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89 Cards in this Set

  • Front
  • Back
Upper GI
Ends with the stomach
Esophagus
Muscular tube that connects the nose and mouth with the stomach. Extension of the pharynx in the back of the oral cavity. It extends down the neck next to the trachea, through the thoracic cavity, and PENETRATES THE DIAPHRAGHM to connect with the stomach in the abdominal cavity
Function of the esophagus
Conveys boluses of food from the pharynx to the stomach. Food is passed through the esophagus by using the process of PERISTALSIS
PERISTALSIS
rhythmic contraction of smooth muscles to propel contents through the digestive tract.
5 Types of esophageal disorders
1) congenital, 2) Motor, 3) Hiatal hernia, 4) esophagitis, 5) neoplasms
Types of congenital disorders
1) tracheoesophageal fistulas, 2) rings, 3) webs, 4) esophageal diverticula
Fistula
abnormal connection or passageway between two epithelium-lined organs or vessels that normally do not connect (in this case between trachea and esophagus)
tracheoesophageal fistulas
Communication between the trachea and esophagus. Most common esophageal anomaly.
Upper and lower boundaries of fistulas
90% of fistulas upper portion of esophagus starts in a blind pouch (ATRESIA), and the lower end communicates with the trachea; Aspiration occurs immediately after birth as Upper blind sac fills with mucus
Esophageal Artesia
failure of the esophagus to develop as a continuous passage. Instead, it ends as a blind pouch. It occurs in approximately 1 in 4425 live births.
5 Classifications of Tracheoesophageal Fistulas
Types A, B, C, D, and H; see slide pic
Type A fistula
Proximal and distal esophageal bud—a normal esophagus with a missing mid-segment.
Type B
Proximal esophageal termination on the lower trachea with distal esophageal bud
Type C
Proximal esophageal ATRESIA (esophagus continuous with the mouth ending in a blind loop superior to the sternal angle) with a distal esophagus arising from the lower trachea or carina. (Most common, up to 90% of cases.)
Type D
Proximal esophageal termination on the lower trachea or carina with distal esophagus arising from the carina.
H-Type
A variant of type D: if the two segments of esophagus communicate; resembles the letter H
Rings and webs
Thin mucosal membranes that project into the esophagus lumen. Can block esophagus either partially or completely; Unknown cause; Generally asymptomatic. Pts may complain of dysphagia or difficult, painless swallowing of solid food. When pain occurs is referred to as odynophagia. Also, acid reflux symptoms may be present.
Rings
bands of normal esophageal tissue that form constrictions around the inside of the lower esophagus (i.e., Schatzki ring).
Webs
arise in the upper esophagus as thin layers of cells that grow across the inside of the esophagus.
Plummer-Vinson Syndrome (sideropenic dysphagia)
Esophageal webs with risk of developing oral cancer; Comes with iron deficiency (sideropenia)and difficulty swallowing;*90% of cases are in middle-aged women since hormonal factors may be involved and it is related to alcohol and tobacco use
Symptoms of Plummer-Vinson Syndrome
1) oropharyngeal mucosal lesions that cause burning mouth syndrome in tongue and oral mucosa; 2) Atrophy of lingual Padilla (dorsal tongue is shiny red and smooth) which causes Glossodynia (tongue pain) , 3) some risk of esophageal cancer but greater risk of oropharyngeal cancer
diverticulum
a sac or pouch arising from a tubular organ
true diverticulum
outpouching of a wall containing all layers of the esophagus
False diverticulum or pseudodiverticulum
outpouching of a wall that lacks a muscular layer
Where do Esophageal Diverticula occur?
