transversus abdominis aponeurosis and the posterior lamina of the internal oblique aponeurosis
- Below the arcuate line, only the anterior layer of the rectus sheath is present, composed of the aponeuroses of the external oblique, internal oblique, and transversus abdominis muscles
- At the arcuate line, the transversus abdominis aponeurosis and the posterior lamina of the internal oblique aponeurosis pass anterior to the rectus muscle. Thus, the lower 1/3rd of the rectus muscle is in direct contact with the peritoneum.
Arcuate Line of the Rectus Sheath (Linea Semicircularis)
- The bow-shaped inferior limit of the posterior rectus sheath, which lies approximately 1/3rd of the distance between the umbilicus and the pubic symphysis
- The inferior epigastric vessels perforate the rectus abdominis here.
Linea Alba
- Tendinous median line that extends from the xiphoid process to the pubic symphysis
- Formed by the fusion of the aponeuroses of the external oblique, internal oblique, and transversus abdominis muscles.
Linea Semilunaris
- Curved vertical line on the anterior abdominal wall at the lateral edge of each rectus abdominis muscle
- Herniation of intra-abdominal contents through the linea semilunaris is known as a Spigelian hernia.
A defect in the upper linea alba can cause _________.
Epigastric hernia
Herniation of intra-abdominal contents through the linea semilunaris is known as a _________.
Spigelian hernia
Femoral Hernia
- Sex: ♀ > ♂ (3:1) (female pelvis is wider than the male and the femoral ring accordingly larger)
- Peak incidence → 40–70 years (femoral ring becomes patulous with increasing age)
- Etiology
- Advancing age and female sex
- Increased intra-abdominal pressure
- Obesity
- Chronic constipation
- Chronic cough (e.g., due to COPD)
- Straining during micturition (e.g., due to prostatic hypertrophy)
- Multiparity
- Previous abdominal surgeries (especially those involving the inguinal region) (approx. 10% of femoral hernias arise after surgical repair of inguinal hernias. Herniorrhaphies may result in cranially directed traction on the inguinal ligament and potentially enlarge the femoral ring)
- In contrast to indirect inguinal hernias, which may occur congenitally, femoral hernias are almost always acquired.
- Typical femoral hernia (common) → protrusion of intraperitoneal contents along with the transverse abdominal fascia through the femoral ring into the femoral canal
- Although femoral hernias account for only about 5% of all hernias, they account for about 40% of all complicated hernias.
- A femoral hernia should be considered among 40–70-year-old women presenting with signs of mechanical bowel obstruction.
- Clinical Features:
- Non-complicated femoral hernia
- A globular, subcutaneous swelling in the groin (easier to detect if patient is standing)
- Localization → inferior to the inguinal ligament, lateral to the pubic tubercle, and medial to the femoral vein
- Swelling enlarges with coughing (palpable cough impulse) or a Valsalva maneuver
- Possibly, non-specific, dragging pain
- Femoral hernias can be difficult to palpate in obese patients. Ultrasound is indicated if a femoral hernia is suspected in this patient group.
- Treatment:
- All femoral hernias should be surgically repaired because of the high risk of complications.
- Richter hernia → herniation of only a part of the circumference of the bowel wall (femoral hernia is the most common site for Richter’s hernia)
Mechanical small bowel obstruction
Multiple air-fluid levels (green overlay) are visible in the mid-abdomen. The opaque appearance of the pelvis (red overlay) is due to fluid-filled loops of small bowel. There is a paucity of gas in the colon, and an air-fluid level is present in the dilated stomach (S).
