Zanki GI Pathology

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ZANKI GI PATHOLOGY

1. What is the most common cause of hematochezia in adults? diverticulosis

2. Aphthous ulcers ("canker sores") are painful, superficial ulcerations of the oral mucosa

3. Aphthous ulcers arise in relation to stress and resolve spontaneously however they often recur

4. Aphthous ulcers are characterized by a grayish base (color) surrounded by erythema

5. Behcet syndrome is characterized by a triad of recurrent aphthous ulcers with genital ulcers and uveitis

6. Behcet syndrome occurs due to immune-complex vasculitis involving primarily small vessels

7. Behcet syndrome can be seen after viral infection but the etiology is unknown

8. Oral herpes ("cold sores") is characterized by painful, shallow, red ulcers involving the oral mucosa

9. Oral herpes is usually due to HSV-1 infection

10. The HSV-1 virus that causes oral herpes remains dormant in the ganglia of the trigeminal nerve

11. Dormant HSV-1 virus may be reactivated by stress and sunlight leading to an episode of oral herpes

12. The major risk factors for squamous cell carcinoma of the oral mucosa are alcohol and tobacco

13. What is the most common location for oral squamous cell carcinoma? Floor of the mouth

14. Oral leukoplakia and erythroplakia are precursor lesions to squamous cell carcinoma

15. Oral leukoplakia is a white deposit on the tongue that cannot be easily scraped away

16. Oral candidiasis is a white deposit on the tongue that can be easily scraped away

17. Hairy leukoplakia is a white rough patch that arises on the lateral tongue

18. Hairy leukoplakia is a squamous cell hyperplasia (not dysplasia) induced by EBV infection

19. Is hairy leukoplakia pre-malignant for oral squamous cell carcinoma? No

20. Oral candidiasis and hairy leukoplakia are usually seen in immunocompromised individuals

21. Oral erythroplakia is a red plaque due to vascularization of leukoplakia

22. Erythroplakia is highly suggestive of squamous cell dysplasia (hyperplasia or dysplasia)

23. Which lesion leukoplakia or erythroplakia is more suggestive of squamous cell dysplasia? Erythroplakia

24. What virus is associated with bilateral inflammation of the parotid glands? Mumps virus

25. In addition to parotitis mumps may also present with orchitis pancreatitis and aseptic meningitis

26. What enzyme is elevated in mumps patients due to involvement of the pancreatic or salivary glands? Œ±-amylase

27. Orchitis due to mumps infection carries risk of sterility especially in teenagers

28. Sialadenitis is inflammation of a salivary gland

29. Sialadenitis most commonly occurs due to sialolithiasis which often leads to Staphylococcus aureus mediated sialadenitis / parotitis

30. Is Warthrin tumor typically unilateral or bilateral? Unilateral

31. Salivary gland tumors are most commonly benign (benign or malignant)

32. Salivary gland tumors most commonly arise in the parotid gland

33. If a salivary gland tumor involves a non-parotid gland it is more likely to be malignant (benign or malignant)

34. Salivary gland tumors typically present as a mobile painless mass/swelling (painful or painless) at the angle of the jaw

35. What is the most common salivary gland tumor? Pleomorphic adenoma

36. Pleomorphic adenoma is a salivary gland tumor composed of chondromyxoid stroma and epithelium

37. Is pleomorphic adenoma a benign or malignant salivary gland tumor? Benign


38. Pleomorphic adenoma is associated with a high rate of recurrence due to incomplete resection or intraoperative rupture

39. Which salivary gland tumor is associated with a high rate of recurrence following resection? Pleomorphic adenoma

40. Warthrin tumor is a cystic salivary gland tumor with abundant lymphocytes and germinal centers

41. Is Warthrin tumor typically benign or malignant salivary gland tumor? Benign

42. Mucoepidermoid carcinoma is a malignant salivary gland tumor composed of mucinous and squamous cells

43. What is the most common malignant salivary gland tumor? Mucoepidermoid carcinoma

44. Malignant salivary gland tumors present with signs of facial nerve damage

45. Esophageal web is a thin protrusion of esophageal mucosa most often in the upper esophagus

46. Esophageal web presents with dysphagia for poorly chewed food

47. Plummer-Vinson syndrome is characterized by a triad of iron deficiency anemia esophageal web and a beefy-red tongue (atrophic glossitis)

48. Zenker diverticulum is an outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum) caused
by cricopharyngeal motor dysfunction

49. Is Zenker diverticulum a true or false diverticulum? False (only involves mucosa and submucosa)

50. Zenker diverticulum classically arises at Killian's triangle between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal
constrictor

51. Zenker diverticulum often presents with oropharyngeal dysphagia obstruction and halitosis (bad breath)

52. What demographic is most commonly affected by Zenker diverticulum? Elderly males

53. Mallory-Weiss syndrome is a linear mucosal laceration at the gastroesophageal (GE) junction

54. The tears in Mallory-Weiss syndrome are caused by a rapid increase in intraabdominal pressure (ex. retching vomiting)

55. Mallory-Weiss syndrome is usually seen in alcoholics and bulimics

56. Mallory-Weiss syndrome presents with hematemesis that can be painful

57. Is the hematemesis seen with Mallory-Weiss syndrome typically painful or painless? Painful

58. Boerhaave syndrome is a transmural laceration of the distal esophagus

59. Boerhaave syndrome presents as esophageal rupture with pneumomediastinum (air in the mediastinum) and subcutaneous emphysema

60. Boerhaave syndrome is usually due to violent retching

61. Esophageal varices are dilated submucosal veins in the lower 1/3rd of the esophagus

62. Esophageal varices arise secondary to portal hypertension

63. In portal hypertension the left gastric vein backs up into the esophageal vein resulting in varices

64. Esophageal varices may rupture which presents with painless hematemesis

65. Is the hematemesis seen with esophageal varices typically painful or painless? Painless

66. Esophageal varices are a common cause of death in patients with cirrhosis

67. Achalasia is characterized by disordered esophageal motility due to inability to relax the lower esophageal sphincter

68. Primary achalasia is due to an autoimmune destruction of ganglion cells in the myenteric (Auerbach) plexus

69. Achalasia may be idiopathic or secondary to a known insult such as Chagas disease and extraesophageal malignancies

70. Does achalasia present with dysphagia for solids or liquids? Both solids and liquids :)

71. Achalasia is characterized by high LES pressure on esophageal manometry

72. Achalasia is characterized by uncoordinated or absent peristalsis in the esophagus

73. Achalasia is characterized by the "Bird's beak" sign on barium swallow


74. Gastroesophageal reflux disease (GERD) is caused by reflux of acid from the stomach due to transiently decreased LES tone

75. What type of hernia increases risk of developing GERD? Sliding hiatal hernia

76. Gastroesophageal reflux disease (GERD) often presents with heartburn which can mimic cardiac chest pain

77. Gastroesophageal reflux disease (GERD) may present with chronic cough and adult-onset asthma

78. Gastroesophageal reflux disease (GERD) may damage the enamel of teeth

79. Late complications of GERD include: - Barrett esophagus - ulcerations followed by esophageal strictures

80. Esophageal stricture is a narrowing of the esophagus

81. Esophageal strictures are associated with caustic ingestion and GERD

82. Barrett esophagus is characterized by specialized intestinal metaplasia of the lower esophageal mucosa

83. In Barrett esophagus non-keratinized stratified squamous epithelium is replaced with non-ciliated columnar epithelium with goblet
cells(metaplasia)

84. Barrett esophagus is seen in 10% of patients with GERD

85. Which type of esophageal cancer (SCC or adenocarcinoma) is associated with obesity GERD and Barrett esophagus? Adenocarcinoma

86. Esophageal carcinoma is subclassified as adenocarcinoma or squamous cell carcinoma

87. Adenocarcinoma of the esophagus is a malignant proliferation of glands

88. Adenocarcinoma of the esophagus is the most common type of esophageal carcinoma in America (location)

89. Adenocarcinoma of the esophagus most commonly arises from pre-existing Barrett esophagus

90. Which part of the esophagus is typically affected by adenocarcinoma? Lower 1/3rd

91. Squamous cell carcinoma of the esophagus is a malignant proliferation of squamous cells

92. Squamous cell carcinoma of the esophagus is the most common type of esophageal carcinoma worldwide (location)

93. The most common causes of squamous cell carcinoma of the esophagus are alcohol and tobacco

94. Which type of esophageal cancer (SCC or adenocarcinoma) is associated with esophageal web (e.g. Plummer-Vinson syndrome)? Squamous
cell carcinoma

95. Which type of esophageal cancer (SCC or adenocarcinoma) is associated with achalasia? Both :)

96. Which type of esophageal cancer (SCC or adenocarcinoma) is associated with very hot tea? Squamous cell carcinoma

97. Which type of esophageal cancer (SCC or adenocarcinoma) is associated with esophageal injury (e.g. lye/caustic ingestion)? Squamous cell
carcinoma