close to upper and lower esophageal sphincters, and in midportion of esophagus
Complications of Esophageal Diverticula (4)
1) regurgitation of undigested food, 2) halitosis, 3) cough, and even 4) aspiration pneumonia
Zenkers diverticulum
upper portion of esophagus
Traction diverticulum
midportion of esophagus
Epiphrenic diverticulum
Lower portion of esophagus, close to diaphragm; *Diverticula are congenital
Motor disorders
Affect peristalsis
2 Types of motor disorders
Achalasia and Scleroderma
Achalasia
Rare motor disorder where there is Failure of the lower esophageal sphincter (a muscular ring at the junction of the esophagus and stomach) to relax during swallowing and there is No peristalsis in the body of the esophagus. Result: Food is retained within esophagus, leading to Esophageal HYPERTROPHY, Dysphagia and regurgitation
Cause of Achalasia
associated with loss or absence of ganglion cells in the mesenteric plexus; Common in Chagas disease (parasitic infection with protozoa Trypanosoma Cruzi where ganglion cells are affected)
Esophageal tissue in Achalasia
Redundant, hyperplastic esophageal squamous epithelium (Looks stretched out instead of narrow and thin)
Scleroderma (progressive systemic sclerosis)
a group of diseases that causes abnormal growth of CONNECTIVE TISSUE. FIBROTIC SMOOTH MUSCLE mainly affecting lower esophageal sphincter and impairs peristalsis. This occurs most often in the esophagus, but may also be seen elsewhere in the GI tract. Cause unknown. Mainly women.
The 2 types of scleroderma
1) Localized scleroderma: affects only the skin. 2) Systemic scleroderma: affects blood vessels and internal organs, as well as skin.
Complications of scleroderma
dysphagia; heartburn caused by peptic esophagitis due to acid reflux from the stomach
Hiatal hernia
Portion of upper stomach bulges through an enlarged esophageal hiatus in the diaphragm.
Two types of Hiatal hernia
1) Sliding Hernia: Common, mostly asymptomatic. Cap of gastric mucosa moves upward above the diaphragm. 2) Paraesophageal Hernia: Uncommon. Herniation of part of gastric fundus alongside the esophagus.
Complications of Hiatal hernia
Large hiatal hernia can allow food and acid to back up into esophagus (gastroesophageal reflux, regurgitation), leading to heartburn and chest pain. Dysphagia, odynophagia.
Esophagitis
Any inflammation, irritation, or swelling of the esophagus
What is the Main barrier to gastroesophageal reflux (GER)
lower esophageal sphincter (LES)
Reflux esophagitis
Most common type of esophagitis; Frequently caused by the backflow of acid-containing fluid and pepsin from the stomach due to decreased pressure of LES
What can cause decreased pressure in LES?
Alcohol, cigarette smoking, fatty foods, chocolate, pregnancy, estrogen tx, certain meds.
Complications of reflux esophagitis
1) Superficial mucosal erosions and ulcers with Vertical line streaks. 2) Reactive proliferation of the lamina propria papillae into basal squamous epithelium which is thickened, 3) Hyperemia; dilated capillary vessels. Increased inflammatory cells in submucosa. 4) Chronic esophagitis may result in esophageal stricture/stenosis where fibrosis can narrow lumen
Barrett esophagus
Metaplastic changes to “specialized epithelium” secondary to chronic gastroesophageal reflux: Esophageal squamous epithelium is replaced by columnar epithelium; Commonly in lower third of esophagus
Causes of Barrett esophagus
Alcohol and tobacco
Complication of Barrett esophagus
Metaplastic epithelium of a Barrett esophagus carries a risk of malignant transformation to an adenocarcinoma (dysphagia occurs and then adenocarcinoma develops); *This disease is considered a PRE-MALIGNANT CONDITION
Symptoms of Candida esophagitis
Dysphagia/odynophagia; Severe candidiasis may result in fibrosis (stricture)
Populations most at risk for Candida esophagitis
Immunosuppressed subjects:AIDS, Diabetes, On Meds for organ transplantation, Cancer chemotherapy, or Antibiotic therapy
Herpetic Esophagitis
due to HSV1 infection; occurs in otherwise healthy ppl
Complications of herpetic esophagitis
Associated with lymphomas and leukemia
Statistics on esophageal carcinoma
Uncommon in USA: Squamous cell carcinoma of esophagus represent 7% of G.I. cancers. Accounts for 2% of cancer deaths; In 2013, about 17,990 Americans were diagnosed with esophageal cancer and 15,210 deaths were estimated to occur in the same year from this type of cancer.