Morgagni Hernia
- Congenital diaphragmatic hernia
-
Failure of fusion of the septum transversum anteriorly with the sternum and ribs → Morgagni hernia (Morgagni-Larrey hernia) (foramen of Morgagni (sternocostal triangle) → small diaphragmatic defects between sternal and costal attachments of the diaphragm)
- Rare → < 5% of CDH
- Anterior (sternocostal/parasternal) CDH (90% are right-sided)
- Infants with Morgagni hernia often present late (asymptomatic at birth since the hernia is often small)
- Clinical Features:
- Presentation depends on the degree of pulmonary hypoplasia and pulmonary hypertension (can present immediately after birth (minutes to hours) or later (days to weeks), and can range from asymptomatic to severe respiratory distress)
- Respiratory distress (e.g., nasal flaring, tachypnea, cyanosis, intercostal retractions, grunting) (respiratory distress is due to severe pulmonary hypoplasia, persistent pulmonary hypertension of the newborn (PPHN), and poor surfactant production, which are typical characteristics of congenital diaphragmatic hernias. Postnatally, the hypoxia and resulting respiratory acidosis → reactive vasoconstriction of the preexisting muscularized pulmonary arteries → persistent pulmonary hypertension of the newborn (PPHN))
- Barrel-shaped chest, scaphoid abdomen (concave anterior abdominal wall), and auscultation of bowel sounds in the chest
- Absent breath sounds on the ipsilateral side
- Mediastinal shift → shift of heart sounds/apex beat to the right side
- Possible syndromic dysmorphism (e.g., craniofacial, spinal dysraphism, cardiac) (∼ 50% of neonates have other congenital anomalies)
- Diagnostics:
- Antenatal ultrasound → most cases are diagnosed on routine antenatal ultrasound
- Fluid-filled stomach/bowel seen in the thorax
- Peristalsis may also be noted in the chest, confirming the diagnosis.
- Esophageal compression can cause polyhydramnios
- Hydrops fetalis may also be seen in severe cases (due to mediastinal shift and compression of the great vessels)
- Chest x-ray
- Abdominal contents, air/fluid-filled bowel, and poorly aerated lung in the ipsilateral hemithorax
- Mediastinal shift to the right and compression of the contralateral lung
- In doubtful cases, a naso-gastric tube is inserted and a chest radiograph is taken → the feeding tube will be seen in the thorax.
- In right-sided CDH → the liver appears as an intrathoracic soft tissue mass + absence of the normal intra-abdominal liver shadow
- Antenatal ultrasound → most cases are diagnosed on routine antenatal ultrasound
- Avoid pleurocentesis in a suspected diaphragmatic hernia because of the risk of bowel perforation, which is suggested by bile in the chest tube.
- Treatment:
- Prenatally diagnosed CDH → antenatal glucocorticoids (to decrease morbidity of pre-term delivery)
- Postnatal therapy
- Initial medical resuscitation
- Correction of hypoxia
- Intubation and mechanical ventilation → indicated in all infants with CDH
- Gastric decompression → insertion of a nasogastric tube and continuous suction (to decompress the stomach/bowel and reduce lung compression)
- Inotropic support may be required to maintain blood pressure
- Correction of hypoxia
- Surgical repair (thoracotomy or laparotomy
- Indicated in all cases of CDH
- Timing → after the infant is stabilized, often after 24–48 hours (longer in infants with severe pulmonary hypoplasia/pulmonary hypertension)
- Procedure → reduction of the hernial contents and primary closure of the defect
Bochdalek Hernia
- Congenital Diaphragmatic Hernia
-
Failure of fusion of the septum transversum postero-laterally with the pleuroperitoneal membranes → Bochdalek hernia (foramen of Bochdalek (Lumbocostal triangle) → small diaphragmatic defects between the lumbar vertebral and costal attachments of the diaphragm)
- Postero-lateral (lumbocostal) CDH (85% are left-sided) (probably because the left pleuroperitoneal membrane fuses later than the right side)
- Most common CDH, accounting for 90% of cases.
- Clinical Features:
- Presentation depends on the degree of pulmonary hypoplasia and pulmonary hypertension (can present immediately after birth (minutes to hours) or later (days to weeks), and can range from asymptomatic to severe respiratory distress)
- Respiratory distress (e.g., nasal flaring, tachypnea, cyanosis, intercostal retractions, grunting) (respiratory distress is due to severe pulmonary hypoplasia, persistent pulmonary hypertension of the newborn (PPHN), and poor surfactant production, which are typical characteristics of congenital diaphragmatic hernias. Postnatally, the hypoxia and resulting respiratory acidosis → reactive vasoconstriction of the preexisting muscularized pulmonary arteries → persistent pulmonary hypertension of the newborn (PPHN))
- Barrel-shaped chest, scaphoid abdomen (concave anterior abdominal wall), and auscultation of bowel sounds in the chest
- Absent breath sounds on the ipsilateral side
- Mediastinal shift → shift of heart sounds/apex beat to the right side
- Possible syndromic dysmorphism (e.g., craniofacial, spinal dysraphism, cardiac) (∼ 50% of neonates have other congenital anomalies)
- Diagnostics:
- Antenatal ultrasound → most cases are diagnosed on routine antenatal ultrasound
- Fluid-filled stomach/bowel seen in the thorax
- Peristalsis may also be noted in the chest, confirming the diagnosis.
