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57 Cards in this Set

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Tracheoesophageal Fistula
= a communication between the trachea and esophagus.

90%: upper portion of the esophagus ends in a blind pouch, and the upper end of the lower segment communicates with the trachea.

Infants develop aspiration immediately after birth.
Esophageal Webs
A thin mucosal membrane projects into the lumen of the esophagus.

Somtimes multiple and can be found ANYWHERE in the esophagus.
Plummer-Vinson Syndrome is characterized by (3):
1. a cervical esophageal web
2. mucosal lesions of the mouth and pharynx
3. iron-deficiency anemia
What is a recognized complication of Plummer-Vinson syndrome?
carcinoma of the oropharynx and upper esophagus.
Define Esophageal Diverticula
an outpouching of the wall that contains all layers of the esophagus.

When the sac lacks a muscular layer, it known as a FALSE DIVERTICULUM.
Where does an esophageal diverticula occur? (3)
in the hypopharyngeal area above the UES

in the middle esophagus

immediately proximal to hte LES
Zenker Diverticulum
An uncommon outpouching that appears HIGH in the esophagus.

Can accumulate large amt of food; frequent regurgitation of previously eaten food.

Serious complication: RECURRENT ASPIRATION PNEUMONIA
Traction Diverticula
Outpouchings that occur princiapally in the MIDPORTION of the esophagus.

Results from adhesions secondary to TB.
Epiphrenic Diverticula
Located immediately ABOVE the diaphragm.

Encountered in YOUNG people.

Nocturnal regurgitation of large amounts of fluid stored in the diverticulum during the day is TYPICAL.
Define dysphagia.


Define odynophagia.
Difficulty swallowing - hallmark of motor disorders of esophagus.


Pain on swallowing.
Achalasia
One time called "CARDIOSPASM"

A disease characterized by the absence of peristalsis in the body of the esophagus and failure of the LES to relax in response to swallowing.

Consensus that loss of absence of GANGLION CELLS in the myenteric plexus of the esophagus is involved.

Latin America: a common complication of CHAGAS DISEASE-- ganglion cells destoryed by TRYPANOSOMA CRUZI.
Scleroderma (Progressive Systemic Sclerosis)
Causes fibrosis in many organs and produces a severe abnormality of esophageal muscle function.

AFFECTS PRINCIPALLY THE LES.

Intimal fibrosis of the small arteries and arterioles is COMMON and may play a role in the pathogenesis of fibrosis.

Patients suffer dysphagia and heartburn caused by PEPTIC esophagitis, owing to reflex of acid from the stomach.
Define hiatal hernia.
A herniation of the stomach through an enlarged hiatus in the diaphragm.

-sliding hernia
-paraesophageal hernia
Sliding hernia.
An enlargement of the diaphragmatic hiatus and a laxity of the circumferential CT that allows a cap of gastric cardia to move upward to a position above the diaphragm.
Paraesophageal Hernia
Characterized by herniation of a portion of the gastric fundus beside the esophagus through a defect in the diaphragmatic CT membrane that defines the esophagus hiatus.

Symptoms: HEARTBURN + REGURGITATION - are attributed to gastroesophageal reflux. Exacerbated when the person is lying down (recumbent) - faciliates acid reflux.
Reflux Esophagitis
An esophageal injury caused by regurgitation of gastric contents into the lower esophagus.
• The combination of acid + pepsin may be very injurious to the esophageal mucosa; gastric fluid often contains refluxed BILE from the duodenum, which is believed to be harmful to the esophageal mucosa.
• PATHOLOGY: If reflux is chronic, then thickening of the epithelium, traditionally termed LEUKOPLAKIA, is seen as irregular, grayish-white patches.
• Areas affected by reflux are susceptible to superficial mucosal ulcerations, which appear as vertical linear streaks.
• The basal layer of the epithelium is thickened, and the papillae of the lamina propria are elongated and extend toward the surface.
• A modest increase in the # of lymphocytes is seen in the lamina propria, and neutrophils and eosinophils may be present within the squamous epithelium.
• Eosphageal stricture may eventuate among those causes in which the ulcer persists and damages the esophageal wall deep to the lamina propria—fibrosis is stimulated and narrows the esophageal lumen.
Barrett Esophagus
Replacement of the squamous epithelium of the esophagus by columnar epithelium secondary to chronic gastroesophageal reflux.