Where in the world are esophageal cancers more prevalent
Asian “Esophageal Cancer Belt”: From Caspian Sea region of northern Iran and Central Asia to northern China......incidence 30-fold greater than USA; Northern China: mortality rate in men 70-fold greater that in USA
6 risk factors for esophageal carcinoma
1) Cigarette smoking: association with esophageal dysphagia, 2) Excessive alcohol consumption, 3) Plummer-Vinson syndrome; Achalasia, 4) Chronic esophagitis, 5) Webs, rings, and diverticula, 6) Diets low in fruits, vegetables, animal protein, trace metals; *Tobacco and alcohol also put people at risk for head and neck carcinomas
Esophageal carcinoma
50% of cases are squamous cell carcinomas in lower third of esophagus with PERSISTENT DYSPHAGIA as most common symptom; Metastasis to lung and liver are common; VERY POOR PROGNOSIS - Mostly unoperable. In those who undergo surgery: ~20% survive for 5 yrs.
3 Types of esophageal carcinomas
1) Ulcerating: possible bleeding, 2) Polypoid: early obstruction of lumen; 3) Infiltrating: gradually narrow lumen
Statistics on Adenocarcinoma of esophagus
Account for ~ 60% of the malignant esophageal tumors in USA
Cause of adenocarcinoma
All adenocarcinomas arise from Barrett epithelium; Thus, endoscopy surveillance is important
Symptoms of adenocarcinoma
Similar to squamous cell carcinoma (SCC); 20% 5-year survival following radical surgery
Stomach
Muscular, sac-like organ that connects the esophagus and small intestine
Function of stomach
Breaking down food. Cells in the stomach lining secrete enzymes, hydrochloric acid, and other chemicals to continue the digestive process begun in the mouth.
Muscles of the stomach (3)
1) Longitudinal muscle layer, 2) Circular muscle layer, 3) Oblique muscle layer
Pylorus
most distal and narrow section of the stomach; Food passes through the pyloric canal into the small intestine
3 Gastric Disorders
1) Gastritis, 2) Peptic Ulcer Disease, 3) Neoplasms
Acute Hemorrhagic Gastritis
Gastric mucosa erosions that can lead to sharp punched-out ulcers and bleeding. Acute inflammatory response. Widespread petechial hemorrhages in any part of stomach (1-25 mm)
Symptoms of Acute Hemorrhagic Gastritis
vague abdominal discomfort to massive, life-threatening bleeding and mucosal perforation.
Risk factors of Acute Hemorrhagic Gastritis (5)
1) Nonsteroidal anti-inflammatory drug use (NSAIDs), 2) Heavy alcohol use, 3) Major surgery, 4) Severe stress: CURLING ULCERS (deep) in severely burned pxs. 5) CNS trauma: CUSHING ULCERS (deep); * Acute Hemorrhagic Gastritis is often associated with acute illness or trauma and all risk factors lead to breakdown of mucosal barrier, which permits acid-induced injury
Helicobacter pylori Gastritis
Most common type of chronic gastritis in the USA. H. pylori has only been found in association with gastric epithelium and/or areas with chronic gastritis. It is not present in other tissues. Prevalence of infection with H. pylori increases with age. By age 60, 50% people is seropositive. Two thirds will show histological evidence of mucosal gastritis; * Strong association with peptic ulcer disease
Treatment of Helicobacter pylori Gastritis
Gastritis is cured following treatment with bismuth or antibiotics; * Antibodies against H. pylori are commonly found in pts with chronic gastritis.
Peptic Ulcer Disease
Focal, chronic ulcers that occur in any portion of the gastrointestinal tract exposed to the aggressive action of gastric secretions (i.e., hydrochloric acid). Peptic ulcers are usually solitary lesions less than 4 cm in diameter. Not normally carcinogenic (less than 1% become cancer)
Stats on peptic ulcer disease
About 10% of population in Western industrialized countries may develop such ulcers at some point during their lifetime
Most common sites of peptic ulcer disease (3 from most common to least common)
1) Proximal duodenum: male preponderance; ~ 30-60 yrs of age, 2) Distal stomach: male = female; middle aged and elderly, 3) At the gastroesophageal junction, in the setting of gastroesophageal reflux or Barrett esophagus
3 Environmental risk factors of peptic ulcer disease
1) Diet: little evidence supports role of food, alcohol, coffee. 2) Cigarette smoking: a definite risk factor, especially for gastric ulcers. 3) Drugs: aspirin, other NSAIDs, and analgesics
3 Genetic risk factors of peptic ulcer disease
1) First-degree relatives of people with peptic ulcers: 3X risk, 2) Risk of duodenal ulcer is 30% higher in people with type O blood, 3) High circulating levels of pepsinogen I: 5X risk for duodenal ulcer
Causes of peptic ulcer disease (3)
1) Hydrochloric acid - Formation and persistence of peptic ulcers in the stomach and duodenum require HCl secretion, 2) Gastric ulcers almost invariably arise following mucosal injury by H. pylori or chemical gastritis. 3) About 75% pts with gastric ulcers harbor H. pylori
2 Complications of peptic ulcer disease
1) Hemorrhage (bleed into the stomach): Most common serious complication in up to 20% of pxs. May manifest as anemia or occult blood in stools. 2) Perforation (now blood leakage out of the stomach): Occurs in ~5% pts. Most common in duodenal ulcers. High mortality rate. * In one third there is no symptoms of peptic ulcer.
