Gastrointestinal Flashcards
Which portion of the small bowel contains villi or finger-like outpouchings that project into the lumen?
Duodenum
What are the crypts of Lieberkuhn and where are they located?
Simple tubular glands that rest on top of the muscular mucosae and deliver secretions to the intervillar spaces of the duodenum.
What is the function of Brunner’s glands?
To secrete alkaline mucous into ducts that track upward through the muscularis mucosae and into the crypts of lieberkuhn for release into the lumen of the duodenum.
Where are peyer’s patches located?
Lymphoid aggregates specific to the lumen.
Increased levels of what enzyme are associated with colonic adenocarcinoma?
COX-2; patients taking a COX inhibitor regularly have a lower incidence of adenomas compared to the general population.
Meckel diverticulum occurs due to a failure of what embryologic process?
Failure of obliteration of the omaphalomesenteric duct.
What are the most common presenting symptoms of intussusception?
Colicky abdominal pain and current jelly stools.
What condition is caused by the failure of ventral and dorsal pancreatic buds to fuse?
Formation of pancreas divisum, an asymptomatic condition usually only found incidentally.
What causes bleeding in Meckel diverticulum?
Ectopic gastric mucosa which produces acid and possible ulceration and bleeding.
Describe the three steps in the adenoma to carcinoma sequence.
- Progression from normal mucosa to small polyp- initial appearance of small adenomatous polyps is caused by a mutation of the APC gene on Ch. 5; 2. Increases in size of polyps- mutation of K-ras protooncogene facilitates this step. Unregulated cell growth occurs; 3. Malignant transformation of adenoma into carcinoma requires mutation of two genes p53 and DCC.
On autopsy and histology, what is characteristic of fulminant hepatitis associated with halothane use?
Atrophied and shrunken liver; histologically there is widespread centrilobular necrosis and inflammation of the portal tracts and parenchyma (appears just like fulminant viral hepatitis).
What are the clinical symptoms of inhaled-anesthetic hepatotoxicity?
Fever, anorexia, nausea, myalgias, arthralgias, rash with tender hepatomeagly and jaundice.
What lab findings are associated with fulminant hepatic necrosis due to inhaled anesthetics?
Elevated serum aminotransferases, prolonged PT, leukocytosis, and eosinophilia.
What causes prolonged prothrombin time in a patient with fulminant hepatic necrosis?
Failure of hepatic synthetic function and deficiency of factor VII.
Where does iron absorption occur?
In the duodenum and proximal jejunum.
Malabsorption of what vitamins/ minerals is common after gastrojejunostomy?
B12, folate, fat-soluble vitamins (esp. Vit. D), calcium, iron.
What effect does mu opioid analgesics have on smooth muscle cells of the sphincter of Oddi?
They contract the sphincter leading to constriction and spasm which may cause biliary colic.
Which opioid is least likely to cause contraction of the sphincter of Oddi and is indicated in biliary and pancreatic pain?
Meperidine.
What is pneumatosis intestinalis?
Air in the bowel wall which can be seen on abdominal xray as thin curvilinear areas of lucency that parallel the lumen.
In an infant with abdominal distention and bloody stool, pneumatosis intestinalis is indicative of what condition?
Necrotizing enterocolitis (NEC).
What triggers necrotizing enterocolitis in newborns?
Bacterial invasion and ischemic necrosis of the bowel wall that is associated with prematurity and initiation of enteral feeding.
What antihyperlipidemia agent causes acute gouty arthritis?
Niacin.
What are the most common adverse affects of fibrates?
Gallstones, myopathy
What are the most common adverse affects of bile acid resins?
GI upset, hypertriglyceridemia, malabsorption.
What is the function of trypsin?
Activation of all of the proteolytic pancreatic enzymes, including its own zymogenic form.
What happens with premature activation of trypsinogen before it reaches the duodenal lumen?
Autodigestion of pancreatic tissues.
What activates trypsin?
Duodenal enterokinase.
Describe symptoms of the ‘prodrome’ phase of Hepatitis B.
Serum sickness like- malaise, fever, skin rash, pruritus, lymphadenopathy, joint pain, anorexia, jaundice, RUQ pain.
What lab findings are characteristic of acute viral hepatitis?
Significant elevations in ALT, AST with ALT> AST followed by rises in billirubin and alk phos.
What is elevated in Gilbert syndrome?
Unconjugated billirubin.
