GI Path: Esophagus & Stomach Flashcards
Esophagus Location
-Extends from the epiglottis to gastroesophageal junction
-Inferior to larynx –> posterior to trachea and anterior to aorta –> penetrates diaphragm at esophageal hiatus –> meets stomach at cardiac orifice = lower esophageal sphincter
Describe the rich lymphatics of the esophagus
-Upper esophagus drains to cervical nodes
-Mid esophagus drains to paratracheal nodes
-Lower esophagus drains to gastric nodes
Esophagus function
-Transports food, liquids, and saliva from pharynx to stomach via peristalsis
- 2 sphincters control opening/closing:
*upper esophageal sphincter
*lower esophageal sphincter
Esophageal Varices
Distended esophageal veins that protrude into lumen
What is the pathogenesis of Esophageal Varices? The oral/clinical signs?
Pathogenesis:
-Portal hypertension –> reverse flow of portal blood from gastric coronary vein into esophageal veins
Oral/Clinical:
-Asymptomatic
-Rupture = massive hematemesis
- 50% of ruptures lead to death
Mallory-Weiss Syndrome
Esophageal linear lacerations - oriented longitudinally
What is the pathogenesis of Mallory-Weiss Syndrome? What is is associated with? The oral/clinical signs?
Pathogenesis:
-Prolonged vomiting prevents relaxation of gastroesophageal musculature and sphincter –> esophageal walls stretch and tear
Associated with:
1) repetitive vomiting - alcoholism/bulimia
2) hiatal hernia
Oral/Clinical:
-Abdominal pain
-Hematemesis - “coffee grinds” in vomitus
-Melana - “black tar” stool
Esophagitis
Inflammation of esophagus
What is the pathogenesis of Esophagitis? Oral/clinical signs?
Pathogenesis:
1) GERD - #1 cause in US men
2) Irritants - alcohol/smoking
3) Allergy
4) Drugs (doxycycline)
5) Chemo/radiation therapy
6) Infections (CMV/HSV)
Oral/Clinical:
-Dysphagia
-Odynophagia
-Chest pain; heart burn; acid reflux
**Can lead to scarring and constriction if untreated
GERD (Gastroesophageal Reflux Disease)
Reflux/backflow of gastric contents into the esophagus
What is the pathogenesis of GERD? Clinical/oral signs? Tx?
Pathogenesis:
1) Incompetent sphincter
2) Hiatal hernia
3) Slowed gastric emptying
**Can lead to Barrett esophagus
Oral/Clinical:
-Erosion of teeth - lingually
-Heartburn
-Adult-onset asthma
-Hoarseness
TX:
-Diet changes
-Lose weight; incline bed
-Meds = antacids; H2 inhibitors; proton pump inhibitors
Hiatal Hernia
Widened opening in the diaphragm where esophagus penetrates allowing part of the stomach to enter the thorax
What is the pathogenesis of Hiatal Hernia? Oral/Clinical signs?
Pathogenesis:
-Muscle weakness of diaphragm
Oral/Clinical:
-Difficulty swallowing
-Heartburn
-Belching
- 50+ yrs
Barrett Esophagus
Intestinal metaplasia within distal esophagus mucosa
**squamous epithelium to non-ciliated columnar epithelium
**most Esophageal Adenocarcinomas are associated with Barrett Esophagus but most Barrett esophagus cases do NOT develop into adenocarcinomas
What is the pathogenesis of Barrett Esophagus? Oral/Clinical signs?
Pathogenesis:
-Chronic GERD –> permanent change in mucosa = resistant to acid –> predisoposed to adenocarcinoma
*10% of chronic GERD cases
Oral/Clinical:
-History of chronic GERD
-Males 4:1
- 40-60yrs
-History of previous radiation exposure
Plummer-Vinson Syndrome
Rare disease - classic triad:
1) Dysphasia
2) Esophageal weba
3) Iron-deficiency anemia
What is the pathogenesis of Plummer-Vinson Syndrome? Oral/Clinical signs?
Pathogenesis:
-Atrophy of oral mucosa + upper esophageal webs
**Transformation of both into squamous cell carcinoma
Oral/Clinical:
-Dysphasia
-Cheilosis
-Glossitis
Esophageal Squamous Cell Carcinoma (SCCA)
Most common malignancy of esophagus
What is the pathogenesis of Esophageal SCCA? Risk factors? Oral/Clinical signs?
Pathogenesis:
-Begins as dysplasia in mid-esophagus –> develop into tumors w/in infiltration of esophageal wall = lumen narrows
Risk Factors:
1) Alcohol/tobacco use/very hot drinks
2) HPV
3) Plummer-Vinson Sx
Oral/Clinical:
-Asymptomatic (early)
-Dysphasia; odynophasia; weight loss (late)
-African Americans 6:1
-Males 4:1
- 45yrs+
Esophageal Adenocarcinoma
Most common malignancy of esophagus in US
What is the pathogenesis of Esophageal Adenocarcinoma? Risk factors? Oral/Clinical signs?