- Esophageal compression can cause polyhydramnios
- Hydrops fetalis may also be seen in severe cases (due to mediastinal shift and compression of the great vessels)
- Chest x-ray
- Abdominal contents, air/fluid-filled bowel, and poorly aerated lung in the ipsilateral hemithorax
- Mediastinal shift to the right and compression of the contralateral lung
- In doubtful cases, a naso-gastric tube is inserted and a chest radiograph is taken → the feeding tube will be seen in the thorax.
- In right-sided CDH → the liver appears as an intrathoracic soft tissue mass + absence of the normal intra-abdominal liver shadow
- Antenatal ultrasound → most cases are diagnosed on routine antenatal ultrasound
- Avoid pleurocentesis in a suspected diaphragmatic hernia because of the risk of bowel perforation, which is suggested by bile in the chest tube.
- Treatment:
- Prenatally diagnosed CDH → antenatal glucocorticoids (to decrease morbidity of pre-term delivery)
- Postnatal therapy
- Initial medical resuscitation
- Correction of hypoxia
- Intubation and mechanical ventilation → indicated in all infants with CDH
- Gastric decompression → insertion of a nasogastric tube and continuous suction (to decompress the stomach/bowel and reduce lung compression)
- Inotropic support may be required to maintain blood pressure
- Correction of hypoxia
- Surgical repair (thoracotomy or laparotomy
- Indicated in all cases of CDH
- Timing → after the infant is stabilized, often after 24–48 hours (longer in infants with severe pulmonary hypoplasia/pulmonary hypertension)
- Procedure → reduction of the hernial contents and primary closure of the defect
Congenital Diaphragmatic Hernias
- Impaired development and/or fusion of embryonic structures (pleuroperitoneal membrane) → defect in the diaphragm persists during fetal development → displacement of abdominal contents into the pleural cavity → compression of lung tissue → pulmonary hypoplasia
- Types
- Failure of fusion of the septum transversum postero-laterally with the pleuroperitoneal membranes → Bochdalek hernia (foramen of Bochdalek (Lumbocostal triangle) → small diaphragmatic defects between the lumbar vertebral and costal attachments of the diaphragm)
- Most common CDH, accounting for 90% of cases.
- Postero-lateral (lumbocostal) CDH (85% are left-sided) (probably because the left pleuroperitoneal membrane fuses later than the right side)
- Failure of fusion of the septum transversum anteriorly with the sternum and ribs → Morgagni hernia (Morgagni-Larrey hernia) (foramen of Morgagni (sternocostal triangle) → small diaphragmatic defects between sternal and costal attachments of the diaphragm)
- Rare → < 5% of CDH
- Anterior (sternocostal/parasternal) CDH (90% are right-sided)
- Infants with Morgagni hernia often present late (asymptomatic at birth since the hernia is often small)
- Failure of fusion of the septum transversum postero-laterally with the pleuroperitoneal membranes → Bochdalek hernia (foramen of Bochdalek (Lumbocostal triangle) → small diaphragmatic defects between the lumbar vertebral and costal attachments of the diaphragm)
- Clinical Features:
- Presentation depends on the degree of pulmonary hypoplasia and pulmonary hypertension (can present immediately after birth (minutes to hours) or later (days to weeks), and can range from asymptomatic to severe respiratory distress)
- Respiratory distress (e.g., nasal flaring, tachypnea, cyanosis, intercostal retractions, grunting) (respiratory distress is due to severe pulmonary hypoplasia, persistent pulmonary hypertension of the newborn (PPHN), and poor surfactant production, which are typical characteristics of congenital diaphragmatic hernias. Postnatally, the hypoxia and resulting respiratory acidosis → reactive vasoconstriction of the preexisting muscularized pulmonary arteries → persistent pulmonary hypertension of the newborn (PPHN))
- Barrel-shaped chest, scaphoid abdomen (concave anterior abdominal wall), and auscultation of bowel sounds in the chest
- Absent breath sounds on the ipsilateral side
- Mediastinal shift: shift of heart sounds/apex beat to the right side
- Possible syndromic dysmorphism (e.g., craniofacial, spinal dysraphism, cardiac) (∼ 50% of neonates have other congenital anomalies)
- Diagnostics:
- Antenatal ultrasound → most cases are diagnosed on routine antenatal ultrasound
- Fluid-filled stomach/bowel seen in the thorax
- Peristalsis may also be noted in the chest, confirming the diagnosis.