4 Severe Diseases associated with peptic ulcer disease
1) Cirrhosis: 10X risk than in normal subjects, 2) Chronic Renal Failure, 3) Hereditary Endocrine Syndromes (Multiple endocrine neoplasia syndrome, type I), 4) Chronic Pulmonary Disease
2 Types of benign neoplasms
Gastrintestinal stromal tumors (GIST) and Epithelial Polyps
Cause of Gastrintestinal stromal tumors (GIST)
Derived from pacemaker cells of Cajal in muscular tissue of the GI tract. Overexpression of c-kit oncogene encodes a tyrosine kinase that promotes cell proliferation. Nonagressive
3 Types of Epithelial Polyps
1) Hyperplastic: most common gastric polyps. Seen in pxs with chronic gastritis. No malignant potential. 2) Adenomatous: usually solitary. Glands lined with dysplastic epithelium. Potential for adenocarcinomas. 3) Fundic gland polyps: No malignant potential
Stats on stomach cancer (malignant neoplasm)
1) About 21,600 Americans were diagnosed with stomach cancer during 2013 and 10,990 deaths were estimated to occur in the same year from this type of cancer. 2) Average age at the time of diagnosis is 71. About two thirds of people with stomach cancer are older than 65. 3) Incidence of Gastric CA is very high in Japan and Chile: 7X-8X USA rates.
3 Causes of stomach cancer
1) Food, 2) Nitrosamines, 3) H. pylori (but cancer can also be found in pts without H. pylori; H. pylori ALONE neither sufficient nor necessary for gastric carcinogenesis)
Food causing stomach cancer
Starch, smoked fish and meat (carcinogen benzopyrene), pickled veggies
Nitrosamines causing stomach cancer
Secondary amines are converted to nitrosamines in the presence of nitrates or nitrites; High nitrate can be found in soil/water, Processed meat and veggies; Nitrosamine is present in cigarettes; However, a good diet of milk and fresh veggies rich in vitamin C can inhibit nitrosation of secondary amines.
Adenocarcinomas of the stomach
Adenocarcinomas greater than 95% of gastric CA; * Primary lymphoma of the stomach accounts for ~5% of all gastric CA
4 Locations of Adenocarcinomas of the stomach
1) Distal Stomach, 2) Lesser curvature of the antrum, 3) Prepyloric region, 4) Rare in the fundus (proximal stomach)
Early gastric cancer
Depth of invasion: limited to mucosa or submucosa (May exhibit an exophytic, flat or depressed, or excavated conformation); May have a more benign course, better prognosis; Metastasis to regional lymph nodes; Distant metastasis: the most common is to a supraclavicular node called Virchow node
3 Types of Advanced gastric cancer
1) Polypoid (fungating): 33% of adeno CA. Solid mass projects into lumen. 2) Ulcerating: 33% of adeno CA. Shallow ulcers with irregular, raised, firm margins and ragged base (in contrast to benign peptic ulcer). 3) Diffuse infiltrating: 10% of adeno CA. No true tumor mass is seen. Wall of stomach is thickened and firm (“leather-bottle-like” lesion). When all stomach is compromised is called linitis plastica.*Most gastric cancers are diagnosed at the advanced stage; Involves Mucosa, submucosa AND MUSCLE INVASION