Esophagus

A. General features. The esophagus is a muscular tube that is continuous with the pharynx and runs in the thorax through the superior and posterior mediastinum. The esophagus pierces the diaphragm to form the esophageal hiatus at vertebral level T10, where it enters the abdominal cavity and meets the stomach at the gastroesophageal junction. The upper esophageal sphincter is skeletal muscle that consists of the cricopharyngeus muscle and the inferior pharyngeal constrictor muscle. It relaxes during swallowing. The lower esophageal sphincter (LES) is smooth muscle and is difficult to identify anatomically. It relaxes during swallowing and prevents gastroesophageal reflux. The esophagus is naturally constricted at three anatomic sites: the junction between the pharynx and esophagus, the level of tracheal bifurcation, and the gastroesophageal junction.

B. Clinical considerations

1. An enlarged left atrium may constrict the esophagus because of the close anatomic relation of these structures.

2. Bronchogenic carcinoma may indent the esophagus as a result of enlargement of the mediastinal lymph nodes. This indentation is seen radiologically during a barium swallow.

3. Malignant tumors of the esophagus most commonly occur in the lower one-third of the esophagus and metastasize below the diaphragm to the celiac lymph nodes.

4. Forceful vomiting, which may tear the posterior wall of the esophagus, often is seen in alcoholism, bulimia, and pregnancy. Clinical findings include severe retrosternal pain after vomiting and extravasated contrast medium. Mallory-Weiss tears involve only the mucosal and submucosal layers. Boerhaave syndrome involves tears through all layers of the esophagus.

5. A sliding hiatal hernia occurs when the stomach and the gastroesophageal junction herniate through the diaphragm into the thorax. Clinical findings include: deep burning retrosternal pain and reflux of gastric contents into the mouth (i.e., heartburn), both of which are accentuated when the patient is in the supine position.

6. A paraesophageal hiatal hernia occurs when only the stomach herniates through the diaphragm into the thorax. There is no reflux of gastric contents, but strangulation or obstruction may occur.

7. Achalasia is failure of the LES to relax during swallowing, probably because of absence of the myenteric plexus. Clinical findings include progressive dysphagia (difficulty in swallowing). Barium swallow shows a dilated esophagus above the LES

and distal stenosis at the LES ("bird beak"). Chagas disease (caused by Trypanosoma cruzi) may lead to achalasia.

8. Esophageal reflux is caused by dysfunction of the LES that allows gastric acid to reenter the lower esophagus. Clinical findings include: substernal pain and heartburn, which may worsen with bending or lying down. Scleroderma may be a systemic cause of esophageal reflux.

9. Esophageal strictures (narrowing)

a. Caustic strictures are the result of injury caused by ingestion of caustic agents (e.g., drain openers, oven cleaners).

b. Other strictures are caused by recurrent mucosal destruction as a result of gastric acid reflux. These strictures most often occur at the gastroesophageal junction.

10. Barrett esophagus is the replacement of stratified squamous epithelium with gastric epithelium in the distal esophagus. Clinical findings include: a long history of heartburn or other reflux symptoms that may lead to esophageal adenocarcinoma.

II. STOMACH (Figure 9-1)

A. General features. The stomach is a muscular organ that functions in food digestion and storage. The stomach is divided into four parts:

1. The cardia, near the gastroesophageal junction

2. The fundus, above the gastroesophageal junction

3. The body, between the fundus and antrum

Junction External Landmarks

Figure 9-1. (A) Diagram showing the various parts of the stomach. High-yield clinical considerations associated with the esophagus, stomach, and duodenum are indicated. A = antrum; B = body; C = cardia; F= fundus; /a = incisura angularis; P = pylorus. (B) Radiograph after barium swallow. Note the parts of the stomach and duodenum. A = antrum; Asc = ascending part of the duodenum; B = body; DC = duodenal cap, or superior part of the duodenum; Des = descending part of the duodenum; F = fundus; Hor = horizontal part of the duodenum; Jej = jejunum. (A adapted with permission from Jarrell BE, Carabasi RA III: NMS Surgery, 3rd ed. Baltimore, Williams & Wilkins, 1996, p 183; B adapted with permission from Ryan S, McNicholas M: Anatomy for Diagnostic Imaging. London, WB Saunders, 1994, p 158.)