- Esophageal compression can cause polyhydramnios
- Hydrops fetalis may also be seen in severe cases (due to mediastinal shift and compression of the great vessels)
- Chest x-ray
- Abdominal contents, air/fluid-filled bowel, and poorly aerated lung in the ipsilateral hemithorax
- Mediastinal shift to the right and compression of the contralateral lung
- In doubtful cases, a naso-gastric tube is inserted and a chest radiograph is taken: the feeding tube will be seen in the thorax.
- In right-sided CDH: the liver appears as an intrathoracic soft tissue mass + absence of the normal intra-abdominal liver shadow
- Antenatal ultrasound → most cases are diagnosed on routine antenatal ultrasound
- Avoid pleurocentesis in a suspected diaphragmatic hernia because of the risk of bowel perforation, which is suggested by bile in the chest tube.
- Treatment:
- Prenatally diagnosed CDH → antenatal glucocorticoids (to decrease morbidity of pre-term delivery)
- Postnatal therapy
- Initial medical resuscitation
- Correction of hypoxia
- Intubation and mechanical ventilation → indicated in all infants with CDH
- Gastric decompression → insertion of a nasogastric tube and continuous suction (to decompress the stomach/bowel and reduce lung compression)
- Inotropic support may be required to maintain blood pressure
- Correction of hypoxia
- Surgical repair (thoracotomy or laparotomy
- Indicated in all cases of CDH
- Timing → after the infant is stabilized, often after 24–48 hours (longer in infants with severe pulmonary hypoplasia/pulmonary hypertension)
- Procedure → reduction of the hernial contents and primary closure of the defect
Hiatal Hernia
- Protrusion of any abdominal structure/organ into the thorax through a lax diaphragmatic esophageal hiatus (in 95% of cases, a portion of the stomach is herniated)
- Saint triad → a combination of cholelithiasis, diverticulosis, and hiatal hernia may occur in ∼ 1.5% of patients (it is not clear whether the combination of these three conditions is a coincidence or due to a common pathophysiological process and etiology. Current research suggests that a connective tissue disorder called herniosis might play a role)
- Incidence increases with:
- Age → affects ∼ 70% of people > 70 years
- ↑ BMI
- The etiology is multifactorial (usually caused by a combination of a lax esophageal hiatus with increased intra-abdominal pressure)
- Lax diaphragmatic esophageal hiatus
- Advanced age (phrenoesophageal ligament weakens with increasing age.)
- Smoking (causes a loss of elastin fibers in the diaphragmatic crura)
- Obesity (deposition of fat in and around the crura widens the hiatus)
- Genetic predisposition (rare)
- Prolonged periods of increased intra-abdominal pressure
- Pregnancy
- Ascites
- Chronic cough
- Chronic constipation
- Defects of the pleuroperitoneal membrane
- Types:
- Type I → sliding hiatal hernia
- Type II → paraesophageal hiatal hernia
- Diagnostics
- Barium swallow → most sensitive test
- Assesses type and size of a hernia (including location of the stomach and the GEJ)
- Endoscopy → used to diagnose hiatal hernia and evaluate for possible complications
- Chest x-ray
- Retrocardiac soft tissue opacity with/without an air-fluid level
- Barium swallow → most sensitive test
Sliding Hiatal Hernia
- Protrusion of any abdominal structure/organ into the thorax through a lax diaphragmatic esophageal hiatus (in 95% of cases, a portion of the stomach is herniated)
- Saint triad → a combination of cholelithiasis, diverticulosis, and hiatal hernia may occur in ∼ 1.5% of patients (it is not clear whether the combination of these three conditions is a coincidence or due to a common pathophysiological process and etiology. Current research suggests that a connective tissue disorder called herniosis might play a role)
- Incidence increases with:
- Age → affects ∼ 70% of people > 70 years
- ↑ BMI
- The etiology is multifactorial (usually caused by a combination of a lax esophageal hiatus with increased intra-abdominal pressure)
- Lax diaphragmatic esophageal hiatus
- Advanced age (phrenoesophageal ligament weakens with increasing age.)
