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GASTRO-1 Flashcards

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1
Q

Choanal Atresia

A
  • 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.
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2
Q

VACTERL Association

A

Mesodermal defects

A group of associated birth defects consisting of

  1. Vertebral anomaly
  2. Anal atresia
  3. Cardiac anomaly
  4. Tracheoesophageal fistula
  5. Esophageal atresia
  6. Renal anomaly
  7. Limb malformation
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3
Q

Duodenal Atresia

A
  • ∼ 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
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4
Q
A

Duodenal Atresia

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5
Q
A

Double Bubble Sign on Ultrasound Seen in Duodenal Atresia

S → stomach

D → proximal duodenum

Shaded area → pyloric sphincter

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6
Q
A

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)

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7
Q

Ileal Atresia

A
  • 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
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8
Q

Jejunal Atresia

A
  • 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
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9
Q
A

Apple Peel or Christmas Tree Seen in Jejunal Atresia

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10
Q

Hypertrophic Pyloric Stenosis

A

Etiology:

  1. 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)
  2. Genetic factors → patients with affected relatives have a higher risk of hypertrophic pyloric stenosis
  3. 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)

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11
Q

Pancreas Location

A
  • 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.
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12
Q

The uncinate process is _______ to the superior mesenteric vessels. The head, body, and tail of the pancreas lie ______ to the superior mesenteric vessels.

A

Posterior; anterior

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13
Q

Tumors in the pancreatic ____ often cause bile duct obstruction and can manifest with painless jaundice (Courvoisier sign).

A

Head

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14
Q

Innervation of the Pancreas

A
  • Innervation → celiac ganglia
    • Sympathetic fibers from T6–12
    • Parasympathetic fibers from the vagus nerve
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15
Q

Lymphatics of the Pancreas

A

Celiac, superior mesenteric, and splenic lymph nodes → paraaortic lymph nodes

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16
Q

Vasculature of the Pancreas

A

Arteries

  • Because the pancreas is embryologically derived from the foregut, it mainly receives arterial supply from the celiac trunk and its branches.
    1. 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
    2. 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)

​Veins

  1. Head and neck:
    • Pancreatic veins → superior mesenteric vein → portal vein
  2. Body and tail:
    • Pancreatic veins → splenic vein → portal vein
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17
Q
A

Microstructure of the exocrine pancreas

The functional unit (acinus) of the exocrine pancreas is visible:

  1. Acinar cells (green overlay; example indicated by A, arrow)
  2. Centroacinar cells (white overlay; example indicated by C)
  3. Acinar lumen (pink overlay, L) with the intercalated duct (dashed line, D)
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18
Q

Exocrine Pancreas

A
  • > 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.
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19
Q

Endocrine Pancreas

A
  • 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).
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20
Q
A

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.

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21
Q
A

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.

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22
Q
A

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.

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23
Q

Pancreatic Ducts

A
  • Smaller ducts have cuboidal epithelium.
  • Larger interlobular ducts have columnar epithelium.
  • Most pancreatic malignancies are adenocarcinomas that originate in the ductal epithelium.
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24
Q

