Gastrointestinal Flashcards
Where does pain typically begin in appendicitis? Where does it migrate to? What are the muscle signs indicative of appendicitis? What does the inflamed appendix rub against?
Pain starts as periumbilical, as it becomes more inflamed it rubs against parietal peritoneum and pain migrates to McBurney’s point. Obturator sign (pain w/ IR of right hip) and Psoas sign (pain w/ hip extension) are muscular signs.
*If appendix is retroperitoneal, the pain won’t be as bad.
Someone presents with persistent bad breath, frequent pneumonia, choking spells, and dysphagia. Imaging shows an outpouching of the esophagus. What muscles are involved, and what is the process in general?
Weakness or paralysis of the cricopharyngeal muscles, resulting in a Zenker diverticulum. Thus, food gets stuck in the diverticulum, some of it goes into lungs (pneumonia), all because the food isn’t getting down like it should.
A patient presents with gout, but also has a history of peptic ulcer disease. What would be the best option for treatment? What is the mechanism of that drug?
Colchicine. This drug inhibits microtubule polymerization and also blocks the attraction of inflammatory factors, thus preventing inflammation in gout.
NSAIDs are first line treatment for gout, but w/ peptic ulcer disease you don’t want to give NSAIDs.
What’s a tumor type in the gut that would cause watery diarrhea, inhibit gastric acid secretion, and respond promptly to somatostatin?
A VIPoma (vasoactive intestinal polypeptide). It would also cause hypokalemia and achlorhydria.
A duodenal biopsy of a patient who has recurrent diarrhea shows crypt hyperplasia and villous atrophy.
Diagnosis? Treatment?
Celiac disease. Anti-TTG antibodies.
Treatment=gluten-free diet
What factors would make you more susceptible to cholera infection?
Decreased acid production, so chronic omeprazole therapy (omeprazole is a PPI).
What is diphenoxylate and what is it used for?
It’s an opioid that is used to reduce motility in relatively benign cases of diarrhea.
It’s given with atropine since atropine causes negative side effects at high doses, to prevent people from using it to get high
An old man comes in with major burns and develops sepsis. While in the hospital, he comes to develop RUQ pain. What do you expect to see, and what type of stones do you think you’ll see?
You should see an inflamed gall bladder with no stones (acute acalculous cholecystitis). In chronically ill patients due to stasis and ischemia.
Look for marked leukocytosis.
Inhibition of which hormone will most likely lead to gall stones?
Cholecystokinin. This normally causes gallbladder contraction. Increased somatostatin will inhibit the release of cholecystokinin from the I cells of the duodenum/jejunum.
A patient has Wilson’s disease–>liver has too much copper. Eventually the copper leaks out and goes to 2 places that cause other clinical findings. Where and what are they?
The the cornea and to the basal ganglia.
You’ll then see the Kayser-Fleischer rings in the eyes, and they will also develop dementia due to the atrophy of the basal ganglia.
Gastric acid secretion is mediated by 3 different stimulants, but all result in one common pathway. What are the 3 stimulants, and what is the one common pathway?
What drug can be used to block the common pathway?
3 stimulants: 1) Histamine 2) Gastrin 3) Acetylcholine
The common pathway=H/K ATPase proton pump.
PPIs (-azole drugs–>omeprazole, lansoprazole, etc.) block that pump, and thus decrease acid production.
*H2 blockers (-dine drugs), block the Histamine receptor pathway.
A patient with T1DM has pernicious anemia. What would you expect their gastrin levels to be and why?
This patient has autoantibodies against the parietal cells of their stomach (already w/ history of an autoimmune process). This results in decreased gastric acid and intrinsic factor production.
As a result, gastrin levels will be HIGH because the body is trying to signal to produce more stomach acid.
You give a diabetic person a glucagon injection. Where will the metabolism in this person change?
How does this differ from epinephrine?
Glucagon will stimulate glucose to be released from the liver (glycogenolysis).
Epinephrine causes glycogenolysis in the liver, decreased glucose uptake in skeletal muscle, increases alanine release from skeletal muscles (used for gluconeogenesis) and breaks down triglycerides in adipose tissue to be used as fuel as well.
A patient has Hirschsprung disease. How often is the sigmoid colon involved? How often is the rectum involved?
Sigmoid colon involved 75% of the time.
Rectum involved 100% of the time.
Remember that the neuronal crest cells migrate caudally, so the rectum is the last part that they reach.
All of migration is done usually within 12 weeks.
Post surgery, a patient is experiencing acute hepatitis with hepatocyte necrosis. What drug class should be suspected?
Halogenated inhaled anesthetics (-flurane/halothane)
