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85 Cards in this Set
- Front
- Back
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What are the 4 layers of the GI tract?
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Mucosa, Submucosa, Muscularis, Serosa/adventitia
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What are the 4 layers of the mucosa of the GI tract?
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1. Epithelium: lines GI. Basement membrane underneath
2. Glands: formed by epithelium invagination 3. Lamina propria: CT tissue beneath basement membrane 4. Muscularis proper: end pt of mucosal layer |
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What is the direction of the muscle of the muscularis in the GI tract?
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Inner circle + outer longitudinal
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What is the serosa/adventitia layer?
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Serosa: visceral peritoneum
Adventitia: where the mesentery attaches |
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What are the 3 congenital abnormalities of the esophagus? (determined first few days of life)
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Atresias, Fistulas and Stenosis.
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What is an atresia of the esophagus?
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Can be in any organ structure of body. In esophagus, there is incomplete development where a blind pouch has formed. You see a blind loop coming down from the oral cavity and another coming up from stomach, but no connection.
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What is a fistula of the esophagus?
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An abnormal connection between 2 organs. Tracheo-esophageal fistula: esophagus connected to trachea. WILL result in airway obstruction. Other intestinal fistulas can be seen in Crohn's diverticulum disease.
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What is stenosis of the esophagus?
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Narrowing or stricture
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How can atresia, fistulas or stenosis be acquired as opposed to congenital?
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May be secondary to sleroderma (fibrous tissue proliferation causing fibrosis in many different organs) or post inflammatory scarring.
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What is the most common combination of atresia, fistulas, stenosis?
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80-90% are a proximal esophageal atresia + distal tracheo-esophageal fistula
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What is dysphagia?
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Painful or difficult swallowing
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What are 5 possible causes of dysphagia?
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1. achalasia
2. Hiatal hernia 3. Infection 4. Esophageal ring or webs (obstruction of flow, mucosa causes obstruction at lumen and reduces flow of food) 5. Laceration of the esophagus |
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What is achalasia?
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Failure of the esophagus to relax. Generally, clinical progression dysphagia to regurgitation. Usually due to aperistalsis, neurogenic stimulation doesn't allow esophagus to relax when swallowing
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What are the two types of esophageal rings and webs?
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Hiatal hernia and diaphragmatic hernia
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What is hiatal hernia?
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A portion of the proximal stomach slips through a weak or slightly enlarged diaphragmatic ostia. 2 main types: sliding: good part of stomach protruding through diaphragm, rolling (para-esophageal): small part of stomach protrudes
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What is a diaphragmatic hernia?
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Congenital abnormality - significan portion of diaphragm has failed to develop allowing abdominal structures (often liver) to be herniated into pleural cavities.
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What is Mallory Weiss syndrome?
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If a patient is undergoing protractive vomiting, they may begin tearing the stratified squamous epithelium of the esophagus
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What is Zenker's diverticulum?
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Diverticulum (small out-pouchings that include some or all of wall of structure) in the esophagus. Problems arise from trapping food that begins to be broke down from bacteria. Inflammation and abscess formation can occur and risk of perforation. Results in halatosis (bad breath)
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What is infectious esophagitis?
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In immunocompromised (HIV, chemo, steroid treatments). Most common forms: CMV, herpes, candida.
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What is the most common type of benign esophageal tumor?
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Leiomyoma - arises from smooth muscle. Rare
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What are the most common form of esophageal carcinoma?
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Adenocarcinoma
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What is the 2nd most common form of esophageal cancer?
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Squamous cell carcinoma. Was the most common type until the 90s when adenocarcinomas increased due to GERD.
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What are 5 other types of esophageal malignancies?
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Leiomyosarcoma, fibrosarcomas, angiosarcomas, liposarcomas and rhabdomyosarcomas
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What part of the esophagus can become cancerous?
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ANY connective tissue surround the esophagus
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What does an esophageal tumor look like and how would it be removed?
