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USMLE World Missed Questions > Gastrointestinal > Flashcards

Flashcards in Gastrointestinal Deck (226):
1

Which portion of the small bowel contains villi or finger-like outpouchings that project into the lumen?

Duodenum

2

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.

3

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.

4

Where are peyer's patches located?

Lymphoid aggregates specific to the lumen.

5

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.

6

Meckel diverticulum occurs due to a failure of what embryologic process?

Failure of obliteration of the omaphalomesenteric duct.

7

What are the most common presenting symptoms of intussusception?

Colicky abdominal pain and current jelly stools.

8

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.

9

What causes bleeding in Meckel diverticulum?

Ectopic gastric mucosa which produces acid and possible ulceration and bleeding.

10

Describe the three steps in the adenoma to carcinoma sequence.

1. 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.

11

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).

12

What are the clinical symptoms of inhaled-anesthetic hepatotoxicity?

Fever, anorexia, nausea, myalgias, arthralgias, rash with tender hepatomeagly and jaundice.

13

What lab findings are associated with fulminant hepatic necrosis due to inhaled anesthetics?

Elevated serum aminotransferases, prolonged PT, leukocytosis, and eosinophilia.

14

What causes prolonged prothrombin time in a patient with fulminant hepatic necrosis?

Failure of hepatic synthetic function and deficiency of factor VII.

15

Where does iron absorption occur?

In the duodenum and proximal jejunum.

16

Malabsorption of what vitamins/ minerals is common after gastrojejunostomy?

B12, folate, fat-soluble vitamins (esp. Vit. D), calcium, iron.

17

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.

18

Which opioid is least likely to cause contraction of the sphincter of Oddi and is indicated in biliary and pancreatic pain?

Meperidine.

19

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.

20

In an infant with abdominal distention and bloody stool, pneumatosis intestinalis is indicative of what condition?

Necrotizing enterocolitis (NEC).

21

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.

22

What antihyperlipidemia agent causes acute gouty arthritis?

Niacin.

23

What are the most common adverse affects of fibrates?

Gallstones, myopathy

24

What are the most common adverse affects of bile acid resins?

GI upset, hypertriglyceridemia, malabsorption.

25

What is the function of trypsin?

Activation of all of the proteolytic pancreatic enzymes, including its own zymogenic form.

26

What happens with premature activation of trypsinogen before it reaches the duodenal lumen?

Autodigestion of pancreatic tissues.

27

What activates trypsin?

Duodenal enterokinase.

28

Describe symptoms of the 'prodrome' phase of Hepatitis B.

Serum sickness like- malaise, fever, skin rash, pruritus, lymphadenopathy, joint pain, anorexia, jaundice, RUQ pain.

29

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.

30

What is elevated in Gilbert syndrome?

Unconjugated billirubin.

31

What is the difference between clinical illness in patients with Hep. B vs Hep. C?

Symptoms are very mild or asymptomatic in Hep C.

32

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.

33

What rare congenital anomalies may occur with imperforate anus?

VACTERL- vertebral defects, anal atresia, cardiac anomalies, tracheoesophageal fistula, esophageal atresia, renal anomalies, limb anomalies.

34

What lab findings are suggestive of Wilson's disease?

Low serum ceruloplasmin levels in conjunction with increased urinary copper excretion or Kayser Fleischer rings.

35

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.

36

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).

37

To where does lymph from the posterior calf drain?

Popliteal lymph nodes.

38

Where does lymph from the prostate drain?

Internal iliac nodes primarily.

39

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.

40

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.

41

What lab findings are associated with lactase deficiency?

Increased stool osmotic gap, increased breath hydrogen content, decreased stool pH on lactose challenge.

42

What increases stool osmotic gap?

The presence of poorly absorbable substances.

43

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.

44

What part of the gut is supplied by the SMA?

Duodenum and pancreas to the left colic flecture. SMA leaves aorta at L1.