98. Which part of the esophagus is typically affected by squamous cell carcinoma? Upper 2/3rds

99. What is the prognosis of esophageal carcinoma? Poor (presents late)

100. Symptoms of esophageal carcinoma include progressive dysphagia (solids to liquids) weight loss pain and hematemesis

101. Squamous cell carcinoma of the esophagus may present with hoarseness due to involvement of the recurrent laryngeal nerve

102. Squamous cell carcinoma of the esophagus may present with cough due to tracheal involvement

103. Esophageal carcinoma in the upper third of the esophagus spreads to cervical lymph nodes

104. Esophageal carcinoma in the middle third of the esophagus spreads to mediastinal tracheobronchial or paratracheal lymph nodes

105. Esophageal carcinoma in the lower third of the esophagus spreads to celiac or gastric lymph nodes

106. Barrett esophagus is characterized by extension of the squamocolumnar junction (Z-line) into the esophageal mucosa

107. Eosinophilic esophagitis is characterized by eosinophilic infiltration of the esophagus often in atopic patients

108. Eosinophilic esophagitis presents with esophageal rings and linear furrows often seen on endoscopy

109. Eosinophilic esophagitis classically presents with dysphagia and food impaction in response to food allergens
110. Does eosinophilic esophagitis respond to GERD therapy (e.g. PPIs)? No

111. What infectious cause of esophagitis presents as punched-out ulcers? HSV-1

112. What infectious cause of esophagitis presents as linear ulcers? CMV

113. What infectious cause of esophagitis presents as white pseudomembranes? Candida

114. Infectious esophagitis is typically seen in immunocompromised patients

115. What connective tissue disease is associated with esophageal dysmotility? Scleroderma

116. Sclerodermal esophageal dysmotility is characterized by low LES pressure on esophageal manometry

117. The low LES pressure in scleroderma predisposes to acid reflux and dysphagia

118. Acute gastritis occurs due to acidic damage to the stomach mucosa

119. Acute gastritis arises due to imbalance between mucosal defenses and acidic environment

120. Mucosal defenses include secretion of mucus HCO3- and normal blood supply

121. Mucosal defenses include normal blood supply which provides nutrients and picks up leaked acids

122. Acute gastritis may arise with severe burns due to hypovolemia which causes mucosal ischemia

123. What type of gastric ulcer is caused by severe burns? Curling ulcer

124. Acute gastritis may arise with NSAID use due to decreased PGE2

125. Acute gastritis may arise with increased ICP due to increased vagal stimulation which increases H+ production

126. What type of gastric ulcer is caused by increased intracranial pressure? Cushing ulcer

127. Acute gastritis may arise with shock which presents as multiple stress ulcers secondary to ischemia

128. Acute gastritis is especially common among alcoholics and patients taking daily NSAIDs (e.g. rheumatoid arthritis patients)

129. Gastric erosion (erosion or ulcer) involves loss of the mucosal layer only

130. Gastric ulcers (erosions or ulcers) may extend into and beyond the submucosa

131. Chronic gastritis occurs due to chronic inflammation of the stomach mucosa

132. Chronic gastritis is associated with atrophy of the gastric mucosa (hypertrophy or atrophy)

133. Chronic gastritis is associated with intestinal metaplasia

134. What is the effect of chronic gastritis on gastric HCl secretion? Decreased (achlorhydria or hypochlorhydria)

135. What is the effect of chronic gastritis on gastrin secretion? Increased (hypergastrinemia)

136. Chronic gastritis is divided into two types based on etiology: autoimmune and H. pylori gastritis

137. Chronic autoimmune gastritis is also referred to as type A gastritis

138. Chronic H. pylori gastritis is also referred to as type B gastritis

139. Chronic autoimmune gastritis is due to autoimmune destruction of parietal cells

140. Which areas of the stomach are affected in chronic autoimmune gastritis? body and fundus

141. Chronic autoimmune gastritis is associated with antibodies against parietal cells and/or intrinsic factor

142. What type of hypersensitivity reaction is chronic autoimmune gastritis? Type IV (T-cell mediated)

143. Chronic autoimmune gastritis is associated with increased risk for pernicious anemia

144. What is the most common (90%) form of chronic gastritis? Chronic H. pylori gastritis

145. Which area of the stomach is initially affected by chronic H. pylori gastritis? antrum

146. Does H. pylori invade the stomach mucosa? No (sits on top of mucosa)

147. Chronic H. pylori gastritis causes increased risk for peptic ulcer disease


148. Chronic H. pylori gastritis causes increased risk for MALT lymphoma

149. What cytotoxin released by H. pylori breaks down the protective mucus barrier? CagA toxin

150. H. pylori produces urease which alkalinizes the local environment enabling bacterial survival

151. H. pylori infection may be diagnosed using the urea breath test

152. Is the intestinal metaplasia seen with H. pylori gastritis reversible? Yes (resolves with treatment of infection)

153. Peptic ulcer disease is a solitary mucosal ulcer involving the proximal duodenum (90%) or distal stomach (10%)

154. Duodenal ulcers are almost always due to H. pylori (~ 90%)

155. Duodenal ulcers rarely may be due to Zollinger-Ellison syndrome

156. Duodenal ulcers present with epigastric pain that improves with meals

157. Duodenal ulcers are diagnosed via endoscopic biopsy which shows an ulcer with hypertrophy of Brunner glands

158. Duodenal ulcers usually arise in the anterior duodenum (anterior or posterior)

159. Duodenal ulcers located in the posterior duodenum may rupture leading to bleeding from the gastroduodenal artery

160. Gastric ulcers are usually due to H. pylori (~ 70%)

161. Less common causes of gastric ulcers include NSAIDs and bile reflux

162. Gastric ulcers present with epigastric pain that worsens with meals

163. What is the most common location for a gastric ulcer? Lesser curvature of stomach

164. Gastric ulcers on the lesser curvature of the stomach may rupture leading to bleeding from the left gastric artery

165. Which type of ulcer (gastric or duodenal) is more likely to be malignant? Gastric

166. Benign gastric ulcers are usually small (< 3 cm), sharply demarcated ("punched-out"), and surrounded by radiating folds of mucosa

167. Malignant gastric ulcers are usually large and irregular with heaped up margins

168. Gastric ulcers (gastric or duodenal) should be biopsied at the margins to rule out malignancy

169. What is the most common ulcer complication (both gastric and duodenal)? Hemorrhage

170. Which type of duodenal ulcer (anterior or posterior) is more commonly associated with hemorrhage? Posterior

171. One possible ulcer complication is obstruction of the pyloric channel or duodenum

172. Which type of duodenal ulcer (anterior or posterior) is more commonly associated with perforation? Anterior

173. Perforation of an anterior duodenal ulcer is characterized by free air under the diaphragm (pneumoperitoneum)

174. Perforation of an anterior duodenal ulcer may present with referred pain to the shoulder via the phrenic nerve

175. What is the most common classification of gastric carcinoma (e.g. SCC lymphoma adenocarcinoma etc.)? Adenocarcinoma

176. Gastric carcinoma is subclassified into intestinal and diffuse types

177. Which type of gastric carcinoma (intestinal or diffuse) is more common? Intestinal type

178. The intestinal type of gastric carcinoma most commonly arises on the lesser curvature of the antrum

179. Which type of gastric carcinoma (intestinal or diffuse) is associated with H. pylori infection? Intestinal

180. Which type of gastric carcinoma (diffuse or intestinal) is associated with chronic gastritis? Intestinal

181. The intestinal type of gastric carcinoma is associated with nitrosamines which are found in smoked foods (common in Japan)

182. The intestinal type of gastric carcinoma is associated with blood type A

183. The diffuse type of gastric carcinoma is characterized by signet ring cells that infiltrate the gastric wall

184. The diffuse type of gastric carcinoma may cause linitis plastica which is a grossly thickened and leathery stomach wall

185. Gastric carcinoma typically presents late (timing) with weight loss early satiety abdominal pain and anemia
186. Gastric adenocarcinoma rarely may present with acanthosis nigricans which is hyperpigmented velvety plaques in the axilla and neck

187. Gastric adenocarcinoma rarely may present with the Leser-Trelat sign which is sudden onset of multiple seborrheic keratoses