Figure 9-1. (A) Diagram showing the various parts of the stomach. High-yield clinical considerations associated with the esophagus, stomach, and duodenum are indicated. A = antrum; B = body; C = cardia; F= fundus; /a = incisura angularis; P = pylorus. (B) Radiograph after barium swallow. Note the parts of the stomach and duodenum. A = antrum; Asc = ascending part of the duodenum; B = body; DC = duodenal cap, or superior part of the duodenum; Des = descending part of the duodenum; F = fundus; Hor = horizontal part of the duodenum; Jej = jejunum. (A adapted with permission from Jarrell BE, Carabasi RA III: NMS Surgery, 3rd ed. Baltimore, Williams & Wilkins, 1996, p 183; B adapted with permission from Ryan S, McNicholas M: Anatomy for Diagnostic Imaging. London, WB Saunders, 1994, p 158.)

Hiatal hernia Achalasia Esophageal reflux Esophageal strictures Barrett esophagus

Hypertrophic pyloric steriosis

Duodenal ulcer

Plica Angularis

Hiatal hernia Achalasia Esophageal reflux Esophageal strictures Barrett esophagus

Hypertrophic pyloric steriosis

Duodenal ulcer

4. The antrum, the distal part of the stomach that begins at the incisura angularis and ends at the pylorus. The pylorus is a well-defined muscular sphincter that controls movement of food out of the stomach and prevents reflux of duodenal contents into the stomach.

B. Clinical considerations

1. Gastric ulcers most often occur within the body of the stomach along the lesser curvature above the incisura angularis. They occur at a histologic transition zone where the gastric glands change from predominantly parietal cells (HCl-producing) to G cells (gastrin-producing). They are caused by damage to the mucosal barrier (because of decreased production of mucus and bicarbonate), usually as a result of smoking, excessive salicylate ingestion, or the use of nonsteroidal anti-inflammatory drugs. Approximately 70% of patients have associated Helicobacter pylori infection. Clinical findings include burning pain in the epigastric or left hypochondriac region that increases after a meal. Treatment is the same as for duodenal ulcers (see 111 B 1).

2. Hypertrophic pyloric stenosis is a congenital condition that presents within weeks after birth. Clinical findings include: projectile vomiting containing no bile, visible peristalsis from the left hypochondriac to the right hypochondriac region, and a hard, mobile mass palpated in the epigastric region.

3. Dumping syndrome is abnormally rapid emptying of hyperosmotic stomach contents (especially high-carbohydrate foods) into the jejunum within 30 minutes after a meal ("early dumping") or 1 to 3 hours after a meal ("late dumping"). It usually occurs after a partial gastrectomy or vagotomy is performed to treat an ulcer or obesity. Clinical findings include: epigastric discomfort, borborygmi (rumbling sounds caused by gas movement), palpitations, dizziness, diarrhea, and hypoglycemia.

4. Cancer of the stomach may metastasize to the supraclavicular lymph nodes (Vir-chow nodes) on the left side. These nodes can be palpated within the posterior triangle of the neck.

III. DUODENUM (see Figure 9-1)

A. General features. The duodenum is divided into four parts.

1. The superior part is intraperitoneal and begins at the pylorus of the stomach (gas-troduodenal junction), which is marked by the prepyloric vein. Radiologists refer to this part of the duodenum as the duodenal cap, or bulb. The superior part has a mesentery and is, therefore, mobile. Posterior relationships include the common bile duct and gastroduodenal artery.

2. The descending part is retroperitoneal and receives the common bile duct and main pancreatic duct on its posterior or medial wall at the hepatopancreatic ampulla (ampulla of Vater).