45

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.

46

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.

47

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.

48

What are the clinical symptoms of mastocytosis?

Nausea, vomiting, abdominal cramps, flushing, pruitis, rash.

49

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.

50

What characterizes the histology of the liver in patients with Hep C?

Lymphoid aggregates within the portal tracts and focal areas of macrovesicular steatosis.

51

What causes congenital pyloric stenosis?

Hypertrophy of the pyloric muscularis mucosae.

52

What characteristically characterizes Crohns disease histologically?

Noncaseating granulomas; linear ulcerations, a cobblestone appearance of mucosa, transmural inflammatory infiltrate.

53

Describe the appearance of noncaseating granulomas on histology.

Accumulation of epitheloid macrophages without central necrosis.

54

In Crohns disease, inflammation involves what structures?

The entire thickness of the intestinal wall (transmural inflammation) with noncaseating granulomas in all tissue layers.

55

String sign on contrast barium studies is present in what condition?

Crohns (due to strictures).

56

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.

57

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.

58

What causes acalculous cholecystitis?

Gallbladder stasis and ischemia which causes inflammation and injury to the gallbladder wall.

59

What appears on light microscopy in acute interstitial pancreatitis?

Focal areas of fat necrosis, calcium deposition and interstitial edema.

60

What appears on examination of tissue in necrotizing (hemorrhagic) pancreatitis?

Chalky white areas of fat necrosis interspersed with hemorrhage.

61

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.

62

Name three osmotic laxatives.

Polyethylene glycol, magnesium hydroxide, magnesium citrate.

63

What is the pathogenesis of Wilson's disease?

Hepatolenticular degeneration.

64

What are potential side effects of bile-acid binding resins?

Constipation, abnormal bloating, hypertriglyceridemia, cholesterol gallstones, and Vit. K. malabsorption.

65

What does keratinization indicate in tumors?

That the tumor is well differentiated.

66

What are the two major risk factors associated with squamous cell carcinoma of the esophagus?

Chronic alcohol consumption and cigarette smoking

67

What are the most common presenting symptoms of toxic megacolon?

Fever, pain and distension, diarrhea, signs of shock.

68

Toxic megacolon is a complication of what condition?

IBD- seen much more often in ulcerative colitis than in Crohn's disease.

69

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.

70

What is the most urgent complication associated with megacolon?

Perforation.

71

What is the most useful diagnostic test for toxic megacolon?

X-ray.

72

What studies are contraindicated in expected toxic megacolon?

Barium contrast and colonoscopy due to potential perforation.

73

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.

74

What structures arise from the ventral pancreatic bud?

Uncinate process, a portion of the pancreatic head, the proximal portion of the main pancreatic duct.

75

To what drug class does cholestyramine belong?

Bile acid binding resins.

76

What is the only part of the duodenum that is not retroperitoneal?

The first part of the duodenum (horizontal part)

77

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).

78

What structures lie close to the third part of the duodenum?

Uncinate process of the pancreas, SMA and SMV.

79

Tumors to the third part of the duodenum put what structures at greatest risk?

Superior mesenteric vessels.

80

What classic triggers may cause symptoms in a patient with Gilbert's disease?

Fasting, hemolysis, exertion, fever, stress, fatigue.

81

What lab abnormalities are associted with Dubin Johnson syndrome?

Chronic conjugated hyperbilirubenemia not associated with hemolysis.

82

What is produced by gastric parietal cells?

HCl

83

What is produced by chief cells?

Pepsinogen

84

What is dumping syndrome?

Accelerated emptying of hyperosmolar food boluses into the small bowel after gastrectomy. Sx include colicky abdominal pain, nausea, diarrhea.

85

What testing abnormalities are most commonly associated with statin use?

Abnormal LFTs. Most hepatotoxicity occurs within 3 months of starting statin therapy.

86

What cell type typically lines the esophagus?