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Granular cobblestone pattern. Removed by cutting out affected portion. Conduct a gastric pull-up (pull up the stomach like a hiatal hernia to reattach the esophagus.
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What are the 2 etiologies of inflammatory lesions of the esophagus?
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Reflux esophagitis (GERD), Barrett's esophagus
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What is reflux esophagitis (GERD)?
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Defect in lower esophageal sphincter allows gastric juices of stomach to enter lower esophagus. Low pH and gastric material causes injury to squam epi. Can cause metaplasia -> can lead to mutations and tumors. Sometimes assoc with hiatal hernia.
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What are the varying forms of injury to the esophagus in GERD, dependent on degree/duration of reflux?
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Mild to sever esophagitis, ulceration of squamous mucosa w/ scar formation in deep ulcers, metaplasia of squam epi to intestinal type or gastric in disorderd fashin (barretts metaplasia), neoplastic transformation - atypical cells growing disordered fashion - displastic changes, neoplastic transformation into adenocarcinomas - can invade basement membrane - metastisize
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What is Barrett's esophagus?
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Displasia of the cells of the esophagus due to GERD. Looks like velvet. Could progress to cancer.
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What are esophageal varices?
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Essentiall varicose veins in the esophagus. Usually due to portal hypertension. May bleed.
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What are the 4 regions of the stomach?
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1. Cardiac: dome of stomach, mucus cells
2. Fundus/body: parietal and chief cells 3. Antrum: gastrin 4. Pylorus |
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What are the 3 muscle wall layers of the stomach?
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Inner circular, outer longitudinal, oblique.
*Note: everywhere else has 2 layers but the stomach has three to churn food |
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What are the 4 cell types in the stomach?
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1. Mucous neck cells: secrete mucus
2. Parietal cells: secrete HCl 3. Chief cells: secrete pepsinogen 4. Neuroendocrine cells: secrete gastrin |
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What are 2 congenital abnormalities of the stomach?
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Diaphragmatic hernia, pyloric stenosis (narrowing, can be surgically fixed, time it takes to make diagnosis depends on symptoms)
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How can gastric dilation and rupture occur?
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Beer binge. Can cause massive gas formation (can be due to a HUGE ingestion of anything - not just beer)
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What are the two broad types of gastritis?
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Acute and Chronic. Can be minimal (no symptoms) to sever (vomiting blood)
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What is the result of acute gastritis?
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Causes reversible damage (erosion) to the gastric mucosa.
Inflammation is limited to the mucosa not the wall. |
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What are the degrees of damage of acute gastritis?
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Acute gastritis: superficial inflammation,
Acute hemorrhagic gastritis: bleeding into mucosa, Acute erosive gastritis: defects in mucosal surface. Depending on severity, may be inflammatory changes or erosive changes w/ widespread sloughing of mucosa. Small petichial hemorrhages may form and develop into ulcers |
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What are the causes of acute gastritis?
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Exposure/ingestion of some sort of toxin, trauma.
Aspirin/other meds, alcohol, infections, sepsis, shock, smoking, food poisoning, severe stress (burns, trauma, surgery), radiation, chemo drugs, physical trauma, ischemia/hypoperfusion |
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What happens in the tissues in acute gastritis?
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Increased acid secretion w/ back diffusion into glands. Decrease in bicarb production, neutrophils found in mucosa and cause erosion/necrosis of mucosa. In severe cases, may be massive hematemesis and melana (tarry stool). May lead to ulcer
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Why are upper GI bleeds dark and lower GI bleeds bright red?
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Blood coming from stomach or upper tract is being digested on its way down. Causes it to be dark: melana.
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What are the clinical features of acute gastritis?
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Variable! May not see any signs/symptoms, vague abdominal discomfort or pain, nausea/vomiting, melana, massive hematemesis
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What is chronic gastritis?