Pathogenesis:
-Begins as dysplasia in distal-esophagus –> develops into large exophytic tumors that ulcerate and deeply infiltrate esophageal wall/gastric wall = lumen narrows
Risk Factors:
1) Barrett esophagus
2) Chronic GERD
Oral/Clinical:
-Asymptomatic (early)
-Dysphasia; odynophasia; weight loss (late)
-Males 7:1
- 45yrs+
Esophageal SCCA and Adenocarcinoma PROGNOSIS
-Asymptomatic until advanced
-Dysphasia/Odynophasia
-Weight loss
-Extensive lymphatic spread:
*cervical nodes - upper esophageal tumors
*mediastinal/tracheal nodes - mid/distal esophageal tumors
-Overall 5yr survival rate = 25%
- 5yr survival rate when diagnosed with symptoms = 10%
Stomach Location
-Extends from lower esophageal sphincter to pyloric sphincter
-Inferior to the diaphragm
Describe the 4 regions of the stomach and the cells found w/in these regions
1) Cardia –> foveolar cells produce mucin
2) Fundus –> parietal cells produces HCl + intrinsic factor & chief cells produce digestive enzymes
3) Body –> parietal cells produce HCl + intrinsic factor & chief cells produce digestive enzymes
4) Antrum –> G-cells produce gastrin –> stimulates parietal cells
The gastric lumen of the stomach is ________
strongly acidic
Describe the mechanisms the stomach has to protect against gastric mucosa
1) Mucus coating
2) Bicarbonate secretion
3) Rich vascular supply
4) Mucosa regenerates
List the sphincters of the stomach
2 sphincters control opening/closing:
-Lower esophageal sphincter
-Pyloric sphincter
List the functions of the stomach
1) Digestive function - proteolytic enzymes; forms/moves chyme
2) Protective function - acidity is hostile to microbes
3) Secretory function - HCl; pepsin; mucus; gastrin; intrinsic factor
4) Temporary storage of food
Acute Gastritis/Gastropathy
Mucosal injury of stomach lining due to acid
- Acute Gastritis = PMNs present
- Gastropathy = no inflammatory cells present
What is the pathogenesis of Acute Gastritis/Gastropathy? Oral/Clinical signs?
Pathogenesis:
-Imbalance between mucosal defenses and acidic environment
-NSAIDS
-Alcohol
Oral/Clinical:
- +/- asumptomatic
- Variable epigastric pain
-Nausea; vomiting
*Acute Gastritis can progress to gastric ulceration = Acute Ulcer
Acute Ulcers
Ulceration of stomach lining
*Usually multiple ulcers occur; less than 1cm in diameter; normal adjacent mucosa; heal with re-epithelialization
What is the pathogenesis of Acute Ulcers? Oral/Clinical signs?
Pathogenesis:
1) Progression of acute gastritis
2) Stress and shock = local ischemia (75% of critically ill patients develop acute ulcers)
Oral/Clinical:
-Nausea; vomiting
-Coffee-ground hematemesis; melena
- 1-4% require transfusion
Helicobactor pylori Gastritis
Bacterial induced neutrophilic inflammation/atrophy of antrum
**Most common cause of chronic gastritis –> 90%
What is the pathogenesis of Helicobactor pylori Gastritis? The oral/clinical signs?
Pathogenesis:
- H. pylori secretes urease –> increased ammonia formed = increased pH around bacteria –> increased gastrin secretion = increased acid from parietal cells of body/fundus = atrophy of mucosa
**Causes imbalance of mucosal defenses resulting in tissue damage
Oral/Clinical:
-Asymptomatic
-Mild epigastric abdominal pain
Helicobactor pylori Gastritis increases the risk for…
1) Ulceration - peptic ulcer disease
2) Adenocarcinoma
3) Marginal zone lymphoma
**H. pylori can be found in dental plaque –> can cause re-infection; stress good OH
Auto-Immune Gastritis
Autoimmune antibodies to parietal cells + intrinsic factor
*triggers T-cell type IV hypersensitivity
What is the pathogenesis of Auto-Immune Gastritis? Oral/Clinical signs?
Pathogenesis:
- T-cell mediated destruction of epithelium of body and fundus including all parietal cells –> metaplasia occurs as gastric mucosa is replaced with intestinal epithelium
*Antrum not affected but G-cells becomes hyperplastic = increases gastrin
Oral/Clinical:
-Pernicious anemia
-Achlorhydria = almost no HCl
Auto-Immune Gastritis increases the risk for….
Adenocarcinoma (higher risk than with H. pylori Gastritis)
Comparison of H. pylori Gastritis and Autoimmune Gastritis
know chart on slide 42
Peptic Ulcer Disease
Solitary, well-demarcated 2-3mm ulcer deep into submucosa or muscle of proximal duodenum (90%) or distal stomach (10%)
What is the pathogenesis of Peptic Ulcer Disease? The locations it is found? The overall risk?