Stratified squamous epithelium.

87

What cell type lines the intestines?

Columnal epithelium.

88

What condition is characterized by intestinal type epithelium in the esophagus?

Barret's esophagus.

89

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.

90

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.

91

Where do femoral hernias most commonly occur?

In women; protrusion through the femoral ring medial to the femoral vessels and inferior to the inguinal ligament.

92

What causes Hirschsprung disease?

Failure of neuronal crest cells to migrate to the ganglion of the submucosal (Meissner) and myenteric (Auerbach) plexi of the bowel wall. THE RECTUM IS ALWAYS INVOLVED.

93

What area should be biopsied for diagnosis of Hirschsprung disease?

Submucosa of the rectum (narrowed segment) to demonstrate the absence of ganglionic cells.

94

What is a common complication of prolonged total parental nutrition?

Gallstone formation secondary to biliary stasis from absent enteral stimulation. The same effect is seen in patients with ileal resections.

95

Describe the three phases of deglutition (swallowing).

ORAL phase is voluntary; PHARYNGEAL phase begins when food reaches posterior wall of the pharynx. This consists of involuntary pharyngeal muscle contractions that propel the bolus to the esophagus; ESOPHAGEAL phase- food enters the esophagus and stretches the walls. Peristalsis moves food downwards.

96

What causes Zenker diverticulum?

Cricopharyngeal muscle dysfunction caused by diminished relaxation of pharyngeal muscles during swallowing. This increases intraluminal pressure in the oropharynx and causes the mucosa to herniate through the wall at the point of muscle weakness forming the false diverticulum.

97

What receptor is the greatest contributor to the removal of cholesterol containing IDL and LDL particles from circulation?

Liver LDL receptors

98

How does Familial hypercholesterolemia affect LDL receptors?

It causes hepatocyte under-expression of functional LDL receptors.

99

How is copper metabolized?

Absorbed copper forms ceruloplasmin in the liver (accounting for 90+% of circulating Cu); Unabsorbed copper is secreted into bile and excreted in stool. Renal tubular secretion is responsible for 5-15% of daily copper excretion.

100

Hemochromatosis is caused by what defect?

HLA-H gene defect on the short arm of Ch6; this encodes for a protein that affects iron absorption in the GI tract.

101

What is present on colonoscopy and biopsy in a patient with cryptosporidum?

Nonulcerative inflammation on colonoscopy; basophilic clusters seen on the surface of intestinal mucosal cells on biopsy.

102

What is present on colonoscopy and biopsy in a patient with entamoeba histolytica?

Numerous discrete, flask shaped ulcerative lesions; biopsy shows trophozoites containing RBCs

103

What is present on colonoscopy and biopsy in a patient with kaposi's sarcoma?

Reddish/ violet, flat macupapular lesions or hemorrhagic nodules; biopsy shows spindle shaped tumor cells with small-vessel proliferation.

104

Alpha-fetoprotein is a serum marker for what malignancy?

Hepatocellular carcinoma.

105

Describe the appearance of carcinoid tumors microscopically.

Nests or sheets of uniform cells with eosinophilic cytoplasm and oval to round stippled nuclei. There is minimal to no variation in shape and size of tumor cells.

106

From where are carcinoid tumors derived?

Enterochromaffin cells of the intestinal mucosa.

107

Where are carcinoid tumors most commonly located?

Ileum; they may also occur in the appendix and rectum.

108

Describe the difference in appearance between hepatocyte ballooning degeneration and death as caused by hepatitis.

Ballooning degeneration causes cytoplasm to appear empty with only an occasional eosinophilic organelle remnant remaining; death is characterized by lobular architectural disruption, cytolysis, apoptosis, and bridging necrosis.

109

What type of virus causes Hepatitis A?

RNA picornavirus.

110

What symptoms are characteristic of acute hepatitis A infection?

fever, malaise, fatigue, anorexia, n/v, abdominal pain, dark urine (due to increased serum billi)

111

What are the classic lab findings associated with hepatitis A?