Exocrine Pancreatic Secretions

A

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
  • Electrolytes (Na+, K+, Cl-, HCO3-) → concentration of Cl- and HCO3- increases with the rate of pancreatic juice secretion
  • Water
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25
Dorsal Pancreatic Bud
* Rest of pancreatic head, neck, body, tail, and accessory pancreatic duct
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Ventral Pancreatic Bud
1. Main pancreatic duct 2. Uncinate process 3. Lower part of pancreatic head Dorsal pancreatic bud: rest of pancreatic head, neck, body, tail, and accessory pancreatic duct
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Intraperitoneal Organs
* Organs covered by visceral peritoneum * Connected by mesentery Organs: 1. Stomach 2. Duodenum (first part) 3. Jejunum 4. Ileum 5. Cecum/appendix 6. Transverse colon 7. Sigmoid colon 8. Liver and gall bladder 9. Spleen 10. Pancreas (tail) 11. Female reproductive organs (ovaries, uterus, and fallopian tubes)
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Extraperitoneal Organs
**Retroperitoneal organs** * Organs that are not covered by visceral peritoneum * Not connected by mesentery Organs: 1. Esophagus 2. Anal canal 3. Kidneys 4. Adrenal glands 5. Ureters 6. IVC 7. Aorta **Secondary retroperitoneal organs** * Organs that were intraperitoneal in utero but became retroperitoneal after fusion of the mesenterywith posterior abdominal wall Organs: 1. Duodenum (second, third, and fourth parts) 2. Ascending colon 3. Descending colon 4. Upper rectum 5. Pancreas (head, neck, and body) **Subperitoneal organs** * Organs that lie inferior to the peritoneal cavity Organs: 1. Lower rectum 2. 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)
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Retroperitoneal Organs
* Organs that are not covered by visceral peritoneum * Not connected by mesentery Organs: 1. Esophagus 2. Anal canal 3. Kidneys 4. Adrenal glands 5. Ureters 6. IVC 7. Aorta **Secondary retroperitoneal organs** * Organs that were intraperitoneal in utero but became retroperitoneal after fusion of the mesenterywith posterior abdominal wall Organs: 1. Duodenum (second, third, and fourth parts) 2. Ascending colon 3. Descending colon 4. Upper rectum 5. Pancreas (head, neck, and body)
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Secondary Retroperitoneal Organs
* Organs that were intraperitoneal in utero but became retroperitoneal after fusion of the mesenterywith posterior abdominal wall Organs: 1. Duodenum (second, third, and fourth parts) 2. Ascending colon 3. Descending colon 4. Upper rectum 5. Pancreas (head, neck, and body)
31
Subperitoneal Organs
* Organs that lie inferior to the peritoneal cavity Organs: 1. Lower rectum 2. 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)
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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
33
Gastrophrenic Ligament
Attachment: * Stomach ←→ Diaphragm Content: * Left inferior phrenic artery Clinical Significance: * Anchors the stomach to the diaphragm * Part of the grater omentum
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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))
35
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
36
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)
37
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
38
Hepatoduodenal Ligament
Attachment: * First part of duodenum ←→ Porta hepatis in the liver Content: * Portal triad: 1. Proper hepatic artery 2. Portal vein 3. 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
39
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
40
Greater Omentum
* Component of visceral peritoneum that extends from the greater curvature of the stomach to cover the intestines. * Contains: 1. Gastrosplenic ligament 2. Gastrophrenic ligament 3. Gastrocolic ligament
41
Lesser Omentum
* Fold of peritoneum that extends from the lesser curvature of the stomach to the liver. * Contains 1. Gastrohepatic ligament 2. Hepatoduodenal ligament
42
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.
43
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
44
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)
45
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
46
Ileum Histology
**Mucosa** * Similar to duodenal mucosa, with thinning out of plicae circulares * Simple columnar epithelium * Structures that increase the absorptive surface area 1. Thin plicae circulares → transverse folds of the mucosa and submucosa (visible to the naked eye) 2. 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. 3. 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
47
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 1. Plicae circulares → transverse folds of the mucosa and submucosa (visible to the naked eye) 2. 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. 3. 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
48
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)
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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)
50
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
51
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
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Duodenum Histology
**Mucosa** * Simple columnar epithelium * Structures that increase the absorptive surface area 1. Plicae circulares → transverse folds of the mucosa and submucosa (visible to the naked eye) and most prominent in the jejunum 2. 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. 3. 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
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Duodenum ## Footnote 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.
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Plicae circulares ## Footnote 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.
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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.
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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.
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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).
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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
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Jejunum 1. Mucosa → composed of villi (finger-like projections; examples indicated by green overlay) and crypts of Lieberkuhn (between two adjacent villi) 2. Plicae circulares → a fold of submucosa (white overlay) and mucosa that protrudes into the lumen 3. Lymphatics and blood vessels within the submucosa 4. Muscularis propria → composed of an inner circular (dotted white bracket) and outer longitudinal (solid white bracket) layer of smooth muscles 5. Subserosa (yellow overlay) and serosa (dotted green line)
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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).
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Peyer Patches ## Footnote 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.
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Posterior to the Stomach
1. Spleen 2. Tail of the pancreas 3. Left kidney 4. Left adrenal gland 5. Transverse colon 6. Transverse mesocolon and lesser sac
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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** 1. Chief cell (basophilic) 2. Parietal cell (eosinophilic; pink) 3. Enterochromaffin-like cell (ECL cell) 4. P/D1 cell **Pylorus and antrum** 1. D cell 2. G cell
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Gastric mucosa ## Footnote 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.
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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. 1. Parietal cells are visible as large eosinophilic cells with a circular nucleus, giving them a fried-egg appearance (green overlay). 2. Chief cells (white dashed outline) are visible as pyramidal cells with basally located nuclei and basophilic cytoplasm that contains zymogen granules. 3. 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.
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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.
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Greater Omentum | (white star)
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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.
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Layers of the Colonic Wall Colonic layers from top to bottom and outside to inside: 1. The mucosa (purple) is lined with columnar epithelium and contains numerous intestinal glands (crypts of Lieberkuhn). 2. The submucosa contains MALT (white and pink), identifiable as the circular aggregates of basophilic cells. 3. The muscularis propria (light pink) is composed of an inner circular and outer longitudinal layer. 4. The serosa (dark pink) is composed of mesothelial tissue.
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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)
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Normal Appendix 1. Mucosa → simple columnar epithelium with multiple crypts 2. Submucosa → Numerous lymphoid follicles (green overlay) distorting the crypts are a characteristic histological feature of the appendix, esp. in children and young adults. 3. Muscular layer 4. Subserosa 5. Serosa
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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: 1. Microfold cells (M cells) → endocytose antigens and deliver them to antigen-presenting cells 2. B lymphocytes in germinal centers become plasma cells and secrete IgA, which prevents pathogens from binding to and invading the intestinal mucosa.
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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
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Celiac Trunk Vertebral Level
T12
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Superior Mesenteric Artery Vertebral Level
L1
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Inferior Mesenteric Artery Vertebral Level
L3
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Middle Suprarenal Artery Vertebral Level
L1
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Renal Artery Vertebral Level
L1–L2
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Gonadal Artery Vertebral Level
L2
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Inferior Phrenic Artery Vertebral Level
T12
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Lumbar Artery (set of four) Vertebral Level
L1–L4
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The right middle suprarenal artery runs ______ to the inferior vena cava.
Posterior
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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: 1. Spinal branches * Spinal canal 2. Terminal branches * Posterior abdominal wall * Muscles of the back