188. Gastric carcinoma may spread and involve the left supraclavicular node also known as Virchow's node

189. Distant metastasis of gastric adenocarcinoma most commonly involves the liver

190. Gastric carcinoma may spread and involve the periumbilical region also known as a Sister Mary Joseph nodule

191. Which type of gastric carcinoma (diffuse or intestinal) is associated with a Sister Mary Joseph nodule? Intestinal

192. Gastric carcinoma may spread and involve the bilateral ovaries also known as a Kruckenberg tumor

193. Which type of gastric carcinoma (diffuse or intestinal) is associated with Kruckenberg tumor? Diffuse

194. Menetrier disease is characterized by hyperplasia of the gastric mucosa and atrophy of the parietal / chief cells

195. Menetrier disease is characterized by hypertrophied gastric rugae that resemble brain gyri

196. Menetrier disease is characterized by excess mucus production with resultant protein loss

197. Menetrier disease is characterized by parietal cell atrophy with decreased acid production

198. Does menetrier disease increase risk for gastric cancer? Yes (pre-cancerous lesion)

199. Meckel diverticulum is an outpouching of all three layers of the bowel wall (true diverticulum)

200. Is Meckel diverticulum a true or false diverticulum? True (outpouching of all layers)

201. Meckel diverticulum arises due to persistence of the vitelline (omphalomesenteric) duct

202. What is the most common congenital anomaly of the GI tract? Meckel diverticulum

203. Meckel diverticulum is associated with the "rule of 2s"

204. Meckel diverticulum is two times more likely to occur in males (gender)

205. Meckel diverticulum is typically two inches long

206. Meckel diverticulum is typically located in the small bowel two feet from the ileocecal valve

207. Meckel diverticulum typically presents during the first two years of life

208. Meckel diverticulum may contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue

209. Meckel diverticulum is diagnosed using a 99mTc-pertechnetate study for uptake by heterotopic gastric mucosa

210. Meckel diverticulum is typically asymptomatic but may present with volvulus intussusception melena RLQ pain or obstruction

211. The vitelline duct connects the yolk sac to the midgut lumen

212. What week does the vitelline duct normally obliterate? Week 7

213. What congenital anomaly is caused by complete failure of the vitelline duct to close? Vitelline fistula

214. What congenital anomaly is caused by only partial closure of the vitelline duct? Meckel diverticulum

215. What congenital anomaly is caused by cystic dilation of the vitelline duct? Vitelline cyst (enterocyst)

216. What congenital anomaly presents with meconium discharge from the umbilicus? Vitelline fistula

217. Volvulus is caused by twisting of a portion of bowel around its mesentery

218. Volvulus can lead to obstruction and infarction of the affected bowel region

219. Volvulus of the sigmoid colon is more commonly seen in the elderly (age group)

220. Volvulus of the midgut is more commonly seen in infants and children

221. Volvulus of the cecum is more common in young adults

222. Intussusception is telescoping of a proximal::(proximal or distal) bowel segment into a distal::(proximal or distal) segment

223. In children the most common cause of intussusception is lymphoid hyperplasia (e.g. due to rotavirus or adenovirus)
224. What is the most common pathologic lead point for intussusception in children over 2? Meckel diverticulum

225. What is the most common lead point for intussusception in adults? Intraluminal mass or tumor

226. Where in the GI tract does intussusception most commonly occur? Ileocecal junction

227. Intussusception results in compromised blood supply, which causes intermittent abdominal pain (frequency) with "currant jelly" stool

228. Intussusception is characterized by a "bull's-eye (target sign)" appearance on ultrasound

229. Acute mesenteric ischemia may occur due to a thrombotic or embolic occlusion of the superior mesenteric artery

230. Acute mesenteric ischemia may occur due to a thrombosis of the mesenteric vein

231. Acute mesenteric ischemia is associated with transmural infarction (mucosal or transmural)

232. Acute mesenteric ischemia is associated with small bowel necrosis and abdominal pain out of proportion to physical findings

233. Acute mesenteric ischemia may present with "currant jelly" stool

234. Chronic mesenteric ischemia may occur due to severe hypotension or atherosclerosis of the celiac artery SMA or IMA

235. Chronic mesenteric ischemia is associated with mucosal infarction (mucosal or transmural)

236. Chronic mesenteric ischemia is typically caused by intestinal hypoperfusion as a result of narrowed vasculature

237. Chronic mesenteric ischemia presents with epigastric pain that occurs after eating (before or after)

238. What risk factor is associated with Warthrin tumors? Smoking

239. Boerhaave syndrome may present with subcutaneous emphysema which is characterized by crepitus felt in the neck region or chest wall

240. Esophagitis may occur with medications such as bisphosphonates tetracyclines NSAIDs iron and potassium chloride

241. Loss of which hormones/neurotransmitters (2) are implicated in the pathogenesis of achalasia? NO and VIP

242. Sigmoid volvulus is associated with the "coffee bean" sign on X-ray

243. What GI pathology is associated with the rotavirus vaccine? Intussusception

244. Lactose intolerance is caused by decreased function of the lactase enzyme found in brush border enterocytes

245. Lactose intolerance presents with abdominal distention and diarrhea upon consumption of milk products

246. Lactose intolerance is typically characterized by normal-appearing villi

247. Temporary lactase deficiency may be seen after small bowel infection (e.g. viral enteritis)

248. Lactose intolerance is characterized by decreased stool pH

249. Lactose intolerance may be diagnosed using the lactose hydrogen breath test

250. The lactose hydrogen breath test is positive for lactose malabsorption if the post-lactose breath hydrogen rises > 20 ppm compared with baseline

251. Celiac disease is immune-mediated damage of small bowel villi due to gluten exposure

252. Celiac disease is associated with HLA-DQ2 and HLA-DQ8

253. What malabsorption disorder is associated with HLA-DQ2 and HLA-DQ8? Celiac disease

254. What is the most pathogenic component of gluten (celiac disease)? Gliadin

255. Once absorbed gliadin is deamidated by the enzyme tissue transglutaminase (tTG)

256. In Celiac disease deamidated gliadin is presented by APCs via MHC class II

257. Which immune cell mediates the tissue damage in Celiac disease? Helper T cells

258. Celiac disease in children (age group) classically presents as abdominal distention steatorrhea and failure to thrive

259. Celiac disease in adults (age group) classically presents with chronic steatorrhea and bloating

260. Celiac disease is classically seen in people of northern European descent

261. Celiac disease is associated with dermatitis herpetiformis which are small herpes-like vesicles on the skin
262. The dermatitis herpetiformis that arises with celiac disease is due to IgA deposition at the tips of the dermal papillae

263. Celiac disease is classically associated with IgA antibodies against endomysium tissue transglutaminase (tTG) and/or deamidated gliadin

264. In patients with IgA deficiency and celiac disease IgG antibodies against endomysium tTG or gliadin are useful for diagnosis

265. There is an increased incidence of IgA deficiency in patients with celiac disease

266. Celiac disease is characterized histologically by flattening of villi

267. Celiac disease is characterized histologically by hyperplasia of crypts

268. Celiac disease is characterized histologically by increased intraepithelial lymphocytes

269. Celiac disease primarily affects the distal duodenum or proximal jejunum

270. Which type of sprue (celiac or tropical) primarily affects the proximal small bowel? Celiac sprue

271. Celiac disease is associated with increased risk for small bowel carcinoma and T-cell lymphoma

272. Celiac disease is associated with decreased bone density

273. What is the treatment for celiac disease? Gluten-free diet

274. Is celiac disease associated with normal or decreased urinary excretion of D-xylose (D-xylose test)? Decreased

275. Tropical sprue is characterized by damage to small bowel villi due to an unknown organism resulting in malabsorption

276. Which malabsorption disorder is more common in tropical regions? Tropical sprue

277. Tropical sprue classically arises after infectious diarrhea

278. Which type of sprue (celiac or tropical) can affect any part of the small bowel? Tropical sprue

279. Tropical sprue presents similarly to celiac disease but responds to antibiotics

280. Tropical sprue may be associated with megaloblastic anemia

281. Is tropical sprue associated with normal or decreased urinary excretion of D-xylose (D-xylose test)? Decreased

282. Whipple disease is characterized by systemic tissue damage with macrophages loaded with Tropheryma whipplei organisms

283. Tropheryma whipplei is an intracellular gram positive organism

284. The granules in macrophages in Whipple disease stain positive for PAS and are diastase resistant

285. Which malabsorption syndrome is associated with PAS positive foamy macrophages? Whipple disease

286. Whipple disease classically involves the lamina propria (mucosal layer) of the small bowel

287. Whipple disease may present with fat malabsorption and steatorrhea due to compression of lacteals by macrophages

288. What lymph nodes are commonly affected in Whipple disease? Mesenteric nodes

289. The symptoms of Whipple disease may be remembered with the mnemonic "Foamy Whipped cream in a CAN": C: cardiac
symptoms A: arthralgias N: neurologic symptoms

290. What demographic is most commonly affected by Whipple disease? Older men

291. Pancreatic insufficiency causes malabsorption of fat fat-soluble vitamins and vitamin B12

292. What test is used to indirectly assess pancreatic function? Fecal elastase

293. Pancreatic insufficiency is associated with decreased excretion of fecal elastase

294. Pancreatic insufficiency is associated with decreased duodenal pH

295. Is pancreatic insufficiency associated with normal or decreased urinary excretion of D-xylose (D-xylose test)? Normal