Early spike in AST and ALT followed by increases in billi and alk phos.

112

What is Whipple disease?

Rare systemic illness involving the small intestine, joints, and CNS. Histologic findings include small intestine mucosa containing enlarged foamy macrophages packed with rod shaped bacilli and PAS positive diastase resistant granules. It is most commonly seen in middle aged white men.

113

What organism causes Whipple disease?

Tropheryma whippelii

114

How is Whipple disease treated?

Antibiotics.

115

What arteries arise from the splenic artery on its route towards the spleen?

Gives rise to vasculature to the stomach and pancreas; pancreatic and short gastric, left gastroepiploic arteries arise from the splenic immediately after it passes the greater curvature of the stomach.

116

What is the difference in blood flow to tissues supplied by the left gastroepiploic artery compared to those supplied by the short gastric?

Many anastamoses with left gastroepiploic thus ischemia is unlikely; short gastric arteries have poor anastamoses.

117

What is the clinical presentation in a patient with abetalipoproteinemia?

Manifests during first year of life with malabsorption. Labs show low plasma triglyceride and cholesterol levels and chylomicrons, VLDLs, and apoB are entirely absent from the blood. Poor lipid absorption causes deficiency of fat soluble vitamins (esp. vitamin D) and essential fatty acids. This causes red blood cell projections (acanthocytes) and neurologic abnormalities (retinitis pigmentosa, progressive ataxia).

118

What is seen on light microscopy in celiac disease?

Atrophy and blunting of the villi with chronic inflammatory infiltrate of the lamina propria.

119

What is the pathology associated with abetalipoproteinemia?

Loss of function of MTP gene causing inability to synthasize apolioprotein B.

120

What is the appearance of intestinal epithelium in a patient with abetalipoproteinemia?

Accumulation of lipids in the intestinal epithelium resulting in enterocytes with clear or foamy cytoplasm.

121

What are curling ulcers?

Ulcers arising in the proximal duodenum in association with severe trauma or burns; patients with high ICP are especially prone.

122

What test is necessary for definitive diagnosis of acute calculous cholecystitis?

A positive HIDA scan that confirms cystic duct obstruction; nonobstructing biliary stones seen by ultrasound are suggestive but NOT diagnostic.

123

What is diffuse esophageal spasm?

Occurs due to uncoordinated contractions of the esophagus. Contractions are inefficient in propelling food into the stomach and may cause dysphagia and chest pain.

124

Patients with diffuse esophageal spasm (DES) often present mimicking what condition?

Unstable angina (intermittent chest pain and dysphagia)

125

What characterizes Primary Biliary Cirrhosis?

Chronic liver disease characterized by autoimmune destruction of the intrahepatic bile ducts and cholestasis.

126

Histology of the liver in a patient with Primary Biliary Cirrhosis shows similar findings to what condition?

Graft vs host disease. Findings include granulomatous bile duct destruction and heavy lymphocyte predominant portal tract infiltrate.

127

What characterizes alcoholic hepatitis histologically?

Hepatocellular swelling and necrosis; mallor bodies, neutrophilic infiltration, fibrosis.

128

What is the histological difference between Acetaminophen toxicity and Reyes syndrome?

Acetaminophen- centrilobular necrosis; Reyes- microvesicular steatosis.

129

What region is most affected by chronic type B gastritis?

Gastric antrum.

130

What is the difference between villious adenomas and tubular adenomas?

Villious are larger, sessile, and more severely dysplastic than tubular adenomas.

131

What is Peutz-Jeghers syndrome?

Associated with multiple hamartomatous polyps and black spots on the skin and mucosa of young patients.

132

Where is H. pylori found in greatest concentration in the case of duodenal ulcer?

Prepyloric area of the gastric antrum.