Majority of patients drink alcohol regularly and smoke tobacco.
3 types of metaplasia of Barrett Esophagus
1. Cardiac-like mucous glands, resembling those ordinarily seen at the gastroesophageal junction, with no parietal or chief cells beings present.
2. An epithelium similar to that of the fundus of the stomach, with short glands containing parietal and chief cells.
3. A distinctive, intestinal-like epithelium composed of goblet cells and surface cells similar to those of the gastric mucosa.
Barrett Esophagus carries what serious risk?
carries a serious risk of malignant transformation to ADENOCARCINOMA.
Candida Esophagitis
Fugal infection has become common because of an increasing # of immunocompromised people who:
1. Receive chemotherapy for malignant disease
2. Are treated with immunosuppressive drugs after organ transplantation.
3. Have contracted AIDS.

Mild cases: few small, elevated white plaques surrounded by a hyperemic zone are present on the mucosa.

Severe cases: confluent pseudomembranes lie on a hyperemic and edematous mucosa.
Herpetic Esophagitis
Esophageal infection with herpesvirus type I

Most frequently associated with lymphomas and leukemias.
Chemical Esophagitis
Usually the result of accidental poisoning in children or attempted suicide in adults.

Produced by intake of strong alkaline agents or strong acids, both of which are used in various cleaning solutions.

Alkali-induced liquefactive necrosis is accompanied by conspicuous inflammation and saponification of the membrane lipids in the epithelium, submucosa, and muscularis of the esophagus and stomach.

Also: thrombosis of small vessels adds ischemic necrosis to the injury.

Strong acids produce immediate coagulation necrosis, which results in a protective eschar that prevents injury and limits penetration.
esophageal varices
= dilated vein immediately beneath the mucosa, which are prone to rupture and hemorrhage.

Arise in the lower 1/3 of the esophagus, virtually always in the setting of portal hypertension secondary to cirrhosis of the liver.
Squamous carcinoma [esophagus]
Accounts for 7% of all gastrointestinal cancers.

Esophageal cancer “belt” extending across Asia from the Caspian Sea region of northern Iran and the former Soviet Union through Central Asia and Mongolia to northern China.
-NORTHERN China, the mortality rate in men is 70-fold greater than that in the U.S.
-Caspian region of Iran has a 30-fold greater incidence, whereas southern zones have a low incidence.
-U.S. = blacks > whites; urban dwellers at greater risk than those in rural areas; males: females = 3:1;
-Scandinavian counties, Holland, and Austria have low frequencies.

~50% of the cases involve the lower 1/3 of the esophagus.

Most common presenting complaint: persistent dysphagia

Prognosis remains DISMAL!
Adenocarcinma [esophagus]
Account for 30-50% of the malignant esophageal tumors.

Virtually all adenocarciomas arise in Barrett epithelium.

20% 5-year survival following radical surgery.
Tumors of squamous carcinoma of the esophagus are 3 types:
1. Polypoid, which projects into the lumen.
2. Ulcerating, which is usually smaller than polypoid.
3. Infiltrating, the principal plan of growth is in the wall.
Congenital Pyloric Stenosis
A concentric enlargement of the pylorus and narrowing of the pyloric canal that obstructs the outlet of the stomach.

Genetic & Familial: associated with Turner syndrome, trisomy 18, esophageal atresia; rubella infection, maternal intake of thalidomide.

Associated with a deficiency of nitric oxide synthase in the nerves of pyloric smooth muscle.

Concentric enlargement of the pylorus and narrowing of the pyloric canal.

After pyloromyotomy, the “tumor” disappears, although occasionally, a small, sympatomatic mass remains.

Infant manifests PROJECTILE VOMITING.
Define Acute Hemorrhagic (EROSIVE) gastritis
The presence of focal necrosis of the mucosa in an otherwise normal stomach.
Environmental factors that contribute strongly to squamous carcinoma of the esophagus: (8)
o Excessive consumption of alcohol
o Cigarette smoking
o Nitrosamines and aniline dyes produce esophageal cancer in ANIMALS.
o Diets lacking in fresh fruits, vegetables, and animal protein.
o Plummer-Vinson syndrome and celiac sprue
o Achalasia
o Esophageal stricture
o Webs, rings, and diverticula
Causes of acute hemorrhagic (erosive) gastritis
intake of aspirin, other NSAID's, excess alcohol.
heavy smoking
tx with cancer chemotherapeutic drugs
uremia
systemic bacterial/viral infections
severe stress
ischemia/shock
suicical attempts with acids/alkali
distal gastrectomy
trauma to the CNS
microcirculatory changes in the staomch
impaired protective mechanisms
Pathology of acute hemorrhagic (erosive) gastritis
widespread petechial hemorrhages in any part of the stomach.

erosions, 1-25 mmacorss

neutrophilic inflammatory response
Clinical symptoms of acute hemorrhagic (erosive) gastritis
Symptoms range from vague abdominal discomfort to massive, life-threatening hemorrhage or clinical manifestations of gastric perforation.