296. What stain is used to screen for fecal fat? Sudan stain

297. Abetalipoproteinemia is characterized by a deficiency of apolipoprotein B-48 and B-100


298. Abetalipoproteinemia is an autosomal recessive inherited malabsorption disorder that is caused by a mutation in the microsomal triglyceride
transfer protein

299. Abetalipoproteinemia is associated with malabsorption due to defective chylomicron formation which requires apoB-48

300. Abetalipoproteinemia is associated with absent plasma VLDL and LDL which require apoB-100

301. Carcinoid tumor is a malignant proliferation of neuroendocrine cells; low-grade malignancy

302. The tumor cells in carcinoid tumors contain secretory granules that stain positive for chromogranin A synaptophysin as well as other
neuroendocrine markers

303. Carcinoid tumors may arise anywhere in the gut however they most commonly arise in the small bowel

304. What is the most common malignancy in the small intestine? Carcinoid tumor

305. What neurotransmitter is often secreted by carcinoid tumors? Serotonin

306. The serotonin released from carcinoid tumors in the small bowel is metabolized in the liver by monoamine oxidase (MAO) producing 5-HIAA

307. Carcinoid tumors are characterized by increased excretion of 5-HIAA in the urine

308. Metastasis of carcinoid tumor to the liver allows serotonin to bypass first-pass metabolism and enter systemic circulation

309. The symptoms of carcinoid syndrome may be remembered with the mnemonic "Be FDR":
Be: bronchospasm F: flushing D: diarrhea R: right-sided heart disease

310. The symptoms of carcinoid syndrome may be triggered by alcohol or emotional stress which stimulate serotonin release from the tumor

311. Carcinoid syndrome may cause right-sided valvular heart lesions such as tricuspid regurgitation and pulmonic stenosis

312. Why are left-sided heart valve lesions NOT seen with Carcinoid syndrome? Lung contains MAO which metabolizes serotonin

313. Does carcinoid syndrome occur with carcinoid tumors that are limited to the GI tract? No

314. What vitamin deficiency may be caused by malignant carcinoid syndrome? Niacin (B3) deficiency

315. Carcinoid syndrome may be treated with surgical resection or with a somatostatin analog

316. Carcinoid syndrome is associated with the "rule of 1/3s"

317. Appendicitis is defined as acute inflammation of the appendix

318. Appendicitis is related to obstruction of the appendix by lymphoid hyperplasia (children)

319. Appendicitis in adults is typically related to obstruction of the appendix by a fecalith

320. Appendicitis presents with diffuse periumbilical pain that eventually localizes to McBurney's point

321. Appendicitis may lead to rupture resulting in peritonitis with guarding and rebound tenderness on physical exam

322. One sign of appendicitis is the obturator sign which is pain on passive flexion and internal rotation of the right hip

323. One sensitive sign of appendicitis and psoas abscess is the psoas sign which is pain on passive extension of the right hip

324. One sign of appendicitis is the Rovsing sign which is pain over the right iliac fossa with palpation of the left iliac fossa

325. Periappendiceal abscess is a common complication of appendicitis

326. What other pathologies should be on a differential when considering appendicitis? diverticulitis (elderly) and ectopic pregnancy

327. Inflammatory bowel disease classically presents in young women (gender) with recurrent bloody diarrhea and abdominal pain

328. Inflammatory bowel disease is more prevalent in the West particularly in caucasians and Eastern European Jews

329. Inflammatory bowel disease is subclassified as ulcerative colitis or Crohn disease

330. Which form of IBD involves only mucosal and submucosal ulcers? Ulcerative colitis

331. Which form of IBD involves transmural inflammation with "knife-like" fissures? Crohn disease

332. Ulcerative colitis (IBD) is characterized by continuous colonic lesions that always involve the rectum

333. Ulcerative colitis always involves the rectum and can extend proximally up to the cecum
334. Crohn disease (IBD) is characterized by skip lesions which can occur anywhere from the mouth to the anus

335. Crohn disease most commonly involves the terminal ileum

336. Crohn disease usually does NOT affect the rectum (rectal sparing)

337. Which form of IBD always causes bloody diarrhea? Ulcerative colitis

338. Which form of IBD may cause bloody or non-bloody diarrhea? Crohn disease

339. Ulcerative colitis is typically characterized by left lower quadrant pain (left or right)

340. Crohn disease is typically characterized by right lower quadrant pain (left or right)

341. Ulcerative colitis (IBD) is characterized histologically by crypt abscesses with neutrophils ulcers and bleeding

342. Crohn disease (IBD) is characterized histologically by lymphoid aggregates with noncaseating granulomas

343. Ulcerative colitis (IBD) is Th2 mediated

344. Crohn disease (IBD) is Th1 mediated

345. Crohn disease (IBD) appears grossly with cobblestone mucosa

346. Crohn disease (IBD) appears grossly with "creeping" fat

347. Crohn disease appears grossly with strictures (lumen size) and bowel wall thickening

348. Crohn disease (IBD) is associated with the "string" sign on imaging, secondary to strictures

349. Ulcerative colitis (IBD) appears grossly with friable mucosal pseudopolyps

350. Ulcerative colitis (IBD) is associated with the "lead pipe" sign on imaging, secondary to loss of haustra

351. Complications of both ulcerative colitis and Crohn disease include malabsorption and colorectal cancer

352. Risk for colorectal cancer development from IBD is based on extent of colonic involvement and duration of disease

353. Complications of ulcerative colitis include toxic megacolon which may perforate and fulminant colitis

354. Complications associated with Crohn disease (IBD) include gallstones and calcium oxalate nephrolithiasis

355. Which form of IBD is associated with fistula formation? Crohn disease

356. One complication of Crohn disease is enterovesical fistula which can cause UTI and pneumaturia

357. Which form of IBD is associated with perianal disease phlegmon/abscess formation and strictures? Crohn disease

358. Extraintestinal manifestations of IBD include arthritis such as ankylosing spondylitis sacroiliitis migratory polyarthritis and peripheral joints

359. Extraintestinal manifestations of IBD include rash such as erythema nodosum and pyoderma gangrenosum

360. Extraintestinal manifestations of IBD include eye inflammation such as uveitis and episcleritis

361. Extraintestinal manifestations of IBD include oral ulcerations (aphthous stomatitis)

362. Ulcerative colitis (IBD) is associated with primary sclerosing cholangitis

363. What biliary tract disease is associated with ulcerative colitis? Primary sclerosing cholangitis

364. Ulcerative colitis (IBD) may be associated with positive serum p-ANCA

365. Crohn disease (IBD) may be associated with positive serum anti-Saccharomyces cervisiae antibodies (ASCA)

366. Treatment for acute exacerbation of Crohn disease often involves corticosteroids

367. What 5-aminosalicylic preparations (2) are useful in the management of ulcerative colitis and Crohn disease? mesalamine and sulfasalazine

368. Treatment of IBD (Crohn's UC) may involve TNF-Œ± inhibitors such as infliximab and adalimumab

369. Treatment of IBD (Crohn's UC) may involve immunosuppressors such as azathioprine and 6-mercaptopurine

370. What treatment is curative for ulcerative colitis? Colectomy

371. Smoking is protective against ulcerative colitis (IBD)


372. Smoking increases risk for Crohn disease (IBD)

373. Hirschsprung disease is characterized by defective relaxation and peristalsis of the rectum and distal sigmoid colon

374. Hirschsprung disease is a congenital megacolon associated with Down syndrome

375. Hirschsprung disease occurs due to a congenital failure of ganglion cells to descend into the myenteric and submucosal plexus

376. The ganglion cells that fail to descend in Hirschsprung disease are derived from neural crest

377. Hirschsprung disease is associated with inactivating mutations in the RET gene

378. Hirschsprung disease is characterized by failure to pass meconium within 48 hours and chronic constipation

379. Hirschsprung disease may present with abdominal distention and bilious vomiting (bilious or nonbilious)

380. Hirschsprung disease is characterized by explosive expulsion of feces ("squirt sign") and an empty rectal vault on digital rectal exam

381. Hirschsprung disease is characterized by massive dilation of the bowel proximal to the aganglionic segment (proximal or distal), resulting in a
"transition zone"

382. Hirschsprung disease is diagnosed by absence of ganglionic cells on rectal suction biopsy

383. Treatment of Hirschsprung disease involves resection of the involved bowel

384. Colonic diverticula are "blind pouches" that communicate with the lumen of the gut

385. Are colonic diverticula typically true or false diverticula? False (only involves mucosa and submucosa)

386. Which gut wall layers are involved in a false diverticulum (psuedodiverticulum)? Mucosa and submucosa

387. Which gut wall layers are involved in a true diverticulum? All three (mucosa submucosa muscularis externa)

388. GI tract diverticula classically arise where the vasa recta perforates the muscularis propria (weak point in colonic wall)

389. Diverticulosis is characterized by many false diverticula in the colon

390. What is the most common location for diverticulosis? Sigmoid colon

391. Diverticulosis is related to wall stress (pulsion diverticulosis) (e.g. constipation straining low fiber diet) and obesity