- Smoking (causes a loss of elastin fibers in the diaphragmatic crura)
- Obesity (deposition of fat in and around the crura widens the hiatus)
- Genetic predisposition (rare)
- Prolonged periods of increased intra-abdominal pressure
- Pregnancy
- Ascites
- Chronic cough
- Chronic constipation
- Defects of the pleuroperitoneal membrane
- Most common type of hiatal hernia (95% of cases)
- The GEJ and the gastric cardia slide up into the posterior mediastinum.
- The gastric fundus remains below the diaphragm (hourglass stomach)
- Clinical features:
- Symptoms of GERD
- Diagnostics
- Chest x-ray
- Retrocardiac soft tissue opacity with/without an air-fluid level
- Endoscopy → used to diagnose hiatal hernia and evaluate for possible complications
- Barium swallow → most sensitive test
- Assesses type and size of a hernia (including location of the stomach and the GEJ)
- Chest x-ray
- Treatment:
- Lifestyle modifications
- Proton pump inhibitors (PPIs) or histamine H2-receptor antagonists if symptoms of GERD occur
- Surgery → laparoscopic/open fundoplication and hiatoplasty
Paraesophageal Hiatal Hernia
- Protrusion of any abdominal structure/organ into the thorax through a lax diaphragmatic esophageal hiatus (in 95% of cases, a portion of the stomach is herniated)
- Saint triad → a combination of cholelithiasis, diverticulosis, and hiatal hernia may occur in ∼ 1.5% of patients (it is not clear whether the combination of these three conditions is a coincidence or due to a common pathophysiological process and etiology. Current research suggests that a connective tissue disorder called herniosis might play a role)
- Incidence increases with:
- Age → affects ∼ 70% of people > 70 years
- ↑ BMI
- The etiology is multifactorial (usually caused by a combination of a lax esophageal hiatus with increased intra-abdominal pressure)
- Lax diaphragmatic esophageal hiatus
- Advanced age (phrenoesophageal ligament weakens with increasing age.)
- Smoking (causes a loss of elastin fibers in the diaphragmatic crura)
- Obesity (deposition of fat in and around the crura widens the hiatus)
- Genetic predisposition (rare)
- Prolonged periods of increased intra-abdominal pressure
- Pregnancy
- Ascites
- Chronic cough
- Chronic constipation
- Defects of the pleuroperitoneal membrane
- Part of the gastric fundus herniates into the thorax.
- The GEJ remains in its anatomical position below the diaphragm.
- Clinical Features:
- Epigastric/substernal pain
- Early satiety (since part of the stomach lies in the thorax)
- Retching
- Symptoms of GERD can occur.
- Diagnostics
- Barium swallow → most sensitive test
- Assesses type and size of a hernia (including location of the stomach and the GEJ)
- Endoscopy → used to diagnose hiatal hernia and evaluate for possible complications
- Chest x-ray
- Retrocardiac soft tissue opacity with/without an air-fluid level
- Barium swallow → most sensitive test
- Treatment
- Conservative management → older patients or those with other comorbidities
- Surgery → laparoscopic/open herniotomy + fundoplication, hiatoplasty, and gastropexy/fundopexy
- Complications:
- Upper gastrointestinal bleeding (occult/massive) → iron deficiency anemia (occurs mainly due to vascular compromise of the herniated portion of the stomach, which leads to mucosal ischemia)
- Gastric ulcers
- Gastric perforation
- Gastric volvulus
- Total gastric obstruction
Dilation of the Esophageal Hiatus
Massive dilation of the esophageal hiatus (green line) and large hiatal hernia. The previously herniated stomach (S) has already been respositioned. (D= diaphragm; E= esophagus; T= thoracic cavity, A= abdomen).