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Inflammation resulting from long standing disease
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What are the range of categories of chronic gastritis?
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Superficial gastritis, atrophic gastritis (atrophic changes increase cancer development possibility) loss of gastric folds, Gastric atrophy (more severe/progressed form of atrophic)
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As severity of inflammation increases in chronic gastritis, associated developments of atrophic changes and flattening of the mucosa occur. What is atrophy associated with?
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Metaplasia. Dysplasia = abnormal change, cancer cells that haven't broken through basement membrane. and Atypia = atypical changes - make sure to watch this closely so it doesn't turn into dysplasia.
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What are the clinical features of chronic gastritis?
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Decrease in parietal cells (-->decrease intrinsic factor and B12 absorption--> decrease acidity), changes in acid secretion (increase or decrease), hypersatrinemia (sometimes), increase in peptic ulcers, increase in polyp formation, increase tendency toward gastric carcinoma
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What is hypersatrinemia in chronic gastritis?
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More gastrin in blood vessels because of overactive neuroendocrine cells (they are trying to get the other cells to produce more HCl to increase acidity)
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Why do peptic ulcers occur in chronic gastritis?
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Mucus neck cells aren't protecting the surface
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What is the danger in polyp formation in chronic gastritis?
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HIGH tendency for developing into gastric cancer.
*Note: if polyps are seen in the colon, there is not nearly as high a chance for colon cancer development |
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What is indicated by chronic inflammation?
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It is a sign of an underlying disease. Peptic ulcer, cancer, Zollinger-Ellison syndrome, pernicious anemia
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What is Zollinger-Ellison syndrome?
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Hypergastrinemia
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What is pernicious anemia?
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Note enough intrinsic factor because of decrease in parietal cells
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How is a diagnosis made for ulcer, Zollinger-Ellison syndrome and pernicious anemia?
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Endoscopy and biopsy
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What are the 2 most common forms that make up 90% of all cases? What make up the other 10% of cases?
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H. polori is the most common (80% of chronic gastritis) and Autoimmune gastritis (10%-second most common). Last 10% due to toxicity, postsurgical w/ assoc duodenal reflux, mechanica/obstructive/motor disorders, radiation/chemo
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What is H pylori?
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GNR curved, flagellated for motility. Colonizes gastric mucosa. Affects antrum and distal areas of fundus. Colonization usually patchy but can become confluent.
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How does H pylori cause ulceration?
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Attaches to the superficial gastric epithelium and breaks down the mucus barrier and exposes undrlying tissue to acid environment of stomach. Produce urease which buffers local acid and contributes to damage of mucus barrier.
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What part of the population does H pylori affect most?
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Increase with age. By age 50 and older over 50% of the population infected, but most are asymptomatic.
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What happens to the tissues in chronic cases over time?
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Atrophic changes (thinning of the mucosa, loss of/flattening gastric folds/rugae, thickening of the muscularis layer), interstinal metaplasia can occur, some increased incidence of gastric carcinoma and gastric lymphoma
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What are the diagnostic tests for H pylori?
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Urease breath test, serology testing for Ab, biopsy from antrom
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What are the treatments for H pylori?
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Antimicrobials, bismuth compounds (pepto bismol)
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What are some of the signs and symptoms of H pylori?
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Nausea, vomiting, abdominal discomfort, hypochloridia (reduction of parietal cells - LOW acid environment), won't necessarily see B12 deficiency because not all parietal cells lost, gastrin levels usually normal
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What percentage of patients with H pylori develop into carcinoma?
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5%
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What is autoimmune gastritis?
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Diffuse gastritis involving fundus and body of stomach (not antrum!) leading to mucosal atrophy
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How does autoimmune gastritis affect the stomach?
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Antibodies produced against parietal cells and intrinsic factor. --> intrinsic factor deficiency and B12 absorption problem
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What are the clinical features of autoimmune gastritis?