3. The horizontal part is retroperitoneal and runs horizontally across vertebra L3 between the superior mesenteric artery anteriorly and the aorta and inferior vena cava posteriorly. In severe abdominal injuries, this part of the duodenum may be crushed against vertebra L3.

4. The ascending part is intraperitoneal and ascends to meet the jejunum at the duodenojejunal flexure, which is supported by the ligament of Treitz. This ligament is the cranial end of the dorsal mesentery.

B. Clinical considerations

1. Duodenal ulcers most often occur in the superior part of the duodenum (i.e, at the duodenal cap). They are caused by damage to the mucosal barrier (caused by decreased mucus and bicarbonate production) and hypersecretion of gastric acid. Almost 100% of patients have associated Helicobacter pylori infection. Clinical findings include severe pain in the epigastric region that decreases after a meal. Treatment includes: H2 receptor antagonists (e.g., cimetidine, ranitidine, nizatidine, famotidine), antacids, sucralfate (a viscous material that provides a protective barrier), omeprazole (H+-K+ ion pump inhibitor), bismuth, metronidazole, and tetracycline. The surgical procedure of choice is a proximal gastric vagotomy, which transects only the vagus nerve (cranial nerve X) fibers to the distal esophagus and fundus of the stomach and results in decreased gastric acid secretion.

2. Perforations occur most often with ulcers located on the anterior surface of the duodenum. Perforations occur less often with ulcers on the posterior surface; however, these may erode the gastroduodenal artery, causing severe hemorrhage.

IV. JEJUNUM, ILEUM, AND LARGE INTESTINE. General features are listed in Table 9-1.

A. Celiac disease is hypersensitivity to gluten and gliadin protein, found in wheat and other grains. When gluten-containing foods are ingested, a large number of lymphocytes, plasma cells, macrophages, and eosinophils accumulate within the lamina propria of the intestinal mucosa. These factors may contribute to the immunologic damage to the mucosa. Gliadin antibodies usually are detectable in the blood. Clinical findings include: chronic diarrhea, flatulence, weight loss, and fatigue.

Table 9-1.

Characteristics of the Small and Large Intestine

Jejunum

Ileum

Large Intestine

Villi (long, finger-shaped) Intestinal glands (crypts)

>3 cm in diameter Large, numerous, and palpable circular folds* Initial 2/5 of the small intestine Located in the umbilical region on the left side of the abdomen Long vasa recta

Main site of absorption

Villi (short, club-shaped) Intestinal glands (crypts)

< 3 cm in diameter Small and few circular folds that disappear distally Terminal 3/5 of the small intestine Located in the hypogastric and inguinal regions on the right side of the abdomen Short vasa recta

Site of vitamin B12 absorption

Often empty (no fecal contents) Prominent Peyer patches

Thicker wall, more vascular, and redder than ileum in a living person

Terminal ileum ends several centimeters above the cecal tip

No villi

Intestinal glands (crypts) 6-9 cm in diameter No circular folds

Teniae coli (three longitudinal bands of smooth muscle) are present Appendices epiploicae

(fatty tags) Haustra (sacculations of the wall) separated by the plicae semilunaris

•Folds of the mucosa and submucosa (also called plicae circularis or valves of Kerckring).

B. Crohn disease is a chronic granulomatous inflammatory bowel disease that most commonly affects the ileum. As the disease progresses, ulcers coalesce into long, serpentine ulcers ("linear ulcers") that are oriented along the long axis of the bowel. A classic feature is the clear demarcation between diseased bowel segments and adjacent uninvolved segments ("skip areas"). Clinical findings include: a mass in the right lower quadrant of the abdomen, intermittent bouts of diarrhea, fever, weight loss, and weakness. Complications include strictures of the intestinal lumen and the formation of fistulas.

