USMLE® Step 1 style questions USMLE
USMLE® Step 2 style questions USMLE
A 23-year-old woman with a history of anxiety comes to the office with abdominal pain and altered bowel habit. The patient has a 4-month history of cramping abdominal pain and fluctuations between diarrhea and constipation. Physical examination shows no abnormalities. Her hemoglobin level is 12.5 grams/dL and celiac disease serology is negative. Which of the following would be considered an alarm symptom in this patient?
It is the most common type of cancer of the gastrointestinal tract, and a major cause of death and disease around the world.
The intraperitoneal space contains the first part of the duodenum, all of the small intestines, the transverse colon, sigmoid colon, and the rectum; the retroperitoneal space contains the distal duodenum, ascending colon, descending colon, and anal canal.
So the large intestines essentially weave back and forth between the intraperitoneal and retroperitoneal spaces.
Now, the walls of the gastrointestinal tract are composed of four layers. The outermost layer is the called serosa for the intraperitoneal parts, and the adventitia for the retroperitoneal parts.
Next is the muscular layer, which contracts to move food through the bowel.
After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves.
And finally, there’s the inner lining of the intestine called the mucosa; which surrounds the lumen of the gastrointestinal tract, and comes into direct contact with digested food.
The mucosa has invaginations called intestinal glands or colonic crypts, and it’s lined with large cells that are specialized in absorption.
Most cases of colorectal tumors happen because of sporadic mutations, but a small number are caused by known genetic mutations that run in a person’s family.
Normally, the APC protein identifies when a cell is accumulating a lot of mutations and forces it to undergo apoptosis, or programmed cell death.
But when the APC gene is mutated, the mutated bowel cells don’t die, and instead some start dividing uncontrollably, giving rise to polyps.
Over time, these polyps might accumulate more mutations in other tumor suppressor genes like the K-ras gene or the p53 gene, and ultimately it might might become a malignant tumor - meaning that the cells might be able to invade neighboring tissues.
Another well known example are genetic mutations in DNA repair genes which help fix up mutations in cellular DNA.
When they’re out of action - cells accumulate mutations and over time can develop into polyps and eventually adenocarcinomas.
So, broadly speaking, adenocarcinomas are the malignant evolution of polyps, and polyps arise when cells start dividing faster than usual.
These pre-malignant polyps can be classified into adenomatous and serrated, according to how they look under the microscope.
When tumors become cancerous, they can be categorized into stages.
Stage 0 is carcinoma in situ, meaning that the tumor has not grown beyond the mucosa.
Stage 1 is when the tumor has grown beyond the mucosa, but has not spread to lymph nodes or distant organs.
Stage 2 is when the tumor has invaded the whole colonic or rectal wall, and may have reached nearby organs or tissues, but still hasn’t spread to lymph nodes or distant organs.
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- "Metastatic Carcinoma Occurring in a Gastric Hyperplastic Polyp Mimicking Primary Gastric Cancer: The First Reported Case" Case Reports in Pathology (2014)
- "Mutation Rate in Human Microsatellites: Influence of the Structure and Length of the Tandem Repeat" The American Journal of Human Genetics (1998)