392. Diverticulosis is associated with low fiber diets

393. What demographic (age group) is commonly associated with diverticulosis? Older adults (risk increases with age)

394. Diverticulosis is usually asymptomatic or associated with vague discomfort

395. Complications of diverticulosis include painless rectal bleeding (hematochezia)

396. Diverticulitis is a complication of diverticulosis due to inflammation of diverticula

397. Diverticulitis classically presents with a triad of LLQ pain fever and leukocytosis

398. What GI tract pathology presents with appendicitis-like symptoms in the LLQ? Diverticulitis

399. Diverticulitis may lead to a colovesical fistula which presents with pneumaturia (e.g. air or stool in the urine)

400. Complications of diverticulitis include abscess perforation and obstruction (inflammatory stenosis)

401. What is the general treatment for diverticulitis? Antibiotics

402. Angio-dysplasia is an acquired malformation resulting in tortuous dilation of vessels of the GI tract

403. Angiodysplasia usually arises in the cecum and right colon (right or left) due to high wall tension

404. Angiodysplasia classically presents as hematochezia in an older adult

405. Angiodysplasia is confirmed by angiography

406. Hereditary hemorrhagic telangiectasia is an autosomal dominant (inheritance) disorder resulting in thin-walled blood vessels especially in
the mouth and GI tract

407. Hereditary hemorrhagic telangiectasia is also known as Osler-Weber-Rendu syndrome


408. Hereditary hemorrhagic telangiectasia presents with blanching skin lesions AV malformations recurrent epistaxis skin discoloration GI
bleeding and hematuria

409. Ischemic colitis is caused by ischemic damage to the colon

410. Ischemic colitis usually occurs at the splenic flexure (griffith's point) which is the watershed area of the SMA and the IMA

411. Ischemic colitis is most commonly due to atherosclerosis of the SMA

412. Ischemic colitis presents with post-prandial abdominal pain followed by hematochezia

413. Ischemic colitis may present with the "thumbprint" sign on imaging due to mucosal edema/hemorrhage

414. Irritable bowel syndrome is recurrent abdominal pain with > 2 of the following: - Pain improves with defecation - Change in stool frequency -
Change in stool consistency

415. What demographic is most commonly associated with irritable bowel syndrome? Middle-aged women

416. The chronic symptoms of irritable bowel syndrome may be diarrhea-predominant constipation-predominant or mixed

417. Is irritable bowel syndrome related to structural abnormalities? No

418. The first line treatment for Irritable bowel syndrome is lifestyle modification and increased dietary fiber

419. Colonic polyps are raised protrusions of colonic mucosa

420. Colonic polyps are grossly characterized as flat sessile or pedunculated (on a stalk)

421. Hyperplastic colonic polyps are due to hyperplasia of glands

422. Hyperplastic colonic polyps classically show a "serrated" appearance on microscopy

423. What is the most common type of colonic polyp? Hyperplastic polyp

424. Hyperplastic colonic polyps are usually small (size) and located in the rectosigmoid region

425. Hyperplastic colonic polyps are benign with no malignant potential

426. Hamartomatous colonic polyps are growths of normal colonic tissue with distorted architecture

427. Do hamartomatous colonic polyps have significant risk of malignant transformation? No

428. What type of colonic polyp is small (< 5 mm) and resembles normal mucosa? Mucosal polyps (clinically insignificant)

429. What type of colonic polyp is a result of mucosal erosion from inflammatory bowel disease? Inflammatory pseudopolyp

430. What type of colonic polyp may include lesions such as lipomas leiomyomas fibromas and others? Submucosal polyps

431. Adenomatous colonic polyps are due to a neoplastic proliferation of glands

432. Adenomatous colonic polyps are benign with some malignant potential

433. Adenomatous colonic polyps may progress to adenocarcinoma via the adenoma-carcinoma sequence

434. The adenoma-carcinoma sequence begins with APC gene mutations

435. Which adenoma-carcinoma sequence mutation results in increased risk for polyp formation? APC mutation

436. Following APC mutation (adenoma-carcinoma sequence) KRAS mutations lead to polyp formation (adenoma)

437. What type of gene is the APC gene? Tumor suppressor gene

438. Progression of colonic adenoma to carcinoma occurs with mutations in the p53 or loss of heterozygosity in the region that encodes
for SMAD 2 / 4

439. Progression of colonic adenomas to carcinoma is associated with overexpression of COX-2

440. What drug class may be used to impede progression of colonic adenoma to carcinoma? NSAIDs (e.g. aspirin)

441. Sessile serrated colonic polyps have a "saw-tooth" pattern similar to hyperplastic polyps, but extend to the crypts and involve lateral crypt
growth

442. Serrated colonic polyps are benign with some malignant potential


443. Serrated colonic poylps may develop into CRC via CpG hypermethylation with microsatellite instability and mutations in BRAF

444. Screening for colorectal polyps/carcinoma is performed by colonoscopy and testing for fecal occult blood (stool guiaic test)

445. Can an adenomatous polyp be distinguished from a hyperplastic polyp on gross examination (e.g. colonoscopy)? No (thus remove all polyps)

446. Which type of polyp has greater malignant potential sessile or pedunculated? Sessile

447. Colonic polyps have a greater risk of progression to carcinoma if they are > 2 cm in size

448. Adenomatous polyps with a tubular histology have less malignant potential than villous histology (tubular or villous)

449. Familial adenomatous polyposis (FAP) is an autosomal dominant (inheritance) disorder characterized by 100s to 1000s of adenomatous
colonic poylps

450. Familial adenomatous polyposis (FAP) is due to an inherited mutation in the APC gene on chromosome 5q

451. Colorectal cancer arises in patients with familial adenomatous polyposis via the "2-hit hypothesis"

452. Familial adenomatous polyposis is pancolonic and always involves the rectum

453. Familial adenomatous polyposis is treated with prophylactic colectomy or else 100% of patients progress to CRC

454. Gardner syndrome is a combination of familial adenomatous polyposis with osteomas and fibromatosis

455. Turcot syndrome is a combination of familial adenomatous polyposis with malignant CNS tumors (e.g. medulloblastoma glioma)

456. Juvenile polyps usually present in childhood as a solitary rectal polyp that prolapses and bleeds

457. Juvenile polyposis syndrome is characterized by numerous harmatomatous polyps WITHOUT hyperpigmentation

458. What demographic (age group) is associated with juvenile polyposis syndrome? Children < 5 years old

459. Juvenile polyposis syndrome is characterized by many juvenile polyps in the stomach colon and small bowel

460. Juvenile polyposis syndrome is associated with increased risk for colorectal carcinoma

461. Peutz-Jeghers syndrome is characterized by numerous harmatomatous polyps WITH hyperpigmentation of the lips mouth hands and genital
skin

462. Peutz-Jeghers syndrome is associated with increased risk of breast GI and gynecologic cancers

463. Colorectal carcinoma is the third most common cause of cancer-related death

464. The peak incidence of colorectal carcinoma is 60 - 70 years of age

465. FAP and most sporadic colorectal carcinomas arise via the chromosomal instability pathway

466. Lynch syndrome and some sporadic colorectal carcinomas arise via the microsatellite instability pathway

467. Microsatellites are repeating sequences of non-coding DNA (coding or non-coding)

468. The microsatellite instability pathway of colorectal cancer is characterized by mutations or methylation of mismatch repair genes

469. Lynch syndrome is due to an inherited defect in DNA mismatch repair enzymes resulting in microsatellite instability

470. Lynch syndrome was previously known as hereditary nonpolyposis colorectal cancer (HNPCC)

471. What is the mode of inheritance of Lynch syndrome (HNPCC)? Autosomal dominant

472. Lynch syndrome progresses to colorectal cancer in ~ 80% of patients

473. Lynch syndrome is usually right-sided and always involves the proximal colon (proximal or distal)

474. Lynch syndrome is associated with increased risk for colorectal endometrial ovarian and skin cancers

475. Screening for colorectal carcinoma in low-risk patients begins at 50 years of age (e.g. colonoscopy fecal occult blood (stool guiaic test))

476. 25% of colorectal cancers arise in patients with a positive family history

477. Patients with a first-degree relative with colon cancer should be screened via colonoscopy starting at age 40 or starting 10 years prior to their
relative's presentation

478. Risk factors for colorectal carcinoma include adenomatous and serrated polyps


479. Risk factors for colorectal carcinoma include tobacco use

480. Risk factors for colorectal carcinoma include diets with processed meat and low fiber

481. Which part of the colon does colorectal carcioma most commonly arise? Rectosigmoid region

482. Left-sided colorectal carcinoma usually grows as a "napkin-ring (infiltrating)" lesion

483. Left-sided colorectal carcinoma presents with decreased stool caliber due to partial obstruction

484. Left-sided colorectal carcinoma presents with colicky pain and hematochezia (stool)

485. Left-sided colorectal carcinoma usually arises as a result of the adenoma-carcinoma sequence

486. Right-sided colorectal carcinoma usually grows as a raised (exophytic) mass

487. Right-sided colorectal carcinoma presents with vague pain weight loss and iron deficiency anemia

488. Right-sided colorectal carcinoma usually arises as a result of the microsatellite instability pathway

489. Iron deficiency anemia in males (especially > 50) and postmenopausal females raises suspicion of colorectal carcinoma