Hiatal hernia
Barium swallow, AP radiograph showing the contrast-enhanced esophagus (1), the herniated esophageal sphincter (arrow), the sliding hiatal hernia (2), and the stomach (3) with typical contour.
Sliding Hiatal Hernia
The zig-zag shaped z-line (green line) seen during gastroscopy marks the the transition from the squamous epithelium of the esophagus (E) to the columnar epithelium of the stomach (S) at the gastroesphageal junction; this is also the physiologic level of the esophageal hiatus, which leads to slight narrowing (N) of the lumen. Here, both z-line and parts of the cardia are located above this narrowing, which points towards a sliding hiatal hernia.
Hiatus hernia
There is a large hiatus hernia in the left hemithorax with a concomitant pyothorax due to gastric gangrene.
Bronchogenic cyst
The lumen is lined by ciliated epithelium (green overlay; examples of cilia indicated by arrowheads) and layers of smooth muscle (yellow overlay) are visible, resembling upper airway tissue. Also, normal adipose tissue (examples of adipocytes indicated by black dashed outlines) can be found in the periphery.
The typical location (suprasternal, behind the manubrium, middle mediastinum) paired with the described histologic appearance leads to the diagnosis of a bronchogenic cyst.
Ranula (retention cyst arising in the sublingual gland)
Asymmetrical, partially white, partially translucent swelling, which extends above the lower teeth.
Pleomorphic Adenoma (Benign Mixed Tumor) of the Salivary Glands
- Peak incidence → 40–60 years
- Most common salivary gland tumor (accounts for 85% of benign salivary gland tumors)
- Etiology → ionizing radiation, environmental/occupational exposure (e.g., rubber manufacturing, cosmetologists, nickel compound exposure)
- Location → usually the parotid gland (∼ 80% of cases)
- Clinical features
- Gradual and painless unilateral swelling of the gland
- Robust, movable tumor
- Ultrasound → diagnostic method of choice in salivary gland tumors
- Histology
- Mixed cellular constitution with myoepithelial cells and chondroid tissue
- Cytokeratin is expressed immunohistochemically
- Malignant transformation may occur (∼ 5% of cases).
- Best treatment is superficial parotidectomy to prevent recurrence
Pleomorphic Adenoma of the Salivary Gland
There is a sharply demarcated, hyperintense, partially lobulated mass arising from the left retromandibular fossa, filling the entire left parapharyngeal space. The lesion is surrounded by a hypointense capsule. This finding is a pleomorphic adenoma. Differential diagnoses include other tumors of the parotid gland.
Pleomorphic Adenoma of the Salivary Gland
Pleomorphic Adenoma of the Parotid Gland
On the left, there is a hypercellular area made up of round epithelial cells with hyperchromatic nuclei and narrow, spindle-shaped myoepithelial cells with flattened nuclei. On the right, there is a paucicellular area predominantly made up of hyalinized stroma (pink acellular material).
This mixed pattern of epithelial (epithelial and myoepithelial cells) and mesenchymal (stroma) components within a salivary gland tumor is pathognomonic for pleomorphic adenoma.
Hypercontractile Esophagus
(Jackhammer Esophagus)
- Vigorous propagative contractions
- Presentation
- Dysphagia
- Regurgitation
- Retrosternal chest pain
- LES relaxation and pressure → normal
- Esophageal barium swallow → typically normal
- Parameters to diagnose hypercontractile esophagus require high-resolution manometry.