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Decreased acid secretion (hypochloridia) w/ HIGH pH, pernicious anemia (secondary to lack of intrinsic factor), assoc w/ other autoimmune dis (hashimoto's thyroiditis, addisons), hypergastrinemia from G-cell hyperplasia secondary to decrease in acid secretion (gastrin increase to try and get more HCl to increase acidity)
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What percentage of patients with autoimmune gastritis progress into carcinoma?
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4%
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What are chronic peptic ulcers?
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98-99% are in stomach or duodenum (of this, most in duodenum). Duodenum: stomach = 4:1. 1-2% anywhere else in GI system
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What are the risks for developing chronic peptic ulcers?
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Cirrhosis, aspirin, cigarettes, genetics, blood type O (30% greater chance for duodenal ulcers), pepsinogen I: high levels in serum = increase risk
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What are the characteristics of chronic peptic ulcers?
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Gastric/duodenal ulcers have a cookie-cutter look (punched out look), malignant ulcer has much more raised folds. Rugae remains present until atrophic changes begin to occur - then rugae disappears
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What are the benign stomach tumors?
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Stromal tumors, leiomyoma, schwannoma, neurofibroma, lipoma, neurogenic tumor, hemangiopericytoma, hemangioma
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What are stromal tumors?
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Benign stomach tumors. <4cm. Most common non-epithelial benign tumor of the stomach, but overall rare. Produced by connective tissue (not epi)! - therefore: outer mucosa will look normal.
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What is a malignant stromal tumor (GIST: gastrointestinal stromal tumor)?
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Enlarged stromal tumor. Will still have normal rugal folds, normal mucosa, normal epi, LOTS of hemorrhaging and necrosis. Very atypical microscopically.
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What are the main types of malignant tumors of the stomach?
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Carcinoma/Adenocarcinoma (90-95%), Lymphoma (4%), Carcinoid (3%), Malignant Spindle cell tumors (2%)
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What is carcinoma/adenocarcinoma of the stomach?
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Malignant tumor. 90-95% of malignant stomach cancers. Epithelial based. Linitis plastica: less common subtype -infiltrates stomach leads to thickened and stiff/firm wall (leathery wall) Rare.
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What is the origin of carcinoid tumors of the stomach?
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Neuroendocrine cells.
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What is the 5 year survival rate with malignant stomach cancer?
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10-15% - poor because not usually diagnosed until later stages.
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What are characteristics of malignant stomach cancer?
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Decrease presence of rugal folds (flat surface). Raised borders = distinctive malignant ulcer
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What are the two main types of stomach polyps?
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Hyperplastic (90%) and Neoplastic (10%)
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What are hyperplastic stomach polyps?
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Exaggerated growth secondary to mucosal regeneration (almost like a wart. No genetic mutation that is allowing it to uncontrollably divide therefore not neoplastic)
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What are neoplastic stomach polyps?
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Adenomatous polyps: 3-4cm still benign. Has to have a mutation to become malignant. 40-60% may progress to malignancy in area of polyp. 40% risk of carcinoma elsewhere in stomach
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What is most stomach cancer associated with?
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Environmental factors. Ingestion of certain food or particular food preparation. Food contains carcinogens or stomach converts food into a carcinogen. Salty meats, pickled raw veggies, salty sauces
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What are risk factors of developing stomach cancer?
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Environmental dietary, hyp/achloriydia (high pH), chronic gastritis, pernicious anemia, partial gastrectomy
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How is a partial gastrectomy a risk for stomach cancer?
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Gastrectomy anastomose site at higher risk, risk increases if hypchlorydia, assoc w/ chronic gastritis, secondary to bile reflux, increase in bacterial colonization, neoplastic gastric polyps increase risk by 40%
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How long does it take for early gastric carcinoma to become invasive?
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About 8 years
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What can decrease the risk of stomach cancer?
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Eating green leafy vegetables and fruits
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