What is the difference between clinical illness in patients with Hep. B vs Hep. C?
Symptoms are very mild or asymptomatic in Hep C.
Imperforate anus is most often associated with what other congenital abnormalities?
Urorecta, urovesical, or urovaginal fistulas; or renal agenesis, hypospadias, epispadias, bladder extrophy. When a fistula is present, meconium may discharge from the urethra or vagina.
What rare congenital anomalies may occur with imperforate anus?
VACTERL- vertebral defects, anal atresia, cardiac anomalies, tracheoesophageal fistula, esophageal atresia, renal anomalies, limb anomalies.
What lab findings are suggestive of Wilson’s disease?
Low serum ceruloplasmin levels in conjunction with increased urinary copper excretion or Kayser Fleischer rings.
What three factors are assessed to calculate the malignant potential of adenomatous polyps?
Size- greater than 4cm indicates 40% risk of malignancy; villous are more likely to be malignant than tubular; degree of dysplasia.
What areas of the body are drained by the superficial inguinal lymph nodes?
Cutaneous lymph from the umbilicus to the feet, including external genitalia and anus (up to the beginning of the rectum, the dentate line).
To where does lymph from the posterior calf drain?
Popliteal lymph nodes.
Where does lymph from the prostate drain?
Internal iliac nodes primarily.
Name six conditions of colitis associated carcinoma compared to sporadic colorectal carcinoma.
More likely to affect younger patients; progresses from flat and non-polypoid dysplasia; histologically appears mucinous and has signet ring morphology; develop early p53 mutations and late APC gene mutations (opposite of sporadic); distributed within the proximal colon; multifocal in nature. They are also often of a higher histological grade.
How does lactase deficiency lead to osmotic diarrhea?
Due to incomplete hydrolysis of the disaccharide lactose into the monosaccharides glucose and galactose. Undigested lactose accumulates within the GI lumen leading to osmotic diarrhea. This lactose is fermented by bacteria causing excessive hydrogen.
What lab findings are associated with lactase deficiency?
Increased stool osmotic gap, increased breath hydrogen content, decreased stool pH on lactose challenge.
What increases stool osmotic gap?
The presence of poorly absorbable substances.
What is SMA syndrome?
When the transverse portion of the duodenum is entrapped between the SMA and aorta causing symptoms of partial intestinal obstruction. It occurs when the aortiomesenteric angle critically decreases, secondary to diminished mesenteric fat, pronounced lordosis, or surgical correction of scoliosis.
What part of the gut is supplied by the SMA?
Duodenum and pancreas to the left colic flecture. SMA leaves aorta at L1.
Where do the majority of anal fissures occur?
Longitudinal tears in the mucosa of the distal anal canal occurring at the posterior midline of the anal verge.
Why do most anal fissues occur at the posterior midline of the anal verge?
Because this area is poorly perfused making its mucosa sensitive to hard fecal masses.
What is mastocytosis?
Abnormal proliferation of mast cells (in the bone marrow and other organs) and increased histamine secretion which increases production of gastric acid by parietal cells. Gastric hypersecretion is common.
What are the clinical symptoms of mastocytosis?
Nausea, vomiting, abdominal cramps, flushing, pruitis, rash.
What histological changes are specific to the hepatitis B virus?
Ballooning degeneration, hepatocyte necrosis, portal inflammation The hepatocellular cytoplasm becomes filled with HBsAg and the cytoplasm appears as finely granular, eosinophilic and ‘ground glass’ like.
What characterizes the histology of the liver in patients with Hep C?
Lymphoid aggregates within the portal tracts and focal areas of macrovesicular steatosis.
What causes congenital pyloric stenosis?
Hypertrophy of the pyloric muscularis mucosae.
What characteristically characterizes Crohns disease histologically?
Noncaseating granulomas; linear ulcerations, a cobblestone appearance of mucosa, transmural inflammatory infiltrate.
Describe the appearance of noncaseating granulomas on histology.
Accumulation of epitheloid macrophages without central necrosis.
In Crohns disease, inflammation involves what structures?
The entire thickness of the intestinal wall (transmural inflammation) with noncaseating granulomas in all tissue layers.
String sign on contrast barium studies is present in what condition?
Crohns (due to strictures).
What is the principle difference between a Mallory-Weiss tear and Boerhaave syndrome?
Mallory weiss tears are upper GI mucosal tears; Boerhaave tears are transmural esophageal tears that are more emergent.