490. Colorectal carcinoma rarely presents with Streptococcus bovis (gallolyticus) bacteremia

491. Colorectal carcinoma may be visualized as an "apple core" lesion seen on barium enema X-ray

492. The T of TNM staging for colorectal carcinoma represents the depth of invasion

493. The N of TNM staging for colorectal carcinoma represents regional lymph node involvement

494. The M of TNM staging for colorectal carcinoma represents distant metastasis

495. Colorectal cancer most commonly metastasizes to the liver

496. What tumor marker is useful for assessing treatment response and recurrence of colorectal carcinoma? CEA

497. Is the CEA tumor marker useful for screening for colorectal carcinoma? No

498. Is the CEA tumor marker useful for monitoring recurrence of colorectal carcinoma? Yes

499. Adhesions are fibrous bands of scar tissue that commonly form after GI surgery

500. What is the most common cause of small bowel obstruction? Adhesion

501. Ileus is an intestinal hypomotility without obstruction that results in constipation and decreased flatus

502. Ileus is associated with a distended/tympanic abdomen and decreased bowel sounds

503. Treatment of ileus includes bowel rest electrolyte correction and cholinergic drugs (stimulate intestinal motility)

504. Meconium ileus is characterized by a meconium plug that obstructs the intestine preventing stool passage at birth

505. Necrotizing enterocolitis is a GI pathology seen in premature formula-fed infants with immature immune systems

506. Necrotizing enterocolitis (NEC) is characterized by necrosis of intestinal mucosa with possible perforation which can lead to: - free air in the
bowel wall (pneumatosis intestinalis) - free air in the abdomen (pneumoperitoneum) - portal venous gas on imaging

507. Acute pancreatitis is due to autodigestion of pancreatic parenchyma by pancreatic enzymes

508. In acute pancreatitis trypsin is prematurely activated which leads to activation of other pancreatic enzymes

509. Acute pancreatitis results in liquefactive necrosis of the pancreas

510. Acute pancreatitis results in fat necrosis of the peripancreatic fat

511. Acute pancreatitis is most commonly due to alcohol or gallstones

512. The causes of acute pancreatitis may be remembered with the mnemonic "I GET PP SMASHED":
I: Idiopathic G: Gallstones E: Ethanol T: Trauma (e.g. automobile accident in children - seatbelt injury) P: Posterior duodenal ulcer
rupture P: Pancreas Divisum S: Steroids M: Mumps A: Autoimmune disease S: {{c8::Scorpion sting
H: HYPERcalcemia or Hypertriglyceridemia/Hyperchylomicronemia E: ERCP (endoscopic retrograde
cholangiopancreatography) D: Drugs (e.g. sulfa drugs, NRTIs, protease inhibitors)
513. Acute pancreatitis is diagnosed by 2 of 3 criteria: - Acute epigastric pain that radiates to the back - Increased serum amylase or lipase to 3x
upper limit of normal - Characteristic imaging findings

514. One criteria for diagnosis of acute pancreatitis is acute epigastric abdominal pain that radiates to the back

515. One criteria for diagnosis of acute pancreatitis is increased serum amylase or lipase

516. Which pancreatic enzyme (amylase or lipase) is more specific for acute pancreatitis? Lipase

517. Acute pancreatitis may present with hypo-calcemia

518. Acute pancreatitis may progress to shock due to pancreatic hemorrhage and fluid sequestration

519. Acute pancreatitis may be complicated by pancreatic pseudocysts which are formed by fibrous tissue surrounding liquefactive necrosis and
pancreatic enzymes

520. Pancreatic pseudocyst presents as an abdominal mass with persistently elevated serum amylase

521. Pancreatic pseudocysts may rupture causing hemorrhage and release of enzymes into the abdominal cavity

522. Pancreatic abscess presents with abdominal pain high fever and persistently elevated serum amylase

523. Pancreatic abscess is often due to E. coli infection

524. Complications of acute pancreatitis include DIC due to activation of coagulation factors

525. Complications of acute pancreatitis include ARDS due to damage to the alveolar capillary interface

526. Chronic pancreatitis is characterized by fibrosis of pancreatic parenchyma

527. Chronic pancreatitis is most often secondary to recurrent acute pancreatitis

528. What are the major causes of chronic pancreatitis in adults? alcohol and genetic predisposition (ex. Cystic Fibrosis)

529. What is the most common cause of chronic pancreatitis in children? cystic fibrosis

530. Pancreatitis (acute and chronic) may present with epigastric abdominal pain that radiates to the back

531. Chronic pancreatitis may present with pancreatic insufficiency which results in malabsorption with steatorrhea and fat-soluble vitamin
deficiences

532. Are serum amylase and lipase useful serum markers for chronic pancreatitis? No (may or may not be elevated)

533. Chronic pancreatitis is characterized by atrophy and dystrophic calcification of pancreatic parenchyma on imaging

534. Contrast studies of chronic pancreatitis reveal a "chain of lakes" pattern due to dilatation of pancreatic ducts

535. What endocrine pathology may arise secondary to chronic pancreatitis? Diabetes mellitus

536. Chronic pancreatitis results in increased risk for pancreatic carcinoma

537. What type of cancer (e.g. SCC adenocarcinoma etc.) is pancreatic carcinoma? Adenocarcinoma

538. Pancreatic adenocarcinoma is a very aggressive tumor arising from the pancreatic ducts (ducts or acini)

539. What age group is most commonly affected by pancreatic adenocarcinoma? Elderly

540. The major risk factors for pancreatic adenocarcinoma are - smoking - chronic pancreatitis (especially > 20 years)

541. Pancreatic adenocarcinoma is more common in Jewish and African American males (ethnicity and gender)

542. What endocrine pathology is a risk factor for pancreatic adenocarcinoma? Diabetes mellitus

543. Pancreatic adenocarcinoma often presents with epigastric abdominal pain that radiates to the back

544. Pancreatic adenocarcinoma often presents with weight loss secondary to malabsorption and anorexia

545. Pancreatic adenocarcinoma often presents as obstructive jaundice with a painless palpable gallbladder

546. A painless palpable gallbladder in pancreatic adenocarcinoma is also known as the Courvoisier sign

547. Pancreatic adenocarcinoma most commonly arises in the head of the pancreas

548. Pancreatic adenocarcinoma in the body or tail may present with secondary diabetes mellitus
549. Pancreatic adenocarcinoma may present with migratory thrombophlebitis which is redness and tenderness in the extremities

550. Migratory thrombophlebitis in pancreatic adenocarcinoma is also known as the Trousseau sign

551. Pancreatic adenocarcinoma is associated with the serum tumor markers CA 19-9 and CEA (less specific)

552. Treatment of pancreatic adenocarcinoma includes the Whipple procedure chemotherapy and radiation

553. What surgical procedure involves the en bloc removal of the head/neck of the pancreas proximal duodenum and gallbladder? Whipple
procedure

554. What is the prognosis of pancreatic adenocarcinoma? Very poor (1-year survival < 10%)

555. Cholelithiasis (gallstones) are solid round stones in the gallbladder

556. Cholelithiasis may arise due increased cholesterol or bilirubin in bile

557. Cholelithiasis may arise due to decreased phospholipids and/or bile acids

558. Cholelithiasis may arise due to stasis of the gallbladder

559. There are two types of gallstones: cholesterol and pigmented

560. Which type of gallstone is the most common especially in the West? Cholesterol stone (80%)

561. Are cholesterol gallstones typically radiolucent or radiopaque? Radiolucent

562. ~ 10 - 20% of cholesterol gallstones are radiopaque due to calcifications

563. Risk factors for cholesterol gallstones may be remembered with the "4 F's": 1. Fat 2. Female (estrogen increases activity of HMG-CoA
reductase) 3. Fertile (pregnant) 4. Forty

564. What classes (2) of lipid lowering drugs are associated with cholesterol gallstone formation? fibrates and bile acid resins

565. Cholesterol gallstones are more common in people of Native American descent

566. Which type of gallstone (cholesterol or pigment) is associated with rapid weight loss? Cholesterol gallstone

567. Which form of IBD has increased risk for gallstones (both cholesterol and pigment)? Crohn disease

568. Black pigment gallstones (color) are radio-opaque and composed of calcium bilirubinate

569. Brown pigment gallstones (color) are radio-lucent and arise with biliary tract infection

570. Biliary tract infections may cause pigment gallstones by deconjugating bilirubin which increases risk of precipitation