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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: 1. Ovarian artery * Ovaries * Lateral third of the fallopian tubes 2. Testicular artery * Testes * Epididymis (via epididymal branches)
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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: 1. Inferior suprarenal artery * Adrenal glands 2. Terminal branches * Kidney * Renal capsule * Ureters
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Splenic Artery
* Runs along the superior margin of the pancreas and enters the splenorenal ligament to supply the spleen * Branches 1. Pancreatic branches → run dorsal to the pancreas to supply the organ * Supply → pancreas 2. 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 3. 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) 4. Posterior gastric artery → runs superiorly within the gastrophrenic ligament to the fundus of the stomach * Supply → Posterior gastric wall and fundus region 5. Short gastric arteries → run within the gastrosplenic ligament to the fundus of the stomach * Supply → Stomach (fundus and greater curvature) 6. 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)
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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 1. 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: 1. 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) 2. Right hepatic artery * Liver (right portion) * Gall bladder (via cystic artery) * Caudate lobe 3. Left hepatic artery * Liver (left portion) * Caudate lobe 2. Gastroduodenal artery → runs posterior to the first part of the duodenum and divides into two branches 3. Right gastroepiploic artery → runs along the greater curvature of the stomach and anastomoses with left gastroepiploic artery * ​Supply: 1. Stomach 2. Duodenum 3. Pancreas 4. Anterior and posterior superior pancreaticoduodenal artery → anastomose with anterior and posterior branches of the inferior pancreaticoduodenal artery around the head of the pancreas * Supply: 1. Stomach 2. Duodenum 3. Pancreas
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The hepatic artery proper lies _______ to the portal vein and ______ to the bile duct within the hepatoduodenal ligament.
Anterior; left lateral
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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
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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 1. Duodenum * Celiac artery → superior pancreaticoduodenal artery * Superior mesenteric artery → inferior pancreaticoduodenal artery 2. Distal third of transverse colon * Superior mesenteric artery → middle colic artery * Inferior mesenteric artery → left colic artery 3. Rectum * Inferior mesenteric artery → superior rectal artery * Internal iliac artery → middle rectal artery * Examples 1. 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) 2. 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
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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)
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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
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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
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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
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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
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Inferior Vena Cava Area of Drainage
1. Lower extremities 2. Abdominal wall 3. Pelvic wall 4. Pelvic organs (except for the proximal rectum) 5. Kidneys and ureters 6. Adrenal glands
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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
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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
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The \_\_\_\_\_\_\_\_, \_\_\_\_\_\_\_\_\_, and ________ veins empty into the left renal vein.
Left suprarenal, left gonadal, and left inferior phrenic veins
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The portal vein drains the structures of ________ and empties indirectly into the ______ via the \_\_\_\_\_\_\_\_.
Gastrointestinal tract; hepatic veins; hepatic sinusoids
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The _______ drains the structures of the gastrointestinal tract and empties indirectly into the hepatic veins via the hepatic sinusoids.
Portal vein
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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
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Hepatic Portal Vein
* Formed by the confluence of the splenic vein and the superior mesenteric vein behind the neck of the pancreas (at the level of L1–L2) * Course * Runs within the hepatoduodenal ligament toward the porta hepatis (the vein runs together with the proper hepatic artery and the bile duct) * Divides into right and left branches at the hilum of the liver * Area of drainage → spleen and gastrointestinal organs (except for the rectum below the pectinate line) * Function * Provides most of the blood supply to the liver (∼ 70–80%) (the hepatic artery provides the remaining blood supply) * Carries nutrient-rich blood from the gastrointestinal organs and spleen to the liver * Portocaval anastomosis in patients with portal hypertension
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Hepatic portal vein is formed by the confluence of the _____ vein and the _____ vein behind the ______ (at the level of \_\_\_\_).
Splenic vein and the superior mesenteric vein; the neck of the pancreas ; L1–L2
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\_\_\_\_\_\_\_\_\_\_ is formed by the confluence of the splenic vein and the superior mesenteric vein behind the neck of the pancreas (at the level of L1–L2)
Hepatic portal vein
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Hepatic Portal Vein Function
1. Provides most of the blood supply to the liver (∼ 70–80%) (the hepatic artery provides the remaining blood supply) 2. Carries nutrient-rich blood from the gastrointestinal organs and spleen to the liver 3. Portocaval anastomosis in patients with portal hypertension
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Left gastric vein empty into the portal vein at the level of \_\_\_\_\_\_\_.
First part of duodenum
111
\_\_\_\_\_\_\_\_\_\_ anastomoses with the lower esophageal veins (caval system), giving rise to esophageal varices.
Left gastric vein
112
Left gastric vein anastomoses with the ________ (caval system), giving rise to esophageal varices.
Lower esophageal veins
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Prepyloric Vein | (via right gastric vein)
* Runs anterior to the pylorus and drains into the right gastric vein * Area of drainage * First part of duodenum * Used as a marker to identify the pylorus of the stomach during surgery * Usually connects the right gastric vein to the right gastroepiploic vein
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\_\_\_\_\_\_\_\_ is used as a landmark in laparoscopic cholecystectomy to prevent injury to the common bile duct.
Cystic vein
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\_\_\_\_\_\_\_\_ veins run in the falciform ligament along with ligamentum teres.
Paraumbilical veins
116
Paraumbilical veins anastomose with the __________ to give rise to caput medusae in patients with portal hypertension.
Superficial epigastric veins of the anterior abdominal wall
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\_\_\_\_\_\_\_\_\_\_ anastomose with the superficial epigastric veins of the anterior abdominal wall to give rise to caput medusae in patients with portal hypertension.
Paraumbilical veins
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Inferior Mesenteric Vein Tributaries
* Tributary of the splenic vein 1. Left colic vein * Runs along the descending colon * Area of drainage: * Distal third of transverse colon * Descending colon 2. Sigmoid veins * Group of veins emerging from the sigmoid colon * Area of drainage: * Sigmoid colon 3. Superior rectal vein * Tributaries from the rectal venous plexus join to form a single vein. * Runs along the mesorectum and sigmoid mesentery to start as the inferior mesenteric vein * Area of drainage: * Rectum and anal canal above the pectinate line
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Caval System
* Veins that drain directly/indirectly into the superior or inferior vena cava * In the GI tract, the esophagus and distal anal canal drain into the caval system.
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Portal System
* Veins that drain directly/indirectly into the portal vein * Most of the GI tract (except for the esophagus and the distal anal canal) drains into the portal system.
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Cavocaval Anastomoses
* Valveless anastomotic connections between the superior vena cava and inferior vena cava (the absence of valves allows for the bidirectional flow of blood in the event of an occlusion) * Function → provide an alternative route for venous drainage in the event of occlusion of the superior/inferior vena cava (e.g., due to tumor) * Sites of anastomosis 1. Anterior abdominal wall * Inferior vena cava ↔︎ common iliac vein ↔︎ external iliac vein ↔︎ inferior epigastric vein ↔︎ superior epigastric vein ↔︎ internal thoracic vein ↔︎ brachiocephalic vein ↔︎ superior vena cava 2. Posterior abdominal wall * Inferior vena cava ↔︎ lumbar veins ↔︎ ascending lumbar vein ↔︎ azygos vein (right)/hemiazygos vein (left) ↔︎ superior vena cava * Inferior vena cava ↔︎ lumbar veins ↔︎ vertebral venous plexus ↔︎ posterior intercostal veins ↔︎ azygos vein (right)/hemiazygos vein (left) ↔︎ superior vena cava
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Portocaval Anastomoses
* Valveless anastomotic connections between the portal vein and the caval system (SVC or IVC) (t he absence of valves allows for the bidirectional flow of blood) * Function → provide an alternative route for venous drainage in patients with portal hypertension (e.g., liver cirrhosis) * Sites of anastomosis 1. Distal esophagus → gives rise to esophageal varices * Portal vein ↔︎ left gastric vein ↔︎ distal esophageal veins ↔︎ azygos vein (right)/hemiazygos vein (left) ↔︎ superior vena cava * Portal vein ↔︎ left gastric vein ↔︎ left inferior phrenic vein ↔︎ inferior vena cava 2. Anterior abdominal wall → gives rise to caput medusae * Portal vein ↔︎ paraumbilical veins ↔︎ superior epigastric vein ↔︎ internal thoracic vein ↔︎ brachiocephalic vein ↔︎ superior vena cava * Portal vein ↔︎ paraumbilical veins ↔︎ thoracoepigastric vein ↔︎ axillary vein ↔︎ subclavian vein ↔︎ brachiocephalic vein ↔︎ superior vena cava * Portal vein ↔︎ paraumbilical veins ↔︎ inferior epigastric vein ↔︎ external iliac vein ↔︎ common iliac vein ↔︎ inferior vena cava 3. Rectum and anal canal → gives rises to anorectal varices) * Portal vein ↔︎ inferior mesenteric vein ↔︎ superior rectal vein ↔︎ middle and inferior rectal veins ↔︎ internal iliac vein ↔︎ inferior vena cava 4. Colon * Portal vein ↔︎ superior/inferior mesenteric vein ↔︎ colonic vein ↔︎ lumbar veins and ascending lumbar veins ↔︎ inferior and superior vena cava