In what type of patient is acute acalculous cholecystitis most often seen?
Hospitalized and severely ill patients (risk factors- sepsis, immunosuppression, trauma, DM, burns, infections, etc). It involves acute inflammation of the gallbladder in the absence of gallstones.
What causes acalculous cholecystitis?
Gallbladder stasis and ischemia which causes inflammation and injury to the gallbladder wall.
What appears on light microscopy in acute interstitial pancreatitis?
Focal areas of fat necrosis, calcium deposition and interstitial edema.
What appears on examination of tissue in necrotizing (hemorrhagic) pancreatitis?
Chalky white areas of fat necrosis interspersed with hemorrhage.
What is the mechanism of action of osmotic laxatives?
Nonabsorbable or poorly absorbable substances that attract water into the intestinal lymen and distend the wall causing peristalsis.
Name three osmotic laxatives.
Polyethylene glycol, magnesium hydroxide, magnesium citrate.
What is the pathogenesis of Wilson’s disease?
Hepatolenticular degeneration.
What are potential side effects of bile-acid binding resins?
Constipation, abnormal bloating, hypertriglyceridemia, cholesterol gallstones, and Vit. K. malabsorption.
What does keratinization indicate in tumors?
That the tumor is well differentiated.
What are the two major risk factors associated with squamous cell carcinoma of the esophagus?
Chronic alcohol consumption and cigarette smoking
What are the most common presenting symptoms of toxic megacolon?
Fever, pain and distension, diarrhea, signs of shock.
Toxic megacolon is a complication of what condition?
IBD- seen much more often in ulcerative colitis than in Crohn’s disease.
Describe the pathological changes that lead to toxic megacolon.
Cessation of neuromuscular activity within the intestinal wall –> rapid colonic distension –> thinning of intestinal wall –> rupture. On light microscopy, segmental necrosis may be seen; the transverse colon is often most dilated.
What is the most urgent complication associated with megacolon?
Perforation.
What is the most useful diagnostic test for toxic megacolon?
X-ray.
What studies are contraindicated in expected toxic megacolon?
Barium contrast and colonoscopy due to potential perforation.
What structures arise from the dorsal pancreatic bud?
Pancreatic tail, body, most of the head, and the small accessory pancreatic duct. Dorsal bud forms the majority of the pancreatic tissue.
What structures arise from the ventral pancreatic bud?
Uncinate process, a portion of the pancreatic head, the proximal portion of the main pancreatic duct.
To what drug class does cholestyramine belong?
Bile acid binding resins.
What is the only part of the duodenum that is not retroperitoneal?
The first part of the duodenum (horizontal part)
The second part of the duodenum lies close to what structures?
The head of the pancreas and the ampulla of vater (where the pancreatic and common bile ducts provide their secretions).
What structures lie close to the third part of the duodenum?
Uncinate process of the pancreas, SMA and SMV.
Tumors to the third part of the duodenum put what structures at greatest risk?
Superior mesenteric vessels.
What classic triggers may cause symptoms in a patient with Gilbert’s disease?
Fasting, hemolysis, exertion, fever, stress, fatigue.
What lab abnormalities are associted with Dubin Johnson syndrome?
Chronic conjugated hyperbilirubenemia not associated with hemolysis.
What is produced by gastric parietal cells?
HCl
What is produced by chief cells?
Pepsinogen
What is dumping syndrome?
Accelerated emptying of hyperosmolar food boluses into the small bowel after gastrectomy. Sx include colicky abdominal pain, nausea, diarrhea.
What testing abnormalities are most commonly associated with statin use?
Abnormal LFTs. Most hepatotoxicity occurs within 3 months of starting statin therapy.
What cell type typically lines the esophagus?
Stratified squamous epithelium.
What cell type lines the intestines?
Columnal epithelium.
What condition is characterized by intestinal type epithelium in the esophagus?
Barret’s esophagus.
In what patients are indirect inguinal hernias most common and what causes these hernias?
Most common in male infants; most commonly caused by persistent processus vaginalis and failure of the internal inguinal ring to close. (Indirect= lateral). Covered by all three spermatic fascial layers.
In what patients are direct inguinal hernias most common and what causes these hernias?
Older men; bulges through Hesselbach’s triangle, medial to the inferior epigastric vessels to reach the external inguinal ring. They are caused by weakness of the transversalis fascia. Protrusion through the external ring only (superficial ring); they are covered by external spermatic fascia.
