When it comes time to sit for USMLE Step 1, you really have to go with your gut. The test can be a difficult thing to stomach, but by focusing on the high-yield aspects of GI physiology and pathophysiology, your efforts will be worthwhile, and your brain will continue to secrete correct answers. While always a challenge, I’ve done my best to distill the subject into a singular blog post. I attempted to winnow this down to a single post, but like so many huge topics out there, one post simply wouldn’t do. Stay tuned for part 2.
High-Yield Gastrointestinal Study for USMLE Step 1
1. Foregut, midgut, and hindgut (8): Having a strong foundation in the embryological divisions of the GI tract will help you lay a sensible framework in figuring out where different organs derive a blood supply, an innervation, and refer their pain. The foregut stretches from esophagus to upper duodenum, and is supplied by the celiac artery. Pain is usually epigastric.
The midgut stretches from distal duodenum to the first ⅔ of the transverse colon. The major artery here is the superior mesenteric artery, and pain is periumbilical. Hindgut describes the region from the last ⅓ of the transverse colon to the rectum. The major artery is the inferior mesenteric artery, and pain is hypogastric. This will at least allow you to narrow a differential when a patient complains of “abdominal pain.”
2. Celiac trunk (7.5): Of all of the branches off of the aorta that supply the gut, the celiac trunk is where you get the most bang for your buck. Put your efforts into understanding the anatomy of this complex region. Major branches of the trunk include left gastric artery, common hepatic artery (which gives rise to gastroduodenal and proper hepatic arteries), and splenic artery. The reason these are so important is because of the foregut organs that they supply: stomach, gallbladder, spleen, liver, pancreas, duodenum, and esophagus.
3. Porto-systemic connections (8): The portal system drains the GI tract and sends all of the absorbed goodies to the liver. There are 3 spots where portal blood can “back up” and flow into the systemic circulation. This is usually a consequence of a diseased and congested liver that make the passage of blood via the portal vein all the more difficult. In the esophagus, the left gastric vein can flow into the azygos causing dreaded esophageal varices. Anastomoses around the umbilicus cause caput medusae. In the rectum, various rectal veins connect to cause anorectal varices.
4. Biliary structures and pathologies (9): There are loads of common and uncommon pathologies that can rip apart the biliary tree. As usual, knowledge of the anatomy of the biliary tree is a necessity. A common theme here is that the body depends on FLOW for so many important functions. When nasal mucus doesn’t flow, a sinus infection develops. Lack of lymphatic flow causes effusions and edema. If bile doesn’t flow, both organ and patient will suffer. Have the spectrum of asymptomatic gallstones → biliary colic → acute cholecystitis → ascending cholangitis down pat. Pathologies like primary sclerosing cholangitis and primary biliary cholangitis often come up on Step 1. Don’t forget choledocholithiasis, a nineteen-letter word just to tell you there’s a stone in the common bile duct. Know how to use lab values (and more importantly, patient history!) to distinguish between these etiologies.
5. Esophageal pathologies (6.5): And you thought it was just a food pipe! There are many esophageal issues that look like one another, and it’s patient history that sets them apart. The most dreaded of the lot is of course, a ruptured esophagus. Nowhere for that air to go but into the chest and mediastinum, so look for crepitus somewhere. Can be a result of trauma or vicious vomiting (Boerhaave syndrome), or the delicate esophageal wall getting pummeled with stomach acid. More benign is the Mallory-Weiss tear, a longitudinal “nick” in the mucosa, also from vomiting. Certainly not life-threatening; care is supportive.
We’ve already mentioned varices in the setting of liver disease. Not a problem unless they are bleeding. Beta-blockers offer a nice prophylaxis, and octreotide can be used in the setting of bleeding.
The most common esophageal pathology you will encounter is metaplasia (Barrett’s esophagus), usually in the setting of GERD. Nip it in the bud by getting acid under control with a PPI before your metaplasia becomes neoplasia.
6. Peptic ulcers (8.5): Ulcers can be anywhere on the spectrum from pesky to life-threatening. Their usual home is in the stomach or duodenum from too much stomach acid. The stomach has a nifty mucus layer to protect its tissue; this barrier can be damaged by overuse of NSAIDs or the dreaded H. Pylori infection (which necessitates triple therapy – 2 antibiotics and a PPI). Untreated, ulcers can erode all the way into the arterial system, causing a hemorrhagic/perforated viscus emergency. The gastroduodenal artery, lying in close proximity deep to the duodenum, is a likely bleeder in this circumstance. The last pearl: if a patient has multiple ulcers or ulcers in strange places, keep Zollinger-Ellison syndrome in your differential, as huge amounts of gastrin make too much acid.
7. Cirrhosis/Portal Hypertension (9) – Understanding the concept of portal hypertension is key. Put simply, a diseased, fibrotic liver is much harder to send blood through than a happy, open, flowy one. This causes an increase in pressure (hypertension) through the portal vein, leader to a backup of blood in the splanchnic circulation. The increased hydrostatic pressure (and hypoalbuminemia) can cause a transudate to form in the abdomen (ascites!).
The liver is such an important organ, and it’s failure wreaks havoc on so many body systems. This is where most proteins and synthesized, so patients often lose clotting factors as well as albumin, causing a bleeding diathesis and edema, respectively. The liver clears toxic substances, quintessentially ammonia (although others are implicated), and their buildup leads to hepatic encephalopathy. Other organ systems can also take a hit, as they do in portopulmonary hypertension, hepatopulmonary syndrome, and hepatorenal syndrome.
Check out this video on Barrett’s Esophagus & High Yield Associations.
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