- Treatment:
- Avoid trigger foods (caffeine; foods that are too hot/cold)
- Medical
- Calcium channel blockers
- Nitrates
- Endoscopic therapy
- Botox injections
- Endoscopic myotomy
- Consider bougie or pneumatic dilation (in patients with associated EGJ obstruction)
- Surgery → long myotomy (for intractable symptoms)
Diffuse Esophageal Spasm
(Distal Esophageal Spasm/Corkscrew Esophagus/Rosary Bead Esophagus)
- Esophageal motility disorder that is characterized by repetitive, uncoordinated, nonprogressive contraction waves of the distal esophagus due to impared inhibitory innervation within the esophageal myenterin plexus
- Presentation
- Dysphagia
- Regurgitation
- Squeezing retrosternal chest pain during meals (similar to angina)
- LES relaxation and pressure → normal
- Esophageal barium swallow → corkscrew esophagus (pseudodiverticulosis)
- Esophageal manometry
- Simultaneous multi-peak premature contractions
- ≥ 10% of swallows have simultaneous contractions with mean amplitude ≥ 30 mm Hg
- Intermittent normal peristalsis (for this reason, 24-hour esophageal manometry is required, since normal peristaltic waves can also be seen)
- Treatment:
- Avoid trigger foods (caffeine; foods that are too hot/cold)
- Medical
- Calcium channel blockers
- Nitrates
- Endoscopic therapy
- Botox injections
- Endoscopic myotomy
- Consider bougie or pneumatic dilation (in patients with associated EGJ obstruction)
- Surgery → long myotomy (for intractable symptoms)
Corkscrew Esophagus
Helical contractions of the lower esophagus (green overlay), resulting in a corkscrew-like appearance.
Seen in patients with diffuse esophageal spasm (DES).
Sialolithiasis
(visible in the duct of the submandibular gland)
Eosinophilic Esophagitis
- Often associated with allergic disorders (e.g., individuals with allergic asthma, allergic rhinitis, food allergies). Ingestion of food containing allergens may lead to dysphagia and bolus obstruction.
- Clinical features
- Dysphagia
- Heartburn refractory to acid suppression therapy
- Food impaction
- Vomiting
- Endoscopic findings
- Trachealization of esophagus → circumferential mucosal lesions (rings/corrugations)
- Longitudinal furrows
- Mucosal fragility
- Biopsy → histological findings include an increased number of eosinophils.
- Treatment
- Dietary therapy → avoid potential food allergens (e.g., milk, egg, wheat, soy, peanuts)
- Acid suppression therapy with PPIs
- Topical glucocorticoids (e.g., budesonide, fluticasone)
- Esophageal dilation is indicated in patients with:
- Esophageal strictures
- Refractory to conservative therapy
Boerhaave Syndrome
- Risk factors
- Intake of large amounts of alcohol or food in the recent past
- Repeated episodes of vomiting
- Prolonged coughing
- Childbirth
- Seizures
- Weightlifting
- Severe vomiting/increased intrathoracic pressure → rupture of all layers of the esophageal wall (transmural perforation)
- In > 90% of cases, the rupture occurs in the distal third of the esophagus on the left dorsolateral wall surface
- Clinical Features
- Mackler triad (esp. in Boerhaave syndrome)
- Vomiting and/or retching
- Severe retrosternal pain that often radiates to the back
- Subcutaneous or mediastinal emphysema → crepitus in the suprasternal notch and neck region or crunching/crackling sound on chest auscultation (Hamman sign)
- Dyspnea, tachypnea, tachycardia
- Dysphagia
- Signs of sepsis
- Delayed presentations → critically ill with sepsis and multiorgan dysfunction
- Mackler triad (esp. in Boerhaave syndrome)
- Diagnostic:
- If esophageal perforation or Boerhaave syndrome is suspected, a neck or a chest x-ray is first conducted, followed by contrast esophagography. If inconclusive, or the patient is unstable/uncooperative, a CT scan is conducted to confirm the diagnosis.
- Initial diagnostic study → neck or chest x-ray
- Widened mediastinum
- Pneumomediastinum, pneumothorax, pneumoperitoneum, subcutaneous emphysema
- Pleural effusion
- Confirmatory test → Contrast leak on contrast esophagography (gold standard) reveals the location and size of the rupture
- Treatment
- ABCDE survey
- Establish airway and/or provide supplemental oxygen as needed.
- IV fluid resuscitation
- Nothing by mouth (NPO) and supply nutritional support
- Broad-spectrum IV antibiotics
- IV proton pump inhibitor (e.g., pantoprazole)
- Parenteral analgesics (see acute pain management)
Esophageal perforation (Boerhaave syndrome)
Mediastinal air (pneumomediastinum) is clearly identifiable as radiolucent shadows (green overlay) adjacent to the left common carotid artery (1) and the contour of the aortic arch and pulmonary trunk (2).