Patients with acute gastritis from aspirin/NSAID's may present with hypochromic, microcytic ANEMIA causedby undetected, chronic bleeding.
causes of CHRONIC gastritis
• Chronic infection by H. pylori
• Immunologic (autoimmune), in association with pernicious anemia
• Toxic, as with alcohol and cigarette smoking
• Postsurgical, especially following antrectomy with gastroenterostomy with reflux of bilious duodenal secretions
• Motor and mechanical, including obstruction, bezoars (luminal concretions), and gastric atony
• Radiation
• Granulomatous conditions (e.g., Crohn disease)
• Miscellaneous-amyloidosis, graft-versus-host disease, uremia.
Autoimmune Gastritis
A chronic, diffuse inflammatory disease of the stomach that is restricted to the body and fundus and is associated with autoimmune phenomena.

Diffuse atrophic gastritis in the body and fundus of the stomach, with lack of or only minimal involvement of the antrum.

Antibodies to parietal cells and intrinsic factor.

Significant reduction in or absence of gastric secretion, including acid.
In the large majority of cases, what is a complciation of autoimmune gastritis?
pernicious anemia.
Superficial Gastritis
 Shows lymphocytes and plasma cells and sometimes neutrophils in the lamina propria of the mucosa of the antrum and body of the stomach.
Atrophic Gastritis
Lymphocytes & plasma cells extend into the DEEPEST reaches of the mucosa --> muscularis mucosae.

Reduction in the # of gastric glands (hence the name “atrophic”)

Inflammatory process abates -->leaves only a thin, atrophic mucosa = “gastric atrophy”
Intestinal Metaplasia
Normal epithelium is replaced by one that is composed of intestinal-type cells.

Many mucin-containing goblet cells and enterocytes line crypt-like glands

Paneth cells present.
People with atrophic gastritis of the autoimmune (or multifocal) type have a high incidence of:
carcinoma of the stomach
Intestinal metaplsia of the stomach in particular has been identified as being...
a pre-neoplastic lesion
Helicobacter pylori Gastritis
(infectious gastritis)
A chronic inflammatory disease of the antrum and body of the stomach caused by infection with H. pylori.

Helicobacter pylori is strongly associated with nonerosive (CHRONIC) gastritis of the antrum and is strongly associated with peptic ulcer disease of the stomach and the duodenum.

H. pylori infection has been found only in association with gastric-type epithelium and does NOT occur in other tissues.

Predominant symptom: dyspepsia (upset stomach).
Peptic ulcer disease
Peptic ulcers are chronic, most often solitary, lesions that occur in any portion of the gastrointestinal tract exposed to the aggressive action of acid/peptic juices.

Peptic ulcer disease refers to breaks in the mucosa of the stomach and small intestine, principally the proximal duodenum, that are produced by the action of gastric secretions.

Peptic ulcer disease affects the distal stomach and the proximal duodenum.

The common factor that unites gastric and duodenal ulcers is gastric secretion of hydrochloric acid—with rare exceptions, a person who does not secrete acid will not develop a peptic ulcer anywhere.
• Peptic ulcers are usually solitary lesions less than 4 cm in diameter, located in the following sites, in order of decreasing frequency:
1. Duodenum, first portion
2. Stomach, usually antrum
3. At the gastroesophageal junction, in the setting of gastroesophageal reflux or Barrett esophagus
4. Within the margins of a gastrojejunostomy
5. In the duodenum, stomach, and/or jejunum of patients with Zollinger-Ellison syndrome
6. Within or adjacent to an ileal Meckel diverticulum that contains ectopic gastric mucosa.
Pathogenesis of Peptic Ulcer Disease
Aspirin and other NSAID’s are contributing factors.

Cigarette smoking is a definite risk factor (alcohol, caffeine, spicy foods NOT risk factors)
Genetic factors: First-degree relatives of people with duodenal ulcers a 3-fold increased risk. Identical twins only show a 50% concordance – environmental factors are definitely involved.

Blood-group antigens: Risk of duodenal ulcer is ~30% higher in people with type O blood. Patients with gastric ulcers don’t exhibit a greater frequency of blood group O.