Pathogenesis:
-Imbalance between mucosal defenses and acidic environment
3 Locations:
1) Gastric
2) Duodenal
3) Jejunal
Overall Risk:
1) Males = 10%
2) Females = 4%
What are the complications of Peptic Ulcer Disease?
1) Bleeding –> most common (30%)
2) Perforation –> most deadly (65% of deaths)
3) Obstruction –> rare
4) Malignancy –> rare complication of gastric ulcers (*non-existent in duodenal ulcers)
What is the treatment for Peptic Ulcer Disease?
1) Test for H. pylori
2) Antibiotics (amoxicillin/metronidazole)
3) Proton Pump Inhibitors (pepcid/zantac/tagamet)
Gastric Peptic Ulcer
Solitary mucosal ulcer of antrum (10%) - chronic and recurring
What is the pathogenesis of Gastric Peptic Ulcer? The oral/clinical signs?
Pathogenesis:
1) H. pylori - 65%
2) Chronic NSAIDs
3) Chronic high dose steroids
4) Cigarettes
5) Stress
**healing followed by recurrent ulcer formation
Oral/Clinical:
-Epigastric pain 1-3hr after eating
-Nausea, vomiting, bloating
-Risk of hemorrhage or perforation
Duodenal Peptic Ulcer
Solitary mucosal ulcer of proximal duodenum (90%)
*Healing followed by recurrent ulcer formation
What is the pathogenesis of Duodenal Peptic Ulcer? The oral/clinical signs?
Pathogenesis:
1) H. pylori (95%) –> bacteria cannot live in duodenum –> H. pylori growth in antrum causes increased acid in duodenum = epithelial metaplasia = H. pylori colonization of duodenum
2) Hypercalcemia –> increased gastrin secretion = parietal cells increase HCl secretion
3) Genetics –> Blood type O
Oral/Clinical:
-Epigastric pain improves after eating
-Risk of hemorrhage or perforation
Zollinger-Ellison Syndrome
Multiple peptic ulcers of stomach, duodenum, and jejunum
What is the pathogenesis of Zollinger-Ellison Syndrome? The oral/clinical signs?
Pathogenesis:
-Nuroendrocrine tumor of pancrease –> spreads to liver/intestine –> secretes increased gastrin = stimulation of parietal cells = increased HCl acid secretion not neutralized
Oral/Clinical:
- Adults - 50yrs+
- Abdominal pain
- Nausea/vomiting
- Diarrhea/weight loss
Gastric Adenocarcinoma
Malignancy of surface epithelial cells
*Most common malignancy of stomach - 90%
What are the 2 types of Gastric Adenocarcinoma?
1) Intestinal type = most common –> diet/chronic gastritis
2) Diffuse type = rare –> blood type A
What is the pathogenesis of Gastric Adenocarcinoma? The oral/clinical signs?
Pathogenesis:
1) Diet
2) Autoimmune gastritis
3) H. pylori gastritis
4) EBV
5) Blood type A
Oral/Clinical:
-Asymptomatic (early)
-Weight loss; abdominal pain; anemia (late)
-Males (2:1) - 55yrs
What is caused by Obstructive/Vascular?
Esophageal Varices
What is caused by trauma?
-Mallory-Weiss Syndrome
-Esophagitis
-GERD
-Hiatal Hernia
-Barrett Esophagus
-Plummer-Vinson Syndrome
What is caused by Neoplasia?
-Squamous Cell Carcinoma
-Adenocarcinoma
-Gastric Adenocarcinoma
-Carcinoma of Ampulla
-Adenomatous Polyps
-Adenocarcinoma - Colorectal Carcinmoa
What is caused by Acute Gastritis/Gastropathy?
Acute Ulcers
What is caused by Chronic Gastritis?
-H. Pylori Gastritis
-Auto-immune Gastritis
-Peptic Ulcer Disease
*Gastric peptic ulcer
*Duodenal peptic ulcer
*Zollinger-Ellison Syndrome
What in the small intestine is caused by developmental problems?
-Pyloric Stenosis
-Meckel Diverticulum
What in the small intestine is caused by obstruction?
-Volvulus
-Hernia
-Adhesions
-Intussesception
What in the small intestine is caused by Vascular/Obstructive?
-Mesenteric Arterial Occlusion
-Mesenteric Venous Occlusion
What in the small intestine is caused by Malabsorption?
-Crohn Disease
-Celiac Disease
What in the large intestine is caused by Obstruction?
-Megacolon (congenital)
*Hirschsprung disease
-Megacolon (acquired)
-Diverticular Disease
What in the large intestine is cause by inflammatory
-Inflammatory bowel disease (IBD)
*ulcerative colitis
*crohn disease
-Pseudomembranous Colitis
-Appendicitis
What in the large intestine is caused by Genetic - Polyposis Syndromes?
-FAP- Familial Adenomatous Polyposis
-Gardner Syndrome
-Peutz-Jeghers Syndrome