133

What causes gynecomastia in a cirrhotic patient?

Hyperestrinism due to decreased catabolism of estrogens and increased sex hormone binding globulin (which decreases the free testosterone to estrogen ratio).

134

Hyperesterinism in a cirrhotic patient leads to what clinical symptoms?

Gyneocomastia, testicular atrophy, decreased body hair, spider angiomata.

135

What is the typical presentation of a patient with biliary atresia?

Complete obstruction of extrahepatic bile ducts with persistent jaundice beginning around week 3 or 4 of life. Dark urine, acholic stools, and conjugated hyperbilirubinemia occur.

136

What is seen on liver biopsy of a patient with biliary atresia?

Intrahepatic bile ductular proliferation, portal tract edema and fibrosis, parenchymal cholestasis.

137

Which structure herniates through the umbilical ring at 6 weeks of embryonic development and returns to complete a 270 degree turn at 10 weeks?

Midgut.

138

What are two main manifestations of intestinal malrotation during early fetal life?

Intestinal obstruction (due to compression by adhesive bands); midgut volvulus (intestinal ischemia due to twisting around blood vessels).

139

What is the difference between a true cyst and a pseudocyst?

Pseudocyst walls consist of granulation tissue and have no epithelial lining; fibrosis and thickening of the walls occurs over time. They contain a fluid rich in enzymes and inflammatory debris. Cysts are lined by epithelial cells.

140

Where and when do pseudocysts most commonly present?

Lesser peritoneal sac, bordered by the stomach, duodenum, and transverse colon. They are a complication of pancreatitis that occur about 4-6 weeks after the episode of pancreatitis.

141

What are the presenting symptoms of arsenic toxicity?

Nausea, vomiting, diarrhea, abdominal pain, decreased consciousness, hypotension, tachycardia, garlic odor of breath.

142

What is the treatment for arsenic poisoning?

Chelating agents- dimercaptrol displaces arsenic ions from sulfhydryl groups of enzymes to facilitate excretion.

143

What is amyl nitrite used to treat?

Cyanide poisoning.

144

What is CaNa2EDTA used to treat?

Acute lead and mercury poisoning.

145

What is porcelain gallbladder?

A bluish, brittle, calcium laden gallbladder wall that can develop in some patients with chronic cholesystitis.

146

What is a major risk associated with porcelain gallbladder?

Gallbladder carcinoma.

147

A patient has gas in the gallbladder and biliary tree as seen on xray. She has pain and abdominal distention. What is the likely diagnosis?

Gallstone ileus. Patient will show signs of small bowel obstruction.

148

What is gallstone ileus?

Caused by longstanding cholelithiasis, it is due the the passage of a large gallstone (greater than 2.5 cm through a cholecystenteric fistula into the small bowel where it causes obstruction of the ileocecal valve.

149

Describe the passage of the esophagus through the thorax as seen on CT.

Courses between the trachea and vertebral bodies down the midline (slightly to pts left). It is typically collapsed with no visible lumen on CT images of the chest.

150

What are the three major gastric acid secretagogues?

Histamine, Gastrin, ACh (vagal stimulation)

151

What enzymatic actions are saturated in the liver due to acetaminophen toxicity?

Glucuronide conjugation and sulfation.

152

What is the mechanism of action of N-acetylcystine in acetaminophen toxicity?

It provides sulfhydryl groups to enhance nontoxic elimination.

153

What does peripheral blood smear of a patient with lead poisoning show?

Microcytic hypochromic anemia and basophilic stippling.

154

Describe the four phases of iron poisoning.

First n/d abdominal pain often accompanied by hemorrhage, hypovolemia and shock; then GI sx resolve and the patient appears better; stage three metabolic acidosis and hepatic dysfunction occur; stage four is marked by scarring of the recovering GI tract.

155

Which two classes of anti-lipid drugs increase hepatic cholesterol synthesis and cause increased risk of gallstones?