571. Which type of gallstone is associated with extravascular hemolysis? Bilirubin (pigment) stones

572. Ascaris lumbricoides is a common roundworm that infects the biliary tract increasing the risk for gallstones

573. Clonorchis sinensis is a liver fluke that infects the biliary tract increasing the risk for gallstones cholangitis and cholangiocarcinoma

574. Which type of gallstone is associated with alcoholic cirrhosis? Pigment stones

575. Which type of gallstone is associated with total parenteral nutrition (TPN)? Cholesterol stones

576. The most common gallstone complication is cholecystitis

577. What imaging technique is used to diagnose gallstones? Ultrasound

578. Gallstones may be treated with elective cholecystectomy if symptomatic

579. Biliary colic is a waxing and waning right upper quadrant pain associated with gallstones; may also have nausea and vomiting

580. Biliary colic occurs due to gallbladder contraction against a stone lodged in the cystic duct

581. Cholecystitis is an acute or chronic inflammation of the gallbladder with gallbladder wall thickening

582. Is cholecystitis typically calculous or acalculous? Calculous

583. Calculous cholecystitis results from an impacted stone in the cystic duct resulting in dilatation with inflammation and bacterial overgrowth

584. What bacteria is a common cause of secondary infection in calculous cholecystitis? E. coli
585. Acalculous cholecystitis is due to gallbladder stasis hypoperfusion or infection (no obstruction); seen in critically ill patients

586. What infection is associated with acalculous cholecystitis? CMV

587. Acute cholecystitis presents with RUQ pain that often radiates to the right scapula

588. Cholecystitis may present with elevated serum alkaline phosphatase if the bile duct is involved

589. Cholecystitis is associated with a positive Murphy's sign which is inspiratory arrest on RUQ palpation due to pain

590. Rokitansky-Aschoff sinus is a herniation of gallbladder mucosa into the muscular wall associated with chronic cholecystitis

591. Chronic cholecystitis presents with vague RUQ pain especially after eating

592. Cholecystitis is diagnosed with ultrasound or HIDA scan

593. Porcelain gallbladder is a calcified gallbladder that results from chronic cholecystitis

594. Porcelain gallbladder is a shrunken hard gallbladder due to chronic inflammation fibrosis and dystrophic calcification

595. Porcelain gallbladder is treated with prophylactic cholecystectomy due to high rates of gallbladder cancer (mostly adenocarcinoma)

596. Ascending cholangitis is a bacterial infection of the bile ducts

597. Ascending cholangitis is usually due to ascending infection with enteric gram-negative bacteria

598. Ascending cholangitis classically presents with the Charcot triad of jaundice fever and RUQ pain

599. In addition to the Charcot triad Ascending cholangitis may also present with altered mental status and shock (Reynolds pentad)

600. There is an increased incidence of ascending cholangitis with choledocholithiasis (stones in the biliary ducts)

601. Choledocholithiasis is the presence of gallstones in the common bile duct often leading to elevated ALP GGT direct bilirubin and/or AST/ALT

602. Gallstone ileus typically involves obstruction of the ileocecal valve by a gallstone

603. Gallstone ileus occurs secondary to cholecystitis with fistula formation between the gallbladder and small bowel

604. Cholecystitis can cause fistula formation with the GI tract resulting in air in the biliary tree (pneumobilia)

605. What type of cancer (e.g. SCC adenocarcinoma etc.) is gallbladder carcinoma? Adenocarcinoma

606. The major risk factor for gallbladder carcinoma is gallstones especially when complicated by porcelain gallbladder

607. Gallbladder carcinoma classically presents as new-onset cholecystitis in an elderly woman (gender)

608. What is the prognosis of gallbladder carcinoma? Poor

609. What is the mode of inheritance of juvenile polyposis syndrome? Autosomal dominant

610. What is the mode of inheritance of Peutz-Jeghers syndrome? Autosomal dominant

611. Jaundice is a yellow discoloration of the skin and/or sclera

612. What is the earliest sign of jaundice? Scleral icterus

613. Jaundice is due to increased serum bilirubin typically > 2.5 mg/dL

614. Does hemolysis result in unconjugated or conjugated hyperbilirubinemia? Unconjugated

615. Hemolysis is associated with dark urine due to increased urine urobilinogen

616. Physiological neonatal jaundice occurs due to transiently low UDP-glucuronyl transferase activity at birth

617. Does physiological neonatal jaundice result in unconjugated or conjugated hyperbilirubinemia? Unconjugated

618. In physiological neonatal jaundice unconjugated bilirubin deposits in the brain especially in the basal ganglia

619. Kernicterus is the deposition of bilirubin in the brain especially basal ganglia causing neurologic deficits and possibly death

620. What is the treatment for physiologic neonatal jaundice? non-UV phototherapy

621. How does phototherapy treat neonatal jaundice? Isomerize UCB to water-soluble form

622. What is the mode of inheritance of hereditary hyperbilirubinemias (e.g. Gilbert Crigler-Najjar Dubin-Johnson)? Autosomal recessive
623. Gilbert syndrome is due to mildly low UDP-glucuronyl transferase activity

624. Gilbert syndrome presents with jaundice during stress illness or fasting

625. Does Gilbert syndrome result in unconjugated or conjugated hyperbilirubinemia? Unconjugated

626. Crigler-Najjar syndrome is due to absent UDP-glucuronyl transferase activity

627. Does Crigler-Najjar syndrome result in unconjugated or conjugated hyperbilirubinemia? Unconjugated

628. Crigler-Najjar syndrome causes jaundice and kernicterus early in life; patients often die within a few years

629. Which form of Crigler-Najjar syndrome is more severe? Type I

630. What are the treatments (2) for Crigler-Najjar syndrome type I? plasmapheresis and phototherapy

631. Crigler-Najjar syndrome type II is less severe and responds to phenobarbital which increases liver enzyme synthesis

632. Dubin-Johnson syndrome is due to a deficiency of bilirubin canalicular transport protein

633. Does Dubin-Johnson syndrome result in unconjugated or conjugated hyperbilirubinemia? Conjugated

634. Dubin-Johnson syndrome presents with a grossly black liver but is otherwise not clinically significant

635. Rotor syndrome is similar to Dubin-Johnson syndrome but milder and WITHOUT black liver

636. Does Rotor syndrome result in unconjugated or conjugated hyperbilirubinemia? Conjugated

637. What type of jaundice is associated with gallstones parasites and liver fluke? Obstructive jaundice

638. What type of jaundice is associated with cholangiocarcinoma and pancreatic carcinoma? Obstructive jaundice

639. Does biliary tract obstruction (obstructive jaundice) result in unconjugated or conjugated hyperbilirubinemia? Conjugated

640. Obstructive jaundice is associated with dark urine due to increased urine conjugated bilirubin

641. Obstructive jaundice is associated with decreased urine urobilinogen

642. Obstructive jaundice is associated with pale stools

643. Obstructive jaundice is associated with increased serum bile acids which may cause pruritus

644. Obstructive jaundice is associated with hypercholesterolemia which may cause xanthomas

645. Obstructive jaundice is associated with steatorrhea with malabsorption of fat-soluble vitamins

646. Does viral hepatitis result in unconjugated or conjugated hyperbilirubinemia? Both :)

647. Viral hepatitis is associated with dark urine due to increased urine conjugated bilirubin

648. Viral hepatitis is associated with normal or decreased urine urobilinogen

649. In addition to hepatitis virus viral hepatitis may also be caused by EBV and CMV

650. Viral hepatitis is characterized by elevated liver enzymes with ALT > AST

651. Acute hepatitis is associated with inflammation that involves the lobules of the liver and portal tracts; characterized by apoptosis of hepatocytes

652. Chronic hepatitis is associated with inflammation that primarily involves the portal tracts

653. Cirrhosis is characterized by disruption of normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes

654. The fibrosis seen in cirrhosis is mediated by TGF-Œ≤ from stellate (ito) cells

655. Alcoholic cirrhosis may be associated with sclerosis around central veins in early disease

656. Cirrhosis is often complicated by portal hypertension

657. Does cirrhosis result in unconjugated or conjugated hyperbilirubinemia? Both :)

658. What is the most common cause of portal hypertension in Western countries? Cirrhosis

659. Portal hypertension may be caused by vascular obstruction such as portal vein thrombosis and Budd-Chiari syndrome

660. What parasitic infection is associated with portal hypertension? Schistosomiasis


661. Portal hypertension can lead to ascites which is fluid in the peritoneal cavity

662. Portal hypertension may lead to portosystemic shunts which can result in esophageal varices gastric varices anorectal varices and caput
medusae

663. Portal hypertension may lead to congestive splenomegaly and hypersplenism

664. Hepatorenal syndrome is a complication of portal hypertension characterized by rapidly developing renal failure secondary to cirrhosis

