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Simple Medicine

GI Uworld images with corresponding questions

Updated: Mar 7, 2022


26 year old woman with fluctuating non bloody stool has a draining fistula near her coccyx. What is her most likely diagnosis?

Crohn's disease: patients are prone to developing fistulas/abscesses as the lesions affect the entire thickness of the bowel wall.



Depletion of somatostatin producing antrum cells will cause what?

Duodenal ulcers: H. pylori antral gastritis is associated with these ulcers due to increase in gastric acid production. Due to lack of somatostatin, gastrin is not inhibited.


Which biochemical conversions require Biotin as a cofactor? Pyruvate to OAA. (particularly for carboxylase enzymes, not succinate to OAA)





How does pancreatic divisum occur? When ventral and dorsal buds do not fuse. The pancreatic systems are drained in 2 separate ducts.




What is the cause of a congenital diaphragmatic hernia? Failure of pleuroperitoneal folds to close. Signs: Immediately after birth, newborn is in respiratory distress, there's unilateral decreased breath sounds and a scaphoid abdomen. Imaging shows thoracic bowel loops and mediastinal shift.


Cause of malrotation? Incomplete physiological rotation of bowel in utero. Presents with bilious emesis in infancy due to duodenal obstruction from abnormally positioned peritoneal bands.


Which medication should patients (who have pre-existing gallbladder disease) avoid? Fibrates

Which medication should be given instead? Fish oil (omega 3) since they reduce the risk of gallstone formation by increasing bile acid synthesis, decreasing cholesterol in bile and increase gallbladder motility.


Fasting gastrin levels are normal but when secretin is given they increase. Cause of this patient's duodenal ulcer? Zollinger Ellison syndrome (gastrin secreting tumor): secretin is released in response to acid and fat in the body, so decreases gastrin secretion. In this case, it has a paradoxical effect, where secretin causes an increase in release of gastrin from gastrinomas due to adenylate cyclase activation.


Patient is prescribed Omeprazole to treat his GERD. Absorption of which nutrients will improve due to admin of this drug?

Dietary fats: Lipase is inactivated by the acidic environment of the stomach. So when PPIs decrease stomach acidity, they increase lipase, which increases breakdown of fat for absorption.

Why during admin of PPI, we have malabsorption of Ca2+, iron, Mg and Vit B12? An acidic environment is needed to absorb these nutrients.


The surgeon occludes the hepatoduodenal ligament but the patient continues to hemorrhage. Which structure is most likely the source of the patient's bleeding?

Inferior vena cava: The portal triad (hepatic artery, portal vein and common bile duct) runs through the hepatoduodenal ligament. If the bleeding does not cease when the portal triad is occluded, then there is damage to the IVC.




Elderly man has dysphagia, halitosis and regurgitation and recurrent aspiration. What is the cause of his symptoms? Diminished relaxation of cricopharyngeal muscles during swallowing: Can cause mucosa to herniate through a zone of weakened muscle, causing a Zenker (false) diverticulum.


What supplements should vegans take? Calcium (lack of animal products like milk), Vit B12 and D


Differentiate between HSV and CMV ulcerations.


What happens in the stomach due to Parietal cells being autoimmune destroyed? Parietal cells can't secrete HCL, thereby increasing the gastric pH. Intrinsic factor can no longer be secreted so Vitamin B 12 cannot be absorbed into the bloodstream.


How can Crohn's disease cause oxalate kidney stones? Crohn's disease most often affects the terminal ileum, which is normally the site of absorption of bile acids back into the gallbladder and absorption of fats also. Due to removal or damage to the terminal ileum, the bile salts are lost in the feces. Normally, dietary calcium and oxalate bind to each other in the intestine and are excreted into the feces. In Crohn's disease, the bile salts bind to excess cholesterol in the intestine and form soaps to be eliminated in the stool. Excess Oxalate then remains unbound and is then filtered into the urine, ultimately causing oxalate kidney stones.



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