C. Appendicitis begins with obstruction of the appendix lumen by a fecal concretion (fecalith) and lymphoid hyperplasia, followed by distension of the appendix. Clinical findings include: initial pain in the umbilical or epigastric region, later pain localizing to the right lumbar region, nausea, vomiting, anorexia, and tenderness to palpation and percussion in the right lumbar region. Complications may include peritonitis as a result of rupture of the appendix. McBurney point is located by drawing a line from the right anterior superior iliac spine to the umbilicus. The midpoint of this line locates the root of the appendix. The appendix is intraperitoneal, being suspended by the mesoap-pendix, and usually is found in the retrocecal fossa, although its position is variable.

D. Toxic megacolon usually is a dilation of the transverse colon that results in perforation of the colonic wall. Clinical signs include: abdominal pain, fever, and leukocytosis.

E. Ogilvie syndrome is most commonly a dilation of the cecum and often is seen in critically ill or bedridden patients.

V. GALLBLADDER, EXTRAHEPATIC BILIARY DUCTS, AND BILE (Figure 9-2)

A. General features

1. The gallbladder is divided into the fundus (anterior portion), body, and neck (posterior portion). A small pouch (Hartmann pouch) may extend from the neck as a result of pathologic changes and is a common site for gallstones to lodge. Roki-tansky-Aschoff sinuses occur when the mucosa of the gallbladder penetrates deep into the muscularis externa. They are an early indicator of pathologic changes (e.g., acute cholecystitis, gangrene). The arterial blood supply is through the cystic artery, a branch of the right hepatic artery. Venous drainage is through cystic veins that empty into the portal vein or directly into liver sinusoids. Lymphatic drainage is into hepatic and pancreaticoduodenal lymph nodes. Sensory nerve fibers for pain from the gallbladder travel with the greater thoracic splanchnic nerve to spinal levels T7—10. Motor nerve fibers for contraction of the gallbladder and relaxation of the sphincter of Oddi (which stimulates bile release into the small intestine) are pre- and postganglionic parasympathetic neurons of the vagus nerve (CN X). Cholecystokinin (CCK), a hormone secreted from 1 cells of the small intestine, mimics the parasympathetic functions of CN X on the gallbladder and sphincter. Motor nerve fibers for relaxation of the gallbladder and contraction of the sphincter of Oddi (which inhibits bile release into the small intestine) are preganglionic sympathetic neurons of the greater thoracic splanchnic nerve and postganglionic sympathetic neurons of the celiac plexus. Functions of the gallbladder include: storage of bile, concentration of bile (approximately tenfold) through absorption of water and electrolytes, acidification of bile, addition of mucus ("white bile") to bile, and release of bile through the simultaneous contraction of the gallbladder and relaxation of the sphincter of Oddi.

2. Extrahepatic biliary ducts. The right and left hepatic ducts join after leaving the liver to form the common hepatic duct. The common hepatic duct is joined at an acute angle by the cystic duct to form the common bile duct. The cystic duct

Hidradenitis Suppurativa Cysts

Figure 9-2. (A) The gallbladder and biliary tree. Note the termination of the common bile duct (CBD) at the hepatoduodenal ampulla (HDA) along with the pancreatic duct (PD). Note the three main sites (X) of gallstone obstruction. (B) Cholangiogram. 1 = endoscope; CD = cystic duct; CHD = common hepatic duct; GB = gallbladder; LHD = left hepatic duct; RHD = right hepatic duct. (A adapted with permission from Jarrell BE, Carabasi RA: NMS Surgery, 3rd ed. Baltimore, Williams & Wilkins, 1996, p 250; B adapted with permission from Ryan S, McNicholas M: Anatomy for Diagnostic Imaging. London, WB Saunders, 1994, p 173.)