Fibrates and bile acid resins.

156

What esophageal pathology occurs in CREST syndrome?

Fibrous replacement of the muscularis which leads to esophageal hypomotility and incompetence of the lower esophageal sphincter. This causes dilation and reflux which increases risk of Barrett esophagus and esophageal adenocarcinoma.

157

What is Budd Chiari syndrome?

Occlusion of the hepatic vein which drains blood from the liver and portal circulation into systemic circulation.

158

What does liver biopsy show in Budd Chiari syndrome?

Centrilobular congestion and fibrosis.

159

What is the difference between a gastric ulcer and a gastric erosion?

Erosions do not fully extend through the muscularis mucosa (limited to mucosal layer) while ulcers penetrate the mucosal layer and extend into the submucosal layers.

160

Name the five layers of the stomach from inside to outside.

Mucosa, muscularis mucosa, submucosa, Muscularis propria, serosa.

161

What is Acute Calculous Cholecystitis (ACC)?

Acute inflammation of the gallbladder that is initiated 90% of the time by obstruction of the gallbladder neck or cystic duct. It is the most common complication of cholelithiasis and results from chemical irritation and inflammation caused by the presence of stones in the gallbladder.

162

Describe the pathogenesis of acute calculous cholecystitis?

Stones disrupt the protective mucous layer leaving the epithelium exposed to the detergent actions of bile salts; PGs released in the gallbladder wall incite inflammation of the mucosa and deeper tissues causing gallbladder hypomotility. Increasing pressure and distension within the gallbladder causes ischemia and bacteria then invade the injured and necrotic tissue causing infection.

163

What is cholestasis?

Deposition of bile pigment within hepatic parenchyma and the presence of green brown plugs in the dilated bile canaliculi. When prolonged, this can cause malabsorption and nutritional deficiencies of fat soluble vitamins (i.e. osteomalacia, etc.)

164

How do levels of total bile salt and phosphatidylcholine affect risk of gallstones?

They increase cholesterol solubility and decrease risk of gallstones.

165

What muscle contracts behind the food bolus initiating a peristaltic wave to propel the bolus downwards?

Cricopharyngeus muscle.

166

What manometry study results are typical for achalasia?

Decreased esophageal body peristalsis and poor relaxation of the LES on manometry

167

What barium swallow results are characteristic of achalasia?

Dilated esophagus and a bird beak deformity of LES.

168

What is Meckel's diverticulum?

Remnant of the omphalomesenteric (vitelline) duct.

169

What is the difference between a true and false diverticula?

True diverticula consist of all parts of intestinal wall (mucosa, submucosa, muscularis, serosa); pseudodiverticulum (ex Zenkers) only contain mucosa and submucosa.

170

What histologic findings are characteristic of GERD?

Basal zone hyperplasia, elongation of the lamina propria papillae, and inflammatory cells (eosinophils, neutrophils, lymphocytes).

171

Metastatic spread of adenocarcinoma to the ovaries is usually in association of primary cancers of what organs?

Stomach, breast, pancreas, gallbladder.

172

What histologic findings are characteristic of Krukenburg tumor?

Mucin producing signet-ring neoplastic cells in the ovarian stroma.

173

What is Virchow's node?

Metastasis of gastric cancer to the left supraclavicular sentinel node.

174

What is a Sister Mary Joseph nodule?

Metastasis of gastric cancer to the periumbilical region.

175

Metastasis of gastric cancer can present most commonly as what three pathologies?

Krukenberg tumor of the ovary, Sister Mary Joseph nodule, Virchow's node.

176

What do PT, billirubin, albumin, and cholesterol levels indicate about the liver?

Functionality

177

What do transaminases indicate about the liver?

Structural integrity and cellular intactness.

178

What do alkaline phosphatase and y-glutamyl transferase levels indicate?

Structural integrity and cellular intactness of the biliary tract.

179

What two organs are the primary source of Alk Phos?