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Inferior Vena Cava Thrombosis
* Etiology 1. Congenital IVC anomaly (venous drainage may be inadequate despite good collateral vessels, leading to venous hypertension and stasis of blood, causing thrombosis) 2. Prothrombotic state (e.g., thrombophilia, malignancy) (other causes include nephrotic syndrome, OCP use, and pregnancy) 3. Renal cell carcinoma 4. Abdominal masses causing extrinsic compression (e.g., large uterine fibroid) (venous stasis can promote thrombus formation as part of the Virchow triad) 5. Abdominal trauma or surgery (compression or shearing forces can cause endothelial injury and promote thrombus formation as part of Virchow triad) 6. Thrombotic occlusion of IVC filter * Clinical features * Acute IVC thrombosis 1. Low back and/or buttock pain 2. Flank pain 3. Hematuria 4. Oliguria/anuria (this is due to bilateral renal vein involvement) 5. Dilated veins over abdomen or legs * Chronic IVC thrombosis 1. Dull aching pain in legs 2. Lower limb swelling (this may increase with exercise and reduce with rest or leg elevation) 3. Postthrombotic syndrome * Diagnosis * Duplex ultrasonography → shows noncompressible veins with monophasic waveform (normally, the veins can be compressed and there is a continuous waveform with respiratory variation) * CT/MRI venography → shows filling defect (this should be avoided in patients with acute kidney injury) * Treatment → depends on etiology, presentation (acute or chronic), and patient factors * Medical management → anticoagulant therapy (e.g., LMW heparin, fondaparinux) (this prevents thrombus propagation, but does not reduce the risk of chronic venous insufficiency or postthrombotic syndrome) * Endovascular therapy → for thrombolytic injection or stent placement * Surgery → thrombectomy
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Lymph node clusters of the abdominal cavity lie along the course of major blood vessels and are divided into three main groups:
1. Preaortic nodes 2. Paraaortic nodes 3. Iliac lymph nodes
125
Common Iliac Lymph Nodes
Location: * Around common iliac vessels Area of Drainage: 1. Lymph from internal and external iliac lymph nodes 2. Middle third of ureter Termination: * Paraaortic lymph nodes
126
External Iliac Lymph Nodes
Location: * Around external iliac vessels Area of Drainage: * Urinary system 1. Lower part of ureter 2. Bladder (some lymph may drain into the internal iliac or common iliac lymph nodes) 3. Urethra (this includes anterior urethra in male individuals and distal portion of urethra in female individuals) * Female individuals → body of uterus, cervix, upper third of vagina * Male individuals → seminal vesicles and vas deferens * Superficial inguinal lymph nodes 1. Anal canal below pectinate line 2. Skin below umbilicus (except popliteal area) (this includes the skin of scrotum, penis, vulva, and perineum) 3. Lower third of vagina * Deep inguinal lymph nodes Termination: * Common iliac lymph nodes
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Internal Iliac Lymph Nodes
Location: * Around internal iliac vessels Area of Drainage: * Lower rectum and anal canal (above the pectinate line) * Urinary system 1. Lower part of ureter 2. Urethra (this includes prostatic, membranous, and a portion of anterior urethra in male individuals and proximal portion of urethra in female individuals) * Female individuals 1. Fallopian tubes 2. Body of uterus and cervix 3. Upper and middle third of vagina * Male individuals 1. Corpora cavernosa and corpus spongiosum 2. Prostate (lymph from the posterior surface of prostate accompanies vesical vessels to drain into the external iliac lymph nodes) 3. Seminal vesicles and vas deferens Termination: * Common iliac lymph nodes
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Paraaortic Lymph Nodes | (Lumbar Nodes)
Location: * Lateral and posterior to aorta and IVC Area of Drainage: 1. Kidney and adrenal gland 2. Upper part of ureter 3. Female individuals → ovaries, uterus (fundus), and fallopian tubes 4. Male individuals → testes 5. Lymph from common iliac lymph nodes Termination: * Lumbar lymphatic trunks
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Preaortic Lymph Nodes
Location: * Anterior to the aorta Area of Drainage: * Structures of the gastrointestinal tract: 1. Celiac lymph nodes → foregut 2. Superior mesenteric lymph nodes → midgut 3. Inferior mesenteric lymph nodes → hindgut Termination: Intestinal lymphatic trunk
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Superficial Inguinal Lymph Nodes
Area of Drainage: 1. Anal canal below pectinate line 2. Skin below umbilicus (except popliteal area) (this includes the skin of scrotum, penis, vulva, and perineum) 3. Lower third of vagina
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Pelvic Splanchnic Nerves
* Visceral nerves that arise from the S2 to S4 spinal levels. * They provide parasympathetic innervation to the pelvic viscera, which includes the bladder, rectum, uterus, cervix, and erectile tissue.
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Parasympathetic Innervation of Abdominal Organs
1. Vagus nerve * Origin → dorsal motor nucleus of the vagus * Enters the abdomen through the esophageal hiatus and runs in close proximity to the esophagus to divide into the following (LARP → Left Anterior, Right Posterior): * Anterior vagal trunk → derived from the left vagus nerve and gives off a hepatic branch * Posterior vagal trunk → derived from the right vagus nerve and joins the celiac plexus * Area of innervation: * Foregut and midgut (via the celiac plexus) * Liver and biliary tree (via hepatic branch) 2. Pelvic splanchnic nerve * Origin → anterior rami of S2–S4 spinal nerves * Runs laterally to join the inferior hypogastric plexus * Some fibers ascend superiorly as hypogastric nerves to join the superior hypogastric and inferior mesenteric plexuses * Area of innervation: * Hindgut (via the inferior mesenteric plexus) * Pelvic organs (e.g., bladder) * The Cannon point (at the left colic flexure) is where parasympathetic innervation transitions from the vagus nerve to the pelvic splanchnic nerves.
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Transjugular Intrahepatic Portosystemic Shunt (TIPS or TIPSS)
Indications 1. Persistent, recurring, or treatment-resistant upper gastrointestinal bleeding resulting from portal hypertension, e.g., from esophageal varices (TIPS ↓ portal pressure → ↓ risk of variceal bleeding) 2. Refractory ascites 3. Acute thrombosis of portal vein 4. Patients with hepatorenal syndrome who are not eligible for or are awaiting liver transplantation (this particular group of patients may benefit from the short-term effects of TIPS implementation; glomerular filtration and plasma creatinine concentration may improve. However, the procedure is not recommended for the general treatment of hepatorenal syndrome because of the risk of hepatic encephalopathy) Procedure * A needle catheter inserted via the internal jugular vein → passed along to hepatic vein → pierced through liver parenchyma to intrahepatic branch of the portal vein → expandable metal stent is placed → side-to-side portocaval shunt **(between portal vein and hepatic vein)** * Assures blood drainage from the portal to the systemic system bypassing the liver, thus lowering portal pressure Contraindications 1. Pre-existing hepatic encephalopathy or cirrhosis → shunt implementation results in reduced hepatic elimination of ammonia and worsening of encephalopathy. 2. Heart failure 3. Severe pulmonary hypertension \> 45 mm Hg 4. Uncontrolled systemic infection or sepsis 5. Hepatic cysts or tumors 6. Cavernous transformation of the portal vein following thrombosis
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Hepatic Capsule
Two layers: 1. 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) 2. 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
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Porta Hepatis Structures
* Fissure between the caudate and quadrate lobes that contains several veins, arteries, and nerves: 1. Common hepatic duct (leaving) 2. Hepatic artery proper (entering) 3. Hepatic portal vein (entering) 4. Hepatic nerve plexus and lymphatic vessels
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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
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Liver Blood Supply
Dual blood supply 1. Hepatic artery proper (supplies 20–40% of blood) → a branch of the common hepatic artery, which branches off the celiac trunk of the abdominal aorta 2. Portal vein (supplies 60–80% of blood) * Forms from the superior mesenteric vein (SMV) and splenic vein * Collects blood from gastrointestinal tract, spleen, and pancreas * Despite being deoxygenated, it still supplies the liver with about half its oxygen demands. * Delivers nutrients and other metabolites
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Liver Venous Drainage
* Hepatic veins, which drain into the inferior vena cava
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Liver Lymphatics
* Celiac lymph node cluster
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Liver Innervation
1. Glisson capsule and serosa → lower intercostal nerves 2. Parenchyma → hepatic plexus (contains sympathetic (from the celiac plexus) and parasympathetic (vagus nerve) nerve fibers, which regulate metabolism, blood flow, and bile secretion) Distention of the capsule results in well-localized, sharp pain, as seen in ascites, inflammation, or hepatic cancer.
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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: 1. Branch of hepatic artery proper (supplies liver with oxygen) 2. Branch of portal vein (contains deoxygenated blood that is rich in nutrients) 3. Bile ductule * Each portal triad is accompanied by the following structures: 1. Lymphatic vessels 2. Branch of the vagus nerve
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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).
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Periportal Zone and Portal Triad of Liver ## Footnote 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).
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The basolateral surface of hepatocytes faces the \_\_\_\_\_\_\_\_.
Sinusoids
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The apical surface of hepatocytes faces the \_\_\_\_\_\_\_\_.
Lumen of the bile canaliculi
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Hepatic Sinusoids
* Large capillaries lined with highly fenestrated endothelial cells * Blood flows through the sinusoids and empties into the central vein of each lobule.
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Kupffer Cells