Figure 9-2. (A) The gallbladder and biliary tree. Note the termination of the common bile duct (CBD) at the hepatoduodenal ampulla (HDA) along with the pancreatic duct (PD). Note the three main sites (X) of gallstone obstruction. (B) Cholangiogram. 1 = endoscope; CD = cystic duct; CHD = common hepatic duct; GB = gallbladder; LHD = left hepatic duct; RHD = right hepatic duct. (A adapted with permission from Jarrell BE, Carabasi RA: NMS Surgery, 3rd ed. Baltimore, Williams & Wilkins, 1996, p 250; B adapted with permission from Ryan S, McNicholas M: Anatomy for Diagnostic Imaging. London, WB Saunders, 1994, p 173.)

drains bile from the gallbladder. The mucosa of the cystic duct is arranged in a spiral fold with a core of smooth muscle known as the spiral valve (valve of Heister). The spiral valve keeps the cystic duct open constantly so that bile can flow freely in either direction. The common bile duct passes posterior to the pancreas and ends at the hepatoduodenal ampulla (ampulla of Vater), where it joins the pancreatic duct. The sphincter of Oddi is an area of thickened smooth muscle that surrounds the bile duct as it traverses the ampulla.

3. Bile is produced primarily by hepatocytes, at an average rate of 600 ml/day. It is composed primarily of: water, electrolytes, bilirubin glucuronide (bile pigment), cholic acid and chenodeoxycholic acid conjugated to glycine or taurine (bile salts), cholesterol and lecithin (lipids), calcium, and secretory IgA. Its function is to emulsify fats. Lactated Ringer solution is a good replacement fluid for bile loss.

B. Clinical considerations

1. Gallstones form when bile salts and lecithin are overwhelmed by cholesterol. Most stones consist of cholesterol (major component), bilirubin, and calcium. There are three main types:

a. Cholesterol stones are large and smooth. They are associated with: obesity, Crohn disease, cystic fibrosis, clofibrate administration, estrogen use, and rapid weight loss. They are common in the general population of the United States, with a noticeably higher rate among Native Americans.

b. Pigment (bilirubin) stones are smooth and green or black. They are associated with: chronic red blood cell hemolysis (e.g., sickle cell anemia, spherocytosis), alcoholic cirrhosis, and biliary infection, and are most common in persons of Asian descent.

c. Calcium bilirubinate stones are associated with infection or inflammation of the biliary tree.

2. Gallstone obstruction occurs at three clinically important sites:

a. Within the cystic duct. A stone may transiently lodge within the cystic duct and cause epigastric pain (biliary colic). An entrapped stone obstructs bile flow from the gallbladder, which results in inflammation of the gallbladder (acute cholecystitis) and causes pain to shift to the right hypochondriac region. Bile becomes concentrated and precipitates in the gallbladder, where it forms a layer of high-density material called "milk of calcium" bile because it contains a large amount of calcium carbonate. Bile flow from the liver remains open (i.e., no jaundice). This situation may lead to Mirizzi syndrome, in which a large gallstone impacted in the cystic duct extrinsically obstructs the nearby common hepatic duct.

b. Within the common bile duct. A stone entrapped within the common bile duct obstructs bile flow from the gallbladder and the liver, and causes inflammation of both. Jaundice is common, and is first observed clinically under the tongue. The jaundice is moderate, and fluctuates, because a stone rarely causes complete blockage of the lumen.

c. At the hepatoduodenal ampulla. If a stone becomes entrapped at the ampulla, it obstructs bile flow from both the gallbladder and the liver. The pancreatic duct also may be blocked. Jaundice and pancreatitis are common.

A. General features. The liver is divided, in classic anatomy, into the right lobe and the left lobe by the interlobar fissure, which is an invisible line that runs from the gallbladder to the inferior vena cava, quadrate lobe, and caudate lobe. The left lobe contains the falciform ligament (a derivative of the ventral mesentery) with the ligamen-tum teres (a remnant of the left umbilical vein) along its inferior border. The bare area of the liver is located on the diaphragmatic surface and is devoid of peritoneum. The liver is secured in its anatomic location by attachment of the hepatic veins to the inferior vena cava. This arrangement allows for very little rotation of the liver during surgery.