Esophageal Perforation
Fluoroscopy (gastrografin swallow; frontal view) of a patient following transesophageal echocardiography
Extravasated oral contrast (green overlay) through a perforation (red overlay) of the mid esophagus parallels the distal esophagus in the mediastinum.
Esophageal Perforation
Mediastinal air (pneumomediastinum) is visible as radiolucent shadows (green overlay) surrounding the trachea, the esophagus and within the anterior mediastinum. Subcutaneous emphysema (red overlay) is also visible.
Pneumomediastinum
CT chest of a patient with Boerhaave syndrome
A large amount of air is seen in the mediastinal soft tissues behind the left atrium in the vicinity of the esophagus. Small bilateral pleural effusions are also present and accompanied by passive atelectasis.
Esophageal Ring
(Schatzki rings)
- Narrowing of the esophagus
- Most commonly seen at the squamocolumnar junction
- Usually caused by chronic acid reflux
- Can lead to dysphagia
Esophageal Ring
(Schatzki rings)
Mallory Weiss Syndrome
- Upper gastrointestinal bleeding caused by tears to the longitudinal mucous membrane at the gastroesophageal junction
- Tears may extend above or below the gastroesophageal junction.
- Precipitating factors
- Severe vomiting
- Blunt abdominal trauma
- Strained defecation
- Predisposing conditions
- Alcoholism
- Bulimia nervosa
- Hiatal hernia (higher pressure gradient)
- Gastroesophageal reflux disease (GERD)
- Treatment
- General measures
- If bleedings stops spontaneously conservative treatment is usually sufficient
- Control of precipitating factors (e.g., omeprazole for GERD)
- Inpatient monitoring
- Treat hemodynamic instability if present
- Surgical treatment
- Indication → actively bleeding lesion
- Gold standard → esophagogastroduodenoscopy
- Therapeutic injection of an adrenaline solution or a fibrin sealant
- Electrocoagulation
- Endoscopic band ligation
- General measures
Plummer-Vinson syndrome (PVS)
- Triad of iron deficiency anemia, postcricoid dysphagia, and upper esophageal webs (upper esophageal webs can be seen on barium swallow and respond well to iron supplementation alone or endoscopic balloon dilation)
- Associated with an increased risk of esophageal squamous cell carcinoma and glossitis
- Etiopathogenesis
- Associated with PICA
Esophageal Web seen in Plummer Vinson Syndrome
Mallory Weiss Syndrome
Barret Esophagus
Barret Esophagus
Erosive Esophagitis
Gastroesophageal Reflux Disease
Barret Esophagus
- Histopathological examination of the mucosa shows a columnar epithelium instead of the normal squamous epithelium.
- A premalignant change that requires close surveillance.
- Risk factors for Barrett esophagus
- Male sex
- European descent
- Age ≥ 50 years
- Obesity
- Symptoms ≥ 5 years
- Reflux esophagitis → stomach acid damages mucosa of distal esophagus → nonkeratinized stratified squamous epithelium is replaced by nonciliated columnar epithelium and goblet cells (intestinal metaplasia, Barrett metaplasia)
- The physiological transformation zone (Z line) between squamous and columnar epithelium is shifted upwards.
- Long-segment (> 3 cm of columnar epithelium between Z line and GEJ) → higher cancer risk
- Complications → esophageal adenocarcinoma
Esophageal Carcinoma
Endoscopic view on an exophytic, irregularly demarcated esophageal carcinoma (green line) with central ulceration (dotted line). Because of the subtotal stenosis of the esophageal lumen, a metal stent will be placed.
Esophageal Carcinoma
Distal Stenosis in Esophageal Cancer
Contrast-enhanced x-ray of the esophagus and stomach (section): contrast enhancement of the distal third of the esophagus, esophagogastric junction, and the fundus (F). Mucosal changes (green areas) and a circular stenotic constriction at the esophagogastric junction (arrows) can be seen.
(C = cardia)
Esophageal Cancer
Barium swallow of the esophagus: stenosis of the distal third of the esophagus (arrows); contrast-enhanced proximal dilation.
Suspected diagnosis: Adenocarcinoma of the distal esophagus in a patient with a history of gastroesophageal reflux disease (Barrett’s esophagus).
Esophageal Cancer
Axial CT scan of the chest → stenotic esophageal cancer with tracheoesophageal fistula