* Type of macrophage * Housed in the sinusoids * Phagocytize foreign particles, bacteria, and damaged, old blood cells.
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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)
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Hepatic Zone II
* Intermediate zone * Affected in yellow fever
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Hepatic Zone III
* Pericentral vein/centrilobular zone * The least oxygenated zone, and thus most susceptible to ischemia * Most sensitive to metabolic toxins (e.g., ethanol, CCl4, halothane, rifampin, acetaminophen) * Has the highest amount of cytochrome P-450
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Hepatic Zone I
* Periportal zone * Best oxygenated and, therefore, is most resistant to ischemia. * Affected first in viral hepatitis and toxic substance ingestion, e.g., cocaine.
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Only _______ are able to synthesize ketone bodies from acetyl-CoA.
Hepatocytes But the liver cannot use them for itself!
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Liver Storage
1. Glycogen (muscle tissue also has large glycogen stores, but only for own use. The liver supplies the whole body with glucose when needed) 2. Lipoproteins (the largest lipid stores are in fat tissue in the form of TAGs) 3. Fat-soluble vitamins (A, K, E, D), folate, and vitamin B12 4. Iron and copper
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Liver Detoxification and Clearance/Excretion
1. Urea cycle (amino acid metabolism) → liver produces urea, which is excreted by the kidneys. 2. Cytochrome-P450 system involved in detoxification 3. Biotransformation → conversion of lipophilic substances into water-soluble substances, which can then be eliminated with the urine or bile (substrates of biotransformation can be endogenous (e.g., bilirubin, steroid hormones) or exogenous (medications, environmental toxins)) * Breakdown of ethanol * Removal of unconjugated bilirubin (liver conjugates it with glucuronate and excretes it in bile)
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Liver is the site of erythropoiesis from ______ until \_\_\_\_\_.
6 weeks' gestation until birth
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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: 1. Anion gap metabolic acidosis 1. Lactic acidosis → increased conversion of pyruvate to lactate by lactate dehydrogenase → ↑ lactate 2. 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 2. 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. 3. 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
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Energy Sources During Fasting and Starvation
1. **Postprandial** * Glycolysis * Aerobic respiration 2. **Fasting (in between meals)** * Glycogenolysis (predominantly) * ß-oxidation of free fatty acids released by adipose tissue (to a smaller extent) * Gluconeogenesis 3. **Starvation days 1–3** * Glycogenolysis * ß-oxidation → muscle and liver now primarily utilize free fatty acids released by adipose tissue instead of glucose. * Gluconeogenesis using the following substrates: * Alanine and lactate, provided by peripheral tissue * Glycerol and propionyl-CoA (the only triacylglycerol component contributing to gluconeogenesis; comes from odd-chain free fatty acids), released by adipose tissue 4. **Starvation after day 3** * Ketogenesis and subsequent ketone bodies consumption * Ketone bodies are synthesized from acetyl-CoA, which is provided by ß-oxidation of free fatty acids that are released by adipose stores. * Synthesized ketone bodies become the brain's main energy source after 3 days of fasting. * Gluconeogenesis * When ketone bodies are depleted, vital proteins are degraded even more quickly in order to serve as substrates in gluconeogenesis. * This process will eventually result in organ failure and ultimately death.
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Gallbladder Composition/Structure
1. Fundus 2. Body 3. Infundibulum → the narrow portion of the body that is continuous with the neck of the gallbladder 4. Neck * Connects to the cystic duct → common hepatic duct → common bile duct * Most common site of gallstone impaction
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Layers of the Gallbladder Wall
* **The gallbladder has no submucosa or muscularis mucosae**. 1. Serosa (on the inferior peritoneal surface) and adventitia (on the superior hepatic surface) 2. Muscularis externa 3. Lamina propria 4. Mucosa * Simple columnar epithelium with microvilli * Secretes mucin
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Layers of the Gallbladder Wall Tissue layers (from top to bottom and from the outside in): 1. Mucosa (dark purple) 2. Lamina propria (purple) 3. Tunica muscularis (pink 4. Tunica subserosa (mottled pink/white; part facing the abdominal cavity pictured here) or adventitia (part facing the liver, not pictured)
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Intrahepatic Bile Ducts
1. Bile canaliculi → intrahepatic bile ductules (canals of Hering) → segmental bile ducts → sectional ducts 2. Common hepatic duct (CHD) → formed by the right and left hepatic ducts
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Extrahepatic Bile Ducts
Common bile duct * Formed by the common hepatic duct and cystic duct * Travels in the free edge of the lesser omentum, in the hepatoduodenal ligament * Posterior to the duodenum and the pancreas * Connects with the main pancreatic duct * Drains into the hepatopancreatic ampulla (ampulla of Vater)
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Hepatobiliary Triangle (Calot triangle)
* An anatomical space formed by the common hepatic duct, the cystic duct, and the lower border of the liver * The Calot triangle contains the cystic artery and the cystic lymph node (Lund's node). * During cholecystectomy, the Calot triangle must be carefully identified to prevent damage to the cystic artery and extrahepatic biliary system.
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Ampulla of Vater (where the common bile duct and the pancreatic duct come together into the 2nd part of the duodenum)
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Bile Composition
* Secretion produced by the liver and stored in the gallbladder that aids in digestion, neutralization of gastric acid, fat absorption, and excretion of bilirubin and cholesterol. 1. Bile pigments * Bilirubin (yellow pigment) * Excreted as water-soluble (conjugated) bilirubin * Conjugated within the liver * Transported in the blood bound to carrier proteins * Lipid soluble (unconjugated) metabolite of hemoglobin * Biliverdin (green pigment) * Byproduct of hemoglobin breakdown 2. Bile acids * Primary bile acids * Cholic acid, chenodeoxycholic acid * Synthesized in the liver from cholesterol (rate-limiting enzyme → cholesterol 7-α hydroxylase) * Stored in the gallbladder * Secondary bile acids * Deoxycholic acid, lithocholic acid * Synthesized in the intestinal lumen by the action of bacterial flora * Bile acids are conjugated with glycine or taurine to form bile salts and become water-soluble. 3. Other components → phospholipids, cholesterol, water, and ions
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Liver cirrhosis in chronic hepatitis B ## Footnote 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)
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Hepatocyte ## Footnote 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.
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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]** 1. Femoral nerve 2. Femoral branch of the genitofemoral nerve 3. Femoral artery 4. Femoral vein 5. Femoral canal 6. 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
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Femoral Sheath
* Connective tissue formed by the iliac fascia and transversalis fasciae about 3–4 cm below the inguinal ligament * Contents * Encloses most contents of the femoral triangle, including: 1. Femoral vein 2. Femoral artery 3. Femoral canal 4. Deep inguinal lymph nodes * **Does not cover the femoral nerve** * Vertical septae divide the sheath into compartments for the contents of the femoral triangle.
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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
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Hesselbach Triangle Borders
* Medially → rectus abdominis muscle * Laterally → inferior epigastric vessels * Inferiorly → inguinal ligament
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Layers of the Anterior Abdominal Wall | (from superficial to deep)
1. Skin and subcutaneous tissue 2. Superficial fascia (above the umbilicus, the superficial fascia is composed of a single sheet of fatty connective tissue. Below the umbilicus, the superficial fascia is composed of two layers → a fatty and a membranous/fibrous one) * Superficial fatty layer (Camper fascia) * Deep membranous layer (Scarpa fascia) (Dartos layer of the scrotum, the superficial fascia of the clitoris and penis, and the superficial fascia of the perineum (Colles fascia) are continuations of the Scarpa fascia) 3. External oblique muscle 4. Internal oblique muscle 5. Transversus abdominis muscle 6. Deep fascia (transversalis fascia) → fuses with the deep fascia of the thigh (fascia lata) (rupture of the spongy urethra leads to accumulation of urine between the Scarpa fascia and the transversalis fascia. Because the Scarpa fascia fuses with the deep fascia of the thigh (fascia lata), extravasated urine cannot enter the thigh) 7. Preperitoneal adipose tissue 8. Parietal peritoneum
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Rupture of the spongy urethra leads to accumulation of urine between the ______ fascia and the _____ fascia.
Scarpa fascia; transversalis fascia. Because the Scarpa fascia fuses with the deep fascia of the thigh (fascia lata), extravasated urine cannot enter the thigh.
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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.
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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.**
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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.
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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.
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A defect in the upper linea alba can cause \_\_\_\_\_\_\_\_\_.
Epigastric hernia
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Herniation of intra-abdominal contents through the linea semilunaris is known as a \_\_\_\_\_\_\_\_\_.
Spigelian hernia
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Spermatic Cord
* Extension of the abdominal wall into the scrotum through the inguinal canal * Contents of the spermatic cord * Three arteries → testicular artery, ductus deferens artery, cremasteric artery * Three nerves → genital branch of genitofemoral, cremasteric nerve, sympathetic nerve fibers * Three other structures → ductus deferens, pampiniform plexus, lymphatic vessels
