Exam 3: GI Pathophysiology Flashcards
After a meal, blood pH shifts:
More alkaline d/t shift of H+ into lumen of stomach, HCO3- into blood
Once food enters duodenum, blood pH shifts:
Back to normal; HCO3- is dumped into lumen to increased pH
Hiatal hernia is caused by:
Stomach moving through opening in diaphragm by esophagus
Sequalae of hiatal hernia:
Trapping of food in esophagus and heartburn/regurg
Achalasia is:
Loss of inhibitory innervation of LES, leading to food sitting in esophagus instead of moving into stomach
Causes of achalasia:
Aperistalsis
Incomplete relaxation of LES
↑ tone of LES
Sequlae of achalasia:
Dysphagia
Mucosal inflammation/ulceration
Squamous cell carcinoma (5%)
Cause of esophageal varices:
Impaired hepatic portal blood flow –> portal HTN –> blood backup to esophagus
% of cirrhosis pts with esophageal varices:
2/3rds
Sequelae of esophageal varices:
Rupture & hemorrhage
Hematemesis
Mortality rate of ruptured esophageal varices:
20-30% per episode with a 70% recurrence rate
Barrett’s esophagus is:
Metaplastic change from esophageal cells to stomach cells
Contributing causes to GERD:
Obesity
Hiatal hernia
Vagal nerve abnormalities
Cause of Barrett’s esophagus:
Long standing GERD
Sequelae of Barrett’s esophagus:
Adenocarcinoma
Two types of esophageal cancers:
Squamous cell carcinoma
Adenocarcinoma
Conditions predisposing to SCC:
Tobacco use
Alcohol use
Achalasia
Drinking very hot tea??
Conditions predisposing to adenocarcinoma:
Barrett’s esophagus/GERD
S/s of esophageal CA:
Dysphagia
Obstruction
(Typically late in progression)
Chronic gastritis can lead to:
Peptic ulcers
Acute gastritis can lead to:
Acute gastric ulceration
Normal stomach pH:
1.5
Gastric pits are:
Depressions in epithelial lining containing gastric glands
Chief cells produce:
Gastric juice enzymes
Parietal cells produce:
Stomach acid
Chronic gastritis/PUD usually caused by:
H. pylori
H. pylori survives in stomach by:
Secreting ammonia as buffer against gastric acid