Bones and liver. 3 fold elevations are quite specific for liver disease

180

What test can be used to clarify the importance of moderately elevated alkaline phosphatase levels?

Hepatic y-glutamyl transpeptidase levels

181

What is the histologic appearance of signet ring carcinomas?

Cells that do not form glands; they often contain abundant mucin droplets that push the nucleus to one side and lead to the characteristic appearance of a signet ring in profile

182

What is the gross appearance of signet ring carcinomas of the stomach?

Diffuse involvement in the stomach wall with a plaque like appearance that is ill defined; often large areas of the stomach wall are infiltrated (leather bottle stomach, linitis plastica)

183

What are the two types of gastric adenocarcinomas?

Intestinal type adenocarcinoma and signet-ring carcinoma.

184

What is the appearance of intestinal-type adenocarcinomas?

Resemble colon cancers; grow as nodular, polypoid and well demarcated masses which on light microscopy form glands that consist of columnar or cubiodal cells.

185

What malignancy is associated with a palpable but non tender gallbladder (Courvosier sign), weight loss, and obstructive jaundice (associated with pruritus, dark urine, and pale stools)?

Adenocarcinoma of the head of the pancreas compressing the common bile duct. Sx are usually not present until invasion of the splanchnic plexus which causes midepigastric abdominal pain.

186

What non genetic factors increase risk of pancreatic cancer?

Smoking, chronic pancreatitis, DM.

187

What two factors are the most common cause of acute pancreatitis?

Alcoholism and gallstones.

188

Name seven less likely causes of acute pancreatitis.

Recent endosopic retrograde cholangiopancreatography (ERCP) procedure, drugs, infections, hypertriglyceridemia, structrual abnormalities of the pancreatic duct, surgery, hypercalcemia.

189

How does hypertriglyceridemia cause acute pancreatitis?

By direct tissue toxicity if levels rise above 1000 mg/dL.

190

What is chronic mesenteric ischemia?

Caused by atherosclerotic narrowing of the celiac trunk, SMA, and IMA; it is characterized by epigastric or periumbilical pain 30-60 mins after food intake as arteries are not able to dilate in response to increased blood flow requirements during digestion and absorption of food. Weight loss is common.

191

What is PBS?

Chronic liver disease characterized by autoimmune destruction of the intrahepatic bile ducts and cholestasis.

192

What physical findings and symptoms are present in a patient with PBS?

First- pruritus and fatigue; then hepatosplenomeagly and xanthomatous lesions in the eyelids or in the skin and tendons. Finally jaundice, steatorrhea, portal hypertension, osteopenia.

193

What are councilman bodies?

Apoptotic hepatocytes that form round acidophilic (pink on H&E) staining. They are caused by necrosis (i.e. hepatitis, etc.)

194

What is Mallory-Weiss syndrome?

Longitudinal mucosal tears at the esophagogastric-squamocolumnar junction.

195

What causes Mallory-Weiss syndrome?

Rapid increases in intraabdominal and intraluminal gastric pressure (caused by retching and vomiting)

196

How does the cause of Mallory Weiss syndrome tears differ from those of varices?

Varices are caused by increased venous pressure; mallory weiss tears are caused by increased intraluminal Gastric pressure due to retching, vomiting, or abdominal straining.

197

What is the toxic byproduct of aspergillus flavus and aspergillus parasiticus?

Aflatoxins.

198

What malignancy is caused by mutations of G-T in the p53 gene?

Hepatocellular carcinoma; caused by aflatoxins.

199

What is biliary sludge?

Bile precipitation secondary to gallbladder hypomotility.

200

What does biliary sludge contain?

Cholesterol monohydrate crystals, calcium bilirubinate, mucus. Complications like cholecystitis occur frequently with biliary sludge.

201

What are two markers of impaired biosynthetic capacity due to liver damage?