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Direct Inguinal Hernia
* Acquired condition * Caused by weakening of the transversalis fascia * Commonly secondary to conditions resulting in increased intraabdominal pressure (e.g., chronic obstructive pulmonary disease with chronic coughing, constipation) * May be associated with long-term glucocorticoid use * Medial to the inferior epigastric blood vessels (within Hesselbach triangle) and lateral to the rectus abdominis * Hernial sac protrudes directly through the posterior wall of the inguinal canal (without involvement of the spermatic cord or round ligament of the uterus) * Only herniates through the superficial (external) ring * Only surrounded by the external spermatic fascia * Palpate the inguinal canal * Invaginate the scrotal skin toward the superficial inguinal ring with the index or little finger. * Ask the patient to perform a Valsalva maneuver. * A bulge palpable on the fingertip confirms the diagnosis of an inguinal hernia * Treatment: * Manual reduction of inguinal hernia should not be attempted if there are any signs of strangulation. (inadvertently reducing ischemic or gangrenous contents of a strangulated hernia can lead to diffuse peritonitis (e.g., due to bowel perforation) and the need for laparotomy and bowel resection) * Incarcerated inguinal hernia causing bowel obstruction (without evidence of strangulation) is not a contraindication for manual reduction of hernial contents. * Surgical repair of the hernial defect is the only definitive treatment of inguinal hernia. The management of direct inguinal hernia and indirect inguinal hernia does not differ.
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Indirect Inguinal Hernia
* Most commonly results from incomplete obliteration of processus vaginalis in males or diverticulum of Nuck in females during fetal development (but can also be acquired). * May not become apparent until adulthood despite being present since birth. * Lateral to the inferior epigastric blood vessels (outside Hesselbach triangle) * Runs from the deep inguinal ring through the inguinal canal to the superficial (external) inguinal ring (in men, along with the spermatic cord) * Surrounded by the external spermatic fascia, cremasteric muscle fibers, and internal spermatic fascia * Indirect inguinal hernia may be associated with a communicating hydrocele. * Treatment: * Manual reduction of inguinal hernia should not be attempted if there are any signs of strangulation (inadvertently reducing ischemic or gangrenous contents of a strangulated hernia can lead to diffuse peritonitis (e.g., due to bowel perforation) and the need for laparotomy and bowel resection) * Incarcerated inguinal hernia causing bowel obstruction (without evidence of strangulation) is not a contraindication for manual reduction of hernial contents. * Surgical repair of the hernial defect is the only definitive treatment of inguinal hernia. The management of direct inguinal hernia and indirect inguinal hernia does not differ.
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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: 1. 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)
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Mechanical small bowel obstruction ## Footnote 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).
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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 * 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 1. Correction of hypoxia * Intubation and mechanical ventilation → indicated in all infants with CDH 2. Gastric decompression → insertion of a nasogastric tube and continuous suction (to decompress the stomach/bowel and reduce lung compression) 3. Inotropic support may be required to maintain blood pressure * 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
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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 * 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 1. Correction of hypoxia * Intubation and mechanical ventilation → indicated in all infants with CDH 2. Gastric decompression → insertion of a nasogastric tube and continuous suction (to decompress the stomach/bowel and reduce lung compression) 3. Inotropic support may be required to maintain blood pressure * 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
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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) * 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 * 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 1. Correction of hypoxia * Intubation and mechanical ventilation → indicated in all infants with CDH 2. Gastric decompression → insertion of a nasogastric tube and continuous suction (to decompress the stomach/bowel and reduce lung compression) 3. Inotropic support may be required to maintain blood pressure * 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
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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) 1. 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) 2. Prolonged periods of increased intra-abdominal pressure * Pregnancy * Ascites * Chronic cough * Chronic constipation 3. Defects of the pleuroperitoneal membrane * Types: 1. Type I → sliding hiatal hernia 2. 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
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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) 1. 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) 2. Prolonged periods of increased intra-abdominal pressure * Pregnancy * Ascites * Chronic cough * Chronic constipation 3. 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) * Treatment: * Lifestyle modifications * Proton pump inhibitors (PPIs) or histamine H2-receptor antagonists if symptoms of GERD occur * Surgery → laparoscopic/open fundoplication and hiatoplasty
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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) 1. 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) 2. Prolonged periods of increased intra-abdominal pressure * Pregnancy * Ascites * Chronic cough * Chronic constipation 3. 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 * Treatment * Conservative management → older patients or those with other comorbidities * Surgery → laparoscopic/open herniotomy + fundoplication, hiatoplasty, and gastropexy/fundopexy * Complications: 1. 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) 2. Gastric ulcers 3. Gastric perforation 4. Gastric volvulus 5. Total gastric obstruction
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Dilation of the Esophageal Hiatus ## Footnote 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).
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Esophageal Hiatus
* Central opening of the diaphragm, which allows the esophagus to pass through into the peritoneal cavity; forms the upper part of the esophageal sphincter and the reflux barrier * Formed by: 1. Left and right paravertebral tendinous crura 2. Median arcuate ligament
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Gastroesophageal Junction (GEJ)
* Normally lies at the level of the esophageal hiatus * Phrenoesophageal ligament (PEL) attaches to the esophagus at the GEJ * Peritoneal fold that encircles the distal portion of the esophagus and gastroesophageal junction and connects them to the peritoneal surface of the diaphragm * Closes the esophageal hiatus and helps maintain the intra-abdominal position of the GEJ
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Hiatal hernia ## Footnote 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.
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Sliding Hiatal Hernia ## Footnote 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.
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Hiatus hernia There is a large hiatus hernia in the left hemithorax with a concomitant pyothorax due to gastric gangrene.
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Bronchogenic cyst ## Footnote 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.
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Secretin
* Source: * S cells (duodenum) * Function: * ↑ Secretion of bile * ↑ Pancreatic secretion of bicarbonate, which neutralizes the acidic chyme arriving from the stomach (necessary for pancreatic enzyme function) * ↓ Secretion of gastric acid * Stimulation: * Postprandial → ↑ gastric acid and fatty acids in the duodenum * Inhibition: * Somatostatin
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Nitric Oxide (NO)
* Source: * Epithelial cells * Smooth muscle cells * Neural cells * Function: * Relaxation of smooth muscle and sphincters (e.g., LES) * Improves circulation (vasodilatory property)
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Vasoactive Intestinal Peptide (VIP)
* Source: * Small intestine * Gallbladder * Parasympathetic neurons in sphincters * APUD cells of the pancreas * Function: * ↑ Secretion of water and electrolytes * ↑ Relaxation of intestinal sphincters and smooth muscle * Stimulation: * Distention of the stomach * Vagal stimulation * Inhibition: * Sympathetic activity
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Motilin
* Source: * Mo cells (small intestine) * Function: * Produces migratory motor complexes (↑ intestinal motility) * Stimulation: * Fasting * Inhibition: * Intake of food Motilin receptor agonists (eg, erythromycin) are used to stimulate intestinal peristalsis
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Gastric Inhibitory Polypeptide (GIP)
* Source: * K cells (duodenum, jejunum) * Function: * ↑ Insulin secretion (more pronounced with the administration of oral glucose compared to intravenous glucose) * ↓ Secretion of gastric acid * ↓ Gastric emptying * Stimulation: * Postprandial → fatty acids, glucose, amino acids entering small intestine * Inhibition: * Fasting
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Bicarbonate
* Source: * Mucosal cells (salivary glands, stomach, pancreas, duodenum) * Brunner glands (duodenum) * Function: * Neutralizes gastric acid * Stimulation: * Secretin * Inhibition: * None
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Pepsin | (converted from prohormone pepsinogen)
* Source: * Gastric chief cells (secrete the prohormone pepsinogen, which is converted to pepsin on contact with gastric acid) * Function: * Protein digestion * Stimulation: * Vagus nerve (ACh) * Low gastric pH * Inhibition: * High gastric pH * Somatostatin
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Intrinsic Factor (IF; vitamin B12 binding protein)
* Source: * Gastric parietal cells * Function: * Binds to vitamin B12 and enables its absorption in the terminal ileum * Stimulation: * Vagus nerve (ACh) * Gastrin * Histamine * Inhibition: * GIP * Prostaglandins * Secretin * Somatostatin
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Gastric Acid (Hydrochloric Acid)