A person with high circulating levels of pepsinogen I is at 5-fold the normal risk of developing a duodenal ulcer.

no association with stress
HCl and peptic ulcers
• The formation and persistence of peptic ulcers in both the stomach and duodenum require the gastric secretion of ACID.
• Gastric secretion of PEPSIN parallels that of HCl.
Diseases associated with peptic ulcers.
• Cirrhosis: incidence of DUODENAL ulcers in patients with cirrhosis is 10-FOLD greater than in normal people.
• Chronic Renal Failure: patients subjected to renal transplantation show a substantially increased incidence of peptic ulceration.
• Hereditary Endocrine Syndromes: Multiple endocrine neoplasia type I is a cause of severe peptic ulceration.
• Chronic Pulmonary Disease: ¼ of the patients with longstanding pulmonary dysfunction suffer from peptic ulcer disease.
Physiological factors in DUODENAL ulcers.
• The maximal capacity for acid production by the stomach is a reflection of the total parietal cell mass.
• Only 1/3 of these patients secrete excess acid.
• Increase in # of parietal cells  increase in chief cells  increased prevalence of hyperpepsinogenemia in patients with ulcers.
• Accelerated gastric emptying can lead to excessive acidification of the duodenum.
• The production of duodenal ulcers requires an acidic pH in the duodenal bulb—an excess of acid over neutralizing secretions (by biliary, pancreatic, duodenal secretions).
• Impaired mucosal defenses may contribute to peptic ulceration.
Physiological factors in GASTRIC ulcers.
• Gastric ulcers almost invariably arise in the soil of chronic, non-erosive antral gastritis.
• Most patients secrete less acid than those with duodenal ulcers and even less in normal people.
• Occurrence of gastric ulcers in the presence of gastric hyposecretion implies these possibilities:
1. Gastric mucosa is particularly sensitive to low concentrations of acid
2. Some material other than acid damages the mucosa
3. Gastric mucosa is exposed to potentially injurious agents for an usually long period of time.
Role of Helicobacter pylori in peptic ulcer disease
• H. pylori has been isolated from the gastric antrum of virtually all patients with duodenal ulcers.
o The converse is NOT TRUE!—only a small # of people infected with H. Pylori suffer from duodenal ulcer disease.
o H. Pylori infection is a necessary, but NOT SUFFICIENT condition for developing peptic ulcer disease of the duodenum.
• Infection with H. pylori may stimulate acid secretion by promoting gastrin release and suppressing somatostatin secretion.
• The release of histamine metabolites by H. pylori may increase basal acid secretion.
• Infection of the metaplastic epithelium by H. pylori may render the mucosa more susceptible to peptic injury.
• ¾ of patients with gastric ulcers harbor H. pylori.
Leiomyoma [stomach]
A benign tumor of smooth muscle cells

Submucosal and covered by intact mucosa
Epithelial Polyps [stomach]
• Classified as either hyperplastic or adenomatous
• Account for almost ½ of all benign gastric tumors.
• The large majority of gastric polyps are found in patients with achlorhydria, and both types occur in association with atrophic gastritis and pernicious anemia, as well as in stomachs that harbor carcinoma.
Hyperplastic Polyps
Represent the large majority of polyps.
Single or multiple

Not true neoplasms; uncertain origin.

Hyperplastic polyps have no malignant potential.
Adenomatous Polyps
True neoplasms

Occur most commonly in the antrum.

Adenomatous polyps manifest a malignant potential, which is variably reported as being from 5% to 75%.
6th most common cause of cancer in the US
carcinoma of the stomach
Pathogenesis of carcinoma of the stomach
Dietary factors: large amts of starch, smoked fish and meat, pickled vegetables.

nitrosamines: vit C is inverly related

blood type A found in 38% of general population, whereas 1/2 of the patients with gastric cancer display this type.

H. pylori +
3 macroscopic types of ADVANCED gastric cancer
Polypoid (fungating) adenocarcinoma: 1/3 of advanced cancers; solid mass that projects into the lumen of the stomach.

Ulcerating adenocarcinoma: 1/3 of advanced cancers; shallow ulcer.

Diffuse or infiltrating adenocarcinoma: 1/10 of ALL stomach cancers.
-When the entire stomach is involved, the term linitis plastica (“leather-bottle stomach”) is applied.
Early gastric cancer
= superficial spreading carcinoma

5-20% are already metastatic to the lymph nodes at the time of detection.

Most found in DISTAL STOMACH.

Metastasizes principally by the lymphatic route to the regional lymph nodes

Distant lymphatic metastases also occur; most common is an enlarged supraclavicular node = VIRCHOW NODE or a SENTINEL NODE.

Carcinoma of the stomach can spread to the OVARY, where it commonly elicits a desmoplastic response = KRUKENBERG TUMOR.