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THE INTEGRATED TEACHING APPROACH Introduction to the Gastrointestinal System. Khaled Jadallah, MD Assistant Professor of Medicine Gastroenterology, Hepatology & Nutrition Department of Internal Medicine. Why the Integrated Gastrointestinal Study Module?.
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THE INTEGRATED TEACHING APPROACHIntroduction to the Gastrointestinal System Khaled Jadallah, MD Assistant Professor of Medicine Gastroenterology, Hepatology & Nutrition Department of Internal Medicine
Why the Integrated Gastrointestinal Study Module? • More organized than classical teaching • Easier to comprehend • More clinically oriented • More interesting and stimulating
Overview • Dramatic growth of knowledge in GI over the last 2-3 decades. • Better understanding of the biology, biochemistry and physiology of the GUT • New insights in the pathophysiology of different GI diseases • Breakthrough in the diagnostic and therapeutic tools and procedures in gastrointestinal diseases
An Endoscopic and Radiologic/Anatomic Journey through the Gastrointestinal Channel
Case 1 A 45-year-old man has had dysphagia of increasing severity over the past year. He has recently lost 3 Kg. Upper endoscopy is normal except for some resistance to passage of the endoscope at the esophagogastric junction. What do you think is going on??
Case 1 (cont’d) • Questions to ask: • Is the dysphagia for solids only or for both solids and liquids?? • Is it a “transfer” dysphagia or “transit” dysphagia?? • What further investigations should we do?? • The diagnosis is: Esophageal achalasia(lack of peristalsis, high pressure LES and incomplete relaxation of LES on swallowing • Manometry is diagnostic
Anatomo-Physiologic Basis of Dysphagia • The process of swallowing depends on the voluntary action of the orophayngeal striated muscles and the involuntary action of the esophageal smooth muscles • Dysphagia secondary to oropharyngeal problems (neurologic or muscular) is called TRANSFER dysphagia • Dysphagia secondary to esophageal problems (Anatomic obstruction or dysmotility) is called TRANSIT dysphagia
Case 2 A 57-year-old man presents with a 3-month history of epigastric pain and voluminous, foul smelling diarrhea. The diarrhea persists despite fasting. Nasogastric suction dramatically decreases stool output. What’s your diagnosis??
Case 2 (cont’d) • This is a case of Zollinger-Ellison Syndrome (Gastrinoma) • The pathophysiology of ZES is explained as follows: • The pain is caused by ulcerations of acid hypersecretion and decreased cytoprotective effect of pancreatic and gastric sodium bicarbonate • The diarrhea is caused by the increased volume of acid and the irritation of the GIT mucosa (secretory diarrhea) • The steatorrhea is provoked mainly by inactivation of pancreatic enzymes and defective micelle formation • These symptoms can be effectively treated by proton pump inhibitirs (e.g. omeprazole, lansoprazole, esomeprazole, ….) which decrease the acid secretion
Case 3 • A 52-year-old obese woman presents with a 4-day history of right upper quadrant pain, associated with nausea and jaundice. The patient also reports dark, tea-colored urine and pale stools. What is the most likely diagnosis??
Case 3 (cont’d) • The antomo-pathology and physiopathology of bilairy pain and jaundice • Biliary pain is caused by obstruction of the bile ducts, especially the CBD. It’s constant and not colicky • Jaundice associated with dark urine (bilirubinuria) and light stools is mostly secondary to obstruction to the flow of bile. • Direct or conjugated bilirubin, but not indirect bilirubin, is water soluble and therefore can be filtrated in the kidneys • The diagnosis is: Choledocholithiasis (stone impacted in the CBD) • The treatment?? ERCP with stone extraction followed by cholecystectomy
Case 4 • A 75-year-old woman with a longstanding history of osteoarthritis and diclofenac (Voltaren) use presents to the ER with hematemesis. EGD is performed and showed multiple ulcers in the antrum. What is the biochemical/physiologic basis of this patient’s ulcers??
Case 4 (cont’d) • Non Steroidal Antinflammatory Drugs (NSAIDs) such as diclofenac inhibit both cycloxygenase-1 (COX-1) and COX-2 enzymes. • COX-1 is enzyme responsible for prostaglandin (PG) production. PG has a cytoprotective effect on the gastric mucosa • COX-2 specific (or COX-1 sparing) NSAIDs (such as celecoxib and rofecoxib) have lower PG inhibition and therefore lower ulceration rate than non selective NSAIDs • A synthetic PG such as MISOPROSTOL can be used along with NSAIDS to decrease the ulceration rate
Take-Home Points • An integrated approach to basic sciences is more effective than classic teaching • Translational basic sciences bridges the gap between basic sciences and patient care • Translational basic sciences can transfer clinical insights into hypothesis that can be tested and validated in the basic research laboratory
Take-Home Points (cont’d) • The integrated teaching approach allows easier application of knowledge and basic research into clinical practice • In the future, multidisciplinary teaching laboratories/seminar rooms will provide venue to teach laboratory sciences such as histology, microbiology, and pathology in un updated clinical context