* Source: * Gastric parietal cells * Function: * ↓ Stomach pH * Activates pepsinogen to pepsin * Kills microorganisms (except Helicobacter pylori) * Stimulation: * Vagus nerve (ACh) * Gastrin * Histamine * Inhibition: * GIP * Prostaglandins (stimulate mucous production and inhibit HCl secretion, which serves to protect the gastric mucosa) * Secretin * Somatostatin * Cholecystokinin
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Ghrelin
* Source: * P/D1 cells (stomach) * Function: * ↑ Appetite and hunger (lateral hypothalamus) * ↑ Neuropeptide Y release (arcuate nucleus of hypothalamus) * ↑ Growth hormone release (anterior pituitary) * ↑ Gastric motility * Stimulation: * Fasting * Sleep deprivation * Inhibition: * Stomach distention (food intake) ↑ in Prader-Willi syndrome ↓ after gastric bypass surgery
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Cholecystokinin
* Source: * I cells (duodenum, jejunum) * Function: * ↑ Contraction of the gallbladder * ↑ Secretion of pancreatic enzymes by acting on neural muscarinic pathways * ↑ Relaxation of the sphincter of Oddi * ↓ Gastric emptying * Stimulation: * Postprandial → fatty acids and amino acids entering the small intestine * Inhibition: * Somatostatin * Fasting
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Somatostatin
* Source: * D cells (duodenum, pancreas) * Hypothalamus * Function: * Inhibits gastrointestinal secretions * ↓ Gastric acid * ↓ Gastrin * ↓ Pepsinogen * ↓ Cholecystokinin * ↓ Secretin * ↓ Pancreatic secretions (VIP, glucagon, insulin) * ↓ Gastric inhibitory polypeptide * Inhibits gall bladder contraction * Decreases motility of the stomach and intestine * Causes splanchnic vasoconstriction (by directly stimulating somatostatin receptors in splanchnic smooth muscle and indirectly by decreasing the secretion of splanchnic vasodilators (e.g., glucagon, VIP)) * Decreases growth hormone and TSH secretion * Stimulation: * Postprandial → gastric acid, fatty acids, and amino acids entering the duodenum * Inhibition: * Vagus nerve (ACh)
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Gastrin
* Source: * G cells (antrum of the stomach, duodenum) * Function: * ↑ Gastric acid secretion (stimulates ECL cells to secrete histamine, which stimulates parietal cells to secrete gastric acid. Gastrin therefore indirectly stimulates gastric acid secretion) * ↑ Gastric motility * Proliferation of the gastric mucosa * Stimulation: * Vagus nerve (via gastrin-releasing peptide and GRP released from presynaptic terminals of postganglionic fibers) (M3) * Amino acids and peptides * Decreased acidity (alkalinization) * Distention of the stomach * Chronic PPI administration * Inhibition: * Somatostatin * Prostaglandins * Gastric pH \< 1.5
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Sialolithiasis
* Formation of stones in the salivary ducts * Etiology * Often idiopathic * Dehydration (decrease salivary flow) * Trauma * Anticholinergics * Location → may occur in any of the larger salivary glands * Primarily in the Wharton duct located in the submandibular gland (∼ 80% of cases; typically a large single stone) * Parotid gland (∼ 20% of cases) * Clinical features * Recurrent, significant pain before and while eating (eating stimulates salivation, which increases the amount of saliva secreted into the ducts, including those that are obstructed by a stone. The resulting increased pressure in the obstructed ducts causes pain and swelling of the gland) * Partial swelling of the glands * Treatment * Mainly conservative * NSAIDs for pain relief * Stimulation of salivary flow by sucking sour candies, massaging the gland, and applying warm compresses * Invasive (only in severe cases) → dilatation of the salivary duct or ultrasonic lithotripsy
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Saliva Function
1. Digestion (contains α-amylase, which breaks down carbohydrates and mucins, which emulsify food particles) 2. Protection of the mucosa and teeth (serves as a buffer, maintaining the pH of the mouth and thus preventing the minerals in the teeth from dissolving. Saliva also lubricates the mucosa and moistens food, allowing it to pass easily to the stomach) 3. Immunological defense (provided by the IgA and IgG that is excreted, as well as lysozyme, which attacks the cell wall of various bacteria) 4. Transport of soluble flavors to the taste buds (taste perception works by diffusing flavor molecules to the taste buds. This mechanism is dependent upon saliva, which dissolves the flavor molecules)
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Parotid Gland
* **Located on the surface of the masseter muscle**, dorsal to the mandibular ramus and ventrocaudal to the external auditory canal in the retromandibular fossa. * Subdivided by the branches of the facial nerve which runs through the parotid gland (parasympathetic innervation of the gland is not through the facial, but the glossopharyngeal nerve) * Its salivary duct (Stensen duct) **runs forward along the masseter muscle and opens adjacent to the 2nd molar in the vestibule of the mouth** (the space between the cheeks and the teeth). * Produces mainly serous fluid and ∼ 40% of the total amount of saliva.
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Submandibular Gland
* Located medial and caudal to the inner surface of the mandible above the mylohyoid and digastric muscles * The salivary duct (Wharton duct) ends in the sublingual caruncle (it can be seen on both sides of the lingual frenulum when the tip of the tongue is pressed to the roof of the mouth) * Produces seromucous fluid and the greater part (∼ 50%) of the secreted saliva
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Sublingual Gland
* Located medial to the mandible above the mylohyoid muscle and below the sublingual fold * Its main salivary duct also ends in the Wharton duct * Produces mainly mucous fluid
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Ranula (retention cyst arising in the sublingual gland) Asymmetrical, partially white, partially translucent swelling, which extends above the lower teeth.
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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
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Pleomorphic Adenoma of the Salivary Gland ## Footnote 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.
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Pleomorphic Adenoma of the Salivary Gland
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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.
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Warthin Tumor | (Papillary Cystadenoma Lymphomatosum)
* Peak incidence → 60–80 years * 2nd most common benign salivary gland tumor (accounting for 10% of benign cases) * Etiology * Ionizing radiation * Smoking * Location → most often the parotid gland (10% bilateral, 10% multifocal) * Rarely malignant transformation * Clinical features → gradual and painless unilateral swelling of the parotid * Diagnostic method of choice in salivary gland tumors * Histology * Cystic structure * Germinal centers * Treatment: * Complete extirpation of the tumor with preservation of facial nerve
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Mucoepidermoid Carcinoma of the Salivary Glands
* Most common malignant salivary gland tumor * Minor salivary glands (gums and the base of the mouth) → most tumors are malignant. * Involves squamous and mucinous cells, both of which arise from excretory stem cells. The distinction between the relative proportion of these cells determines if the carcinoma is low, intermediate, or high grade * Treatment * Curative → parotidectomy (superficial or total), if possible, with preservation of the facial nerve * Palliative → chemotherapy
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Achalasia
* Esophageal motility disorder characterized by inadequate relaxation of the lower esophageal sphincter (LES) and nonperistaltic contractions in the distal two-thirds of the esophagus due to the degeneration of inhibitory neurons * **Atrophy of inhibitory neurons in the Auerbach plexus** → lack of inhibitory neurotransmitters (e.g., NO, VIP) → inability to relax and increased resting pressure of the LES, as well as dysfunctional peristalsis → esophageal dilation proximal to LES * Etiology * Primary achalasia (most common) → cause is unknown (autoimmune process or viral infections (e.g., HSV-1, measles) could be involved) * Secondary achalasia (pseudoachalasia) → the presentation and manometric findings of a mechanical cause of obstruction (e.g., a malignancy) that mimics achalasia 1. Esophageal cancer 2. Stomach cancer and other extraesophageal cancers (symptoms may be due to mass effect or paraneoplasia) 3. Chagas disease 4. Amyloidosis 5. Neurofibromatosis type I 6. Sarcoidosis * Typically manifests with progressive dysphagia to solids and liquids while esophageal obstruction manifests with dysphagia to solids only. * Diagnostics * In general, all patients with suspected achalasia should initially undergo upper endoscopy and/or esophageal barium swallow; findings may support the diagnosis * Bird-beak sign * Delayed barium emptying or barium retention * Esophageal manometry is indicated to establish the diagnosis (confirmatory test of choice), irrespective of the initial imaging findings. * Peristalsis is absent or uncoordinated in the lower two-thirds of the esophagus. * Incomplete or absent LES relaxation * High LES resting pressure * No evidence of mechanical obstruction * Endoscopy should be performed to rule out pseudoachalasia because the presentation and manometric findings of a mechanical cause of obstruction (e.g., a malignancy) may mimic achalasia * Treatment * If a low surgical risk * Pneumatic dilation * LES myotomy (Heller myotomy) * If a high surgical risk * Botulinum toxin injection in the LES * If other measures are unsuccessful → nitrates or calcium channel blockers * Complications * Pulmonary complications (e.g., pneumonia, abscess, asthma) caused by aspiration * Megaesophagus * Increased risk of esophageal cancer.
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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: 1. Avoid trigger foods (caffeine; foods that are too hot/cold) 2. Medical * Calcium channel blockers * Nitrates 3. Endoscopic therapy * Botox injections * Endoscopic myotomy * Consider bougie or pneumatic dilation (in patients with associated EGJ obstruction) 4. Surgery → long myotomy (for intractable symptoms)
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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: 1. Avoid trigger foods (caffeine; foods that are too hot/cold) 2. Medical * Calcium channel blockers * Nitrates 3. Endoscopic therapy * Botox injections * Endoscopic myotomy * Consider bougie or pneumatic dilation (in patients with associated EGJ obstruction) 4. Surgery → long myotomy (for intractable symptoms)
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Corkscrew Esophagus ## Footnote Helical contractions of the lower esophagus (green overlay), resulting in a corkscrew-like appearance. Seen in patients with diffuse esophageal spasm (DES).