Elevated PT, hypoalbuminemia

202

What is a marker of impaired transport and metabolic capacity of the liver?

Elevated bilirubin.

203

What are two markers of hepatocyte injury?

Elevated AST and ALT (AST usually > than ALT in cirrhosis)

204

What are two markers of cholestasis due to liver injury?

Elevated alkaline phosphatase, elevated gamma glutamyl transpeptidase.

205

Levels of which three factors is the greatest prognostic indicator of cirrhosis?

PT, albumin levels, billi levels.

206

Describe the pathogenesis of Crigler-Najjar syndrome.

AR disorder of billirubin metabolism caused by lack of UGT enzyme needed to catalyze bile glucuronidation. This causes unconjugated hyperbilirubinemia (as billi is not properly conjugated by the liver) and indirect billirubin levels rise.

207

What is the difference in excretion patterns between congugated and unconjugated billi?

Conjugated is water soluble, loosely bound to albumin and excreted in urine when present in excess; unconjugated binds tightly to albumin and is insoluble (so cant be excreted in urine)

208

What factors are involved in the pathogenesis of crohn's disease?

Increased activity of Th1 helper T cells causing increased production of IL-2, interferon-y, and TNF which cause subsequent intestinal injury and non-caseating granulomas.

209

What is the function of NF-kB?

It triggers cytokine response to infectious pathogens.

210

What AST:ALT ratio is indicative of alcoholic hepatitis?

Ratio greater than 2; elevated GGT is also characteristic.

211

Inflamatory infiltrate of what layer of the small bowel is characteristic of Crohns?

Inflammatory infiltrate of the lamina propria.

212

Describe the inflammation associated with temporal arteritis.

Granulomatous inflammation of the media.

213

Transmural inflammation of the arterial wall with fibrinoid necrosis is characteristic of what condition?

Polyarteritis nodosa.

214

What renal pathology is associated with Crohn's disease?

Calcium oxalate stones.

215

In what gastric layers are chief cells and parietal cells found?

Parietal cells- superficial region of the gastric glands; Chief cells- deeper region of the gastric glands

216

What is the pathology of hepatic steatosis?

Triglyceride accumulation in the hepatocyte cytoplasm. This is caused by a decrease in free fatty oxidation secondary to excess NADH production by alcohol and aldehyde dehydrogenase.

217

What symptoms are characteristic of a VIPoma?

Watery diarrhea, achlorhydria, hypokalemia.

218

What histology is characteristic of Reye's syndrome?

Microvesicular steatosis- small fat vacuoles in the cytoplasm of hepatocytes. No necrosis or inflammation is present. EM shows glycogen depletion, swelling, and a decreased number of mitochondria.

219

What is the most common location for colon cancer?

Rectosigmoid colon.

220

Describe the properties of a left sided tumor of the colon and its presenting symptoms.

Smaller than right sided; tend to infiltrate the wall and encircle the colon causing obstruction, altered bowel habits, constipation, abdominal distention, nausea, vomiting.

221

Name six inciting factors of hepatic encaphalopathy.

Drugs, hypotension, excess nitrogen load (bleeding, constipation), portal hypertension, infections, metabolic disturbances.

222

What BUN value is associated with liver disease?

Decreased BUN due to inefficient conversion of ammonia into urea.

223

Pink discoloration due to PAS stain indicates the presence of what?

Glycoproteins (can show cell walls of actinomycete tryphermia whipilli in whipple's disease).

224

What type of mutation is associated with Lynch Syndrome or HNPPC?

Mutation in one allele for genes coding for mismatch repair; the other mutation occurs in adult life.

225

Describe the location of cancers in Lynch syndrome compared to sporadic colon cancer?

Lynch on right; sporadic on left.

226

Why are patients with Crohn's disease more susceptible to gallstones?

Due to decreased bile reabsorption and its loss in feces increases bile lithogenecity; cholesterol then precipitates to form gallstones.