B. Clinical considerations

1. Liver biopsies often are performed by needle puncture through right intercostal space 8, 9, or 10 just after the patient exhales. The needle passes through the following structures: skin > superficial fascia > external oblique muscle * intercostal muscles costal parietal pleura > costodiaphragmatic recess _> diaphragmatic parietal pleura diaphragm -> peritoneum.

2. Congenital biliary atresia affects the development of the intrahepatic and extra-hepatic bile ducts. It usually presents within weeks after birth and is the most common cause of persistent jaundice in infancy. Clinical findings include: jaundice (does not start immediately after birth, as in physiological jaundice); dark urine; and clay-colored stools. Liver biopsy shows bile duct proliferation with dilation of bile canali-culi and bile plugs.

Left Lobe Inferior Mesenteric Vein

Figure 9-3. (/\) Anterior surface of the liver. Note the right (R) and left (L) lobes, which are divided by the interlobar fissure (IF). FL = falciform ligament; GB = gallbladder; IVC = inferior vena cava. (B) Inferior surface of the liver. Note the quadrate (Q) and caudate lobes (C). (C) The five liver segments and nine liver subsegments used in liver resectioning.The five liver segments include the posterior and anterior segments of the right lobe, the medial and lateral segments of the left lobe, and the caudate lobe. Note the hepatic veins (HV) at the periphery of the liver segments. The nine liver subsegments include the posterior superior (PS), posterior inferior (PI), anterior superior (>4S), anterior inferior (Al), medial superior (MS), medial inferior (Ml) [which corresponds to the classic quadrate lobe (O)], lateral superior (LS), lateral inferior (/_/), and classic caudate lobe (C).

Figure 9-3. (/\) Anterior surface of the liver. Note the right (R) and left (L) lobes, which are divided by the interlobar fissure (IF). FL = falciform ligament; GB = gallbladder; IVC = inferior vena cava. (B) Inferior surface of the liver. Note the quadrate (Q) and caudate lobes (C). (C) The five liver segments and nine liver subsegments used in liver resectioning.The five liver segments include the posterior and anterior segments of the right lobe, the medial and lateral segments of the left lobe, and the caudate lobe. Note the hepatic veins (HV) at the periphery of the liver segments. The nine liver subsegments include the posterior superior (PS), posterior inferior (PI), anterior superior (>4S), anterior inferior (Al), medial superior (MS), medial inferior (Ml) [which corresponds to the classic quadrate lobe (O)], lateral superior (LS), lateral inferior (/_/), and classic caudate lobe (C).

3. Primary biliary cirrhosis is caused by granulomatous destruction of medium-sized intrahepatic bile ducts. Cirrhosis appears late in the course of the disease. Primary biliary cirrhosis is characterized by mitochondrial pyruvate dehydrogenase autoantibodies, the role of which is not clear.

4. Primary sclerosing cholangitis is caused by inflammation, fibrosis, and segmental dilation of both the intrahepatic and the extrahepatic bile ducts. It often occurs in association with chronic ulcerative colitis. Clinical findings include: right hypochondriac region pain or painless jaundice, no fever or chills, pruritus, fatigue, and nausea.

5. Surgical resection of the liver may be performed by removing one of the liver segments (five total segments) or one of the liver subsegments (nine total subsegments). Hepatic veins form the surgical landmarks that mark the periphery of a liver segment during segmental resection. (Recall that pulmonary veins form the surgical landmarks that mark the periphery of a bronchopulmonary segment during segmental resection of the lung.)

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Pregnancy Diet Plan

Pregnancy Diet Plan

The first trimester is very important for the mother and the baby. For most women it is common to find out about their pregnancy after they have missed their menstrual cycle. Since, not all women note their menstrual cycle and dates of intercourse, it may cause slight confusion about the exact date of conception. That is why most women find out that they are pregnant only after one month of pregnancy.

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Responses

  • valente schiavone
    Which clinical consideration involves tears through all layers of the esophagus?
    7 years ago

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