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Sialolithiasis (visible in the duct of the submandibular gland)
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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
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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) 1. Vomiting and/or retching 2. Severe retrosternal pain that often radiates to the back 3. 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 * 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)
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Esophageal perforation (Boerhaave syndrome) ## Footnote 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).
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Esophageal Perforation ## Footnote 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.
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Esophageal Perforation ## Footnote 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.
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Pneumomediastinum ## Footnote 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.
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Chronic Mediastinitis | (Fibrosing Mediastinitis)
* Inflammation of the tissues in the mediastinum * Proliferation of fibrous and collagenous tissue in the mediastinum * Etiology * Etiology remains unclear. * Several studies report that Histoplasma capsulatum is causative. * Clinical features * Retrosternal and/or back pain * Subcutaneous emphysema in the neck and face * Fever, tachycardia, tachypnea * Sternal wound drainage * Superior vena cava syndrome * Obstruction of the upper airways * Pleuritis and pericarditis (facilitated by contiguous spread to the pleura and pericardium) * Bacteremia leading to sepsis and signs of shock * Diagnostics * Chest x-ray shows a widened mediastinum and mediastinal emphysema. * Chest CT (confirmatory test) shows attenuation of mediastinal fat, as well as mediastinal fluid collections and gas. * CBC may show leukocytosis. * Treatement: * Resuscitation * IV antibiotic therapy * Surgical debridement
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Acute Mediastinitis
* Inflammation of the tissues in the mediastinum * Acute infection of the mediastinum * Etiology * Cardiothoracic surgical procedures (most common cause) → mediastinitis **typically occurs within 14 days of the procedure** * Perforation of mediastinal structures (e.g., esophagus, trachea) * Descending spread of infection from oropharyngeal foci * Clinical features * Retrosternal and/or back pain * Subcutaneous emphysema in the neck and face * Fever, tachycardia, tachypnea * Sternal wound drainage * Superior vena cava syndrome * Obstruction of the upper airways * Pleuritis and pericarditis (facilitated by contiguous spread to the pleura and pericardium) * Bacteremia leading to sepsis and signs of shock * Diagnostics * Chest x-ray shows a widened mediastinum and mediastinal emphysema. * Chest CT (confirmatory test) shows attenuation of mediastinal fat, as well as mediastinal fluid collections and gas. * CBC may show leukocytosis. * Treatement: * Resuscitation * IV antibiotic therapy * Surgical debridement
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Esophageal Stricture
* Etiology: * Most common sequela of reflux esophagitis (inflamed esophageal mucosa heals via fibrosis, forming a stricture that narrows the esophageal lumen) or ingestion of caustic substances * Clinical features: * Solid food dysphagia * Diagnostics * Barium esophagram (best initial test) → narrowing of the esophagus at the gastroesophageal junction * Endoscopy with biopsies → to rule out malignancy and eosinophilic esophagitis * Treatment * First-line treatment → dilation with bougie dilator/balloon dilator and PPIs in patients with reflux (reduce the risk of recurrence)
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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
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Esophageal Ring | (Schatzki rings)
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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
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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
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Esophageal Web seen in Plummer Vinson Syndrome
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Mallory Weiss Syndrome
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Sclerodermal Esophageal Dysmotility
* Smooth muscle atrophy and fibrosis → esophageal dysmotility and decreased LES pressure → dysphagia, gastroesophageal reflux, heartburn → aspiration, Barrett esophagus, stricture * Part of CREST syndrome
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Gastroesophageal Reflux Disease (GERD) Risk Factors/Associations
1. Smoking; caffeine and alcohol consumption (all three substances decrease LES tone. Alcohol and caffeine also stimulate gastric acid secretion, which, in combination frequent transient lower esophageal sphincter relaxations (TLESRs), increases the risk of esophageal mucosal injury from the gastric refluxate) 2. Stress 3. Obesity 4. Pregnancy (GERD is present in up to 80% of pregnancies. The underlying pathophysiology involves increased abdominal pressure, decreased LES tone (due to high estrogen and progesterone levels during pregnancy), and prolonged gastric emptying as a result of reduced gastric motility) 5. Angle of His enlargement (\> 60°) (angle that is formed between the esophagus and the gastric fundus (esophageal-gastric angle). In healthy adults, it is 50–60°. Infants usually have an undeveloped, flat angle of His. Therefore, the regurgitation of stomach contents after meals is a common finding during the first 12 months of life and is not considered pathological) 6. Iatrogenic (e.g., after gastrectomy) (gastrectomy may result in a widened angle of His) 7. Inadequate esophageal protective factors (i.e., saliva, peristalsis) 8. Gastrointestinal malformations and tumors → gastric outlet obstruction, gastric cardiac carcinoma 9. Scleroderma 10. Sliding hiatal hernia: ≥ 90% of patients with severe GERD 11. Asthma
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Gastroesophageal Reflux Disease (GERD) Histopathological Findings
* May vary depending on the severity of mucosal damage 1. Superficial coagulative necrosis in the nonkeratinized squamous epithelium 2. Thickening of the basal cell layer 3. Elongation of the papillae in the lamina propria and dilation of the vascular channels at the tip of the papillae (leading to hyperemia) 4. Inflammatory cells (granulocytes, lymphocytes, macrophages) 5. Transformation of squamous into columnar epithelium leads to Barrett metaplasia
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Drops in esophageal pH to ___ or less correlate with symptoms of acid reflux into the esophagus.
4 Normal esophageal pH is ∼ 7, with small variations throughout the day.
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Barret Esophagus
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Barret Esophagus
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Erosive Esophagitis
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Gastroesophageal Reflux Disease
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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
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Esophageal Carcinoma ## Footnote 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.
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Esophageal Carcinoma
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Distal Stenosis in Esophageal Cancer ## Footnote 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)
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Esophageal Cancer ## Footnote 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).
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Esophageal Cancer ## Footnote Axial CT scan of the chest → stenotic esophageal cancer with tracheoesophageal fistula
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Adenocarcinoma of the Esophagus
* Carcinoma arises in context of Barrett esophagus (columnar epithelium with goblet cells) and high-grade dysplasia * Gland-forming tumors with different possible growth patterns (tubular, papillary, tubulopapillary) * Mucinous differentiation possible * Lower 1/3 of the esophagus * Lymphatics drain caudally to the gastric and celiac nodes. Metastatic disease may present with abdominal lymphadenopathy * Risk factors * Chronic GERD * Barrett esophagus * Visceral obesity * Smoking * Achalasia * Foods containing nitroso compounds (eg, processed meats) * Medications that decrease esophageal sphincter pressure (eg, nitroglycerin)
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Squamous Cell Carcinoma of the Esophagus
* Breakdown of uniform tissue structure * Squamous cell carcinoma clusters with circular keratinization * Lymphocytic infiltration between the carcinoma clusters * Upper 2/3 (increase frequency in the middle 1/3) * Metastatic disease → mediastinal lymphadenopathy * Risk Factors: * Alcohol * Hot liquids * Caustic strictures * Smoking * Achalasia * Plummer-Vinson syndrome * Atrophic gastritis * Nitrosamine rich foods * Betel nut or areca nut chewing
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Dumping Syndrome
* Complication of dysfunctional or bypassed pyloric sphincter (e.g., post-gastrectomy) with symptoms occuring due to rapid gastric emptying. * There are two types → early and late, referring to the timing of symptoms after meals. **Early Dumpling** * Dysfunctional or bypassed pyloric sphincter → rapid emptying of undiluted hyperosmolar chyme into the small intestine → fluid shift to the intestinal lumen → small bowel distention → vagal stimulation → increased intestinal motility * Clinical Features * Occur within 15–30 minutes after meal ingestion * Include nausea, vomiting, diarrhea, and cramps * Vasomotor symptoms such as sweating, flushing, and palpitations **Late Dumpling** * Dysfunctional pyloric sphincter → rapid emptying of glucose-containing chyme into the small intestine → quick reabsorption of glucose → hyperglycemia → excessive release of insulin → hypoglycemia and release of catecholamines * Clinical features * Occur hours after meal ingestion * Include signs of hypoglycemia (e.g., hunger, tremor, lightheadedness) * GI discomfort * Suspect late dumping syndrome in a patient with previous gastric surgery and hypoglycemia.
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Dieulafoy Lesion
* Minor mucosal trauma to an abnormal submucosal artery (usually located in the proximal stomach) leads to major bleeding (acute upper GI bleeding) * It can be hard to visualize on endoscopy because it is missing an ulcer base. * Treatment includes endoscopic hemostasis (injection therapy, hemoclips, etc.) or excision of the susceptible mucosa
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