665. Cirrhosis may present with neuropsychiatric symptoms due to increased serum ammonia (NH3)

666. Neuropsychiatric symptoms of cirrhosis include hepatic encephalopathy and asterixis ("flapping tremor")

667. Is hepatic encephalopathy reversible or irreversible? Reversible

668. Hepatic encephalopathy may be triggered by increased NH3 production or absorption such as increased dietary protein

669. Hepatic encephalopathy may be triggered by decreased NH3 removal such as renal failure

670. What antibiotics (2) are used to treat hepatic encephalopathy? rifaximin and neomycin

671. What osmotic laxative is used to treat hepatic encephalopathy? Lactulose

672. Dermatologic symptoms of cirrhosis include jaundice spider angiomas palmar erythema and petechiae/purpura

673. How do levels of estrogen change in cirrhosis? Increased

674. Increased estrogen in cirrhosis may lead to spider angiomas and palmar erythema (dermatologic symptoms)

675. Increased estrogen in cirrhosis may lead to gynecomastia testicular atrophy and amenorrhea (reproductive symptoms)

676. Cirrhosis may present with peripheral edema secondary to hypoalbuminemia

677. Cirrhosis may present with coagulopathies due to decreased synthesis of clotting factors

678. Is liver failure followed with PT or PTT? PT

679. What odor may be associated with cirrhosis? Fetor hepaticus

680. What is the most common cause of liver disease in the West? Alcohol consumption

681. Which alcoholic liver disease is characterized by macrovesicular fatty change with a heavy greasy liver? Hepatic steatosis

682. Hepatic steatosis is characterized by macro-vesicular fatty change

683. Which form of alcoholic liver disease may be reversible with abstinence? Hepatic steatosis

684. Alcoholic hepatitis is characterized by swelling of hepatocytes with necrosis and neutrophilic infiltration

685. Alcoholic hepatitis is characterized histologically by mallory bodies which are intracytoplasmic eosinophilic inclusions of damaged keratin
(intermediate) filaments

686. The liver damage in alcoholic hepatitis is mediated by acetaldehyde

687. Alcoholic hepatitis may present with painful hepatomegaly (painful or painless)

688. Alcoholic hepatitis is characterized by elevated liver enzymes with ALT < AST

689. Non-alcoholic fatty liver disease is associated with obesity and metabolic syndrome

690. Nonalcoholic fatty liver disease is characterized by fatty infiltration of hepatocytes with cellular "ballooning" and eventual necrosis

691. Nonalcoholic fatty liver disease is characterized by elevated liver enzymes with ALT > AST

692. Hemochromatosis is characterized by organ damage secondary to excess iron

693. The tissue damage in hemochromatosis is mediated by the generation of free radicals

694. Hemochromatosis may be primary; due to autosomal recessive (inheritance) mutations in iron absorption

695. Hemochromatosis typically presents after age 40 when total body iron > 20g

696. Hemochromatosis has a slowed progression in women (gender)


697. Why does hemochromatosis have a slowed progression in women? Iron loss through menstruation

698. Hemochromatosis may be secondary; due to chronic transfusions

699. Primary hemochromatosis is due to mutations in the HFE gene on chromosome 6 leading to increased expression of DMT1 and decreased
synthesis of Hepcidin

700. Hemochromatosis is associated with HLA-A3

701. What point mutations in the HFE gene are typically seen with primary hemochromatosis? C282Y (more common) and H63D

702. Hemochromatosis classically presents with a triad of cirrhosis diabetes mellitus and bronze skin

703. Hemochromatosis can cause restrictive cardiomyopathy (classically) or dilated cardiomyopathy

704. Hemochromatosis may cause gonadal dysfunction due to testicular atrophy

705. Hemochromatosis may cause arthropathy especially in metacarpophalangeal (MCP) joints

706. The arthropathy in hemochromatosis occurs due to calcium pyrophosphate deposition

707. What is a common cause of death in hemochromatosis? Hepatocellular carcinoma

708. Hemochromatosis is characterized by increased ferritin

709. Hemochromatosis is characterized by decreased TIBC

710. Hemochromatosis is characterized by increased serum iron

711. Hemochromatosis is characterized by increased % saturation

712. Liver biopsy of a patient with hemochromatosis reveals accumulation of brown pigment (color) in hepatocytes

713. The coarse yellowish-brown pigment in hepatocytes / kupffer cells from hemochromatosis may be distinguished from lipofuscin by staining
with Prussian blue

714. Lipofuscin is a yellow-brown "wear and tear" pigment associated with normal aging

715. Which part of the cell does lipofuscin accumulate? Lysosomes

716. Treatment for hemochromatosis may include repeated phlebotomy

717. What type of drug are deferasirox deferoxamine and deferiprone (oral)? Iron chelators

718. What GI disorder may be treated with deferasirox deferoxamine and oral deferiprone? Hemochromatosis

719. Wilson disease is caused by an autosomal recessive (inheritance) defect in ATP-mediated hepatocyte copper transport

720. Wilson disease is due to mutations in the ATP7B gene on chromosome 13

721. Wilson disease results in lack of copper transport into bile and lack of incorporation into ceruloplasmin

722. Wilson disease is also known as hepatolenticular degeneration

723. Wilson disease is characterized by accumulation of copper especially in the liver brain cornea and kidneys

724. Wilson disease typically presents before age 40

725. Wilson disease often presents with cirrhosis due to copper accumulation in the liver

726. Wilson disease often presents with neuropsychiatric manifestations due to copper deposition and resultant cystic degeneration in
the putamenand other adjacent structures

727. Wilson disease presents with Kayser-Fleisher rings due to copper deposits in Descemet's membrane of the cornea

728. Wilson disease may present with renal disease such as Fanconi syndrome

729. Wilson disease is characterized by decreased serum ceruloplasmin

730. Wilson disease is characterized by increased urinary copper

731. What type of drug are penicillamine and trientine? Copper chelators

732. Wilson disease may be treated with oral zinc or chelating agents (e.g. penicillamine trientine)
733. Biliary tract diseases (e.g. PSC PBC) present with features of obstructive jaundice

734. Does biliary tract disease (e.g. PBC PSC) result in unconjugated or conjugated hyperbilirubinemia? Conjugated

735. Biliary tract diseases (e.g. PBC PSC) are associated with increased serum cholesterol

736. Primary biliary cholangitis is an autoimmune granulomatous destruction of intra-hepatic bile ducts

737. Does primary biliary cholangitis (PBC) effect intra- or extrahepatic bile ducts? Intrahepatic

738. Histologically Primary biliary cholangitis is characterized by lymphocytic infiltrate and granulomas

739. What demographic is classically affected by primary biliary cholangitis (PBC)? Middle-aged women (~ 40 y.o)

740. Which biliary tract disease is classically seen in middle-aged women and presents with generalized pruritis and fatigue? Primary biliary
cholangitis (PBC)

741. Primary biliary cholangitis is associated with other autoimmune diseases

742. Primary biliary cholangitis (PBC) is associated with anti-mitochondrial antibody

743. Which biliary tract disease is caused by extrahepatic biliary obstruction? Secondary biliary cholangitis

744. Secondary biliary cholangitis occurs in patients with known obstructive lesions (e.g. gallstones biliary strictures pancreatic carcinoma)

745. Secondary biliary cholangitis may be complicated by ascending cholangitis

746. Primary sclerosing cholangitis is characterized by inflammation and fibrosis of both intra- and extrahepatic bile ducts

747. Does primary sclerosing cholangitis (PSC) effect intra- or extrahepatic bile ducts? Both :)

748. Primary sclerosing cholangitis causes periductal fibrosis with an "onion-skin" appearance histologically

749. Primary sclerosing cholangitis is characterized by a "beading" appearance of intra- and extrahepatic bile ducts on ERCP and MRCP

750. What demographic is classically affected by primary sclerosing cholangitis (PSC)? Middle-aged men (classically with IBD)

751. Primary sclerosing cholangitis is associated with p-ANCA antibody

752. Primary sclerosing cholangitis and primary biliary cholangitis are associated with increased serum IgM

753. Primary sclerosing cholangitis is associated with increased risk for cholangiocarcinoma and gallbladder cancer

754. What is a late complication associated with biliary tract disease (e.g. PBC PSC)? Cirrhosis

755. Reye syndrome is fulminant liver failure and encephalopathy in children with viral illness who take aspirin

756. Reye syndrome may occur due to decreased Œ≤-oxidation secondary to reversible inhibition of mitochondrial enzymes in hepatocytes by
aspirin metabolites

757. Reye syndrome presents with micro-vesicular fatty change in the liver hypoglycemia vomiting hepatomegaly and eventually coma/death

758. What viruses classically cause Reye syndrome when treated with aspirin? Influenza B and VZV

759. Hepatic adenomas are rare benign tumors associated with OCP and anabolic steroid use; regress upon cessation of drug

760. Hepatic adenomas may rupture causing intraperitoneal bleeding especially during pregnancy

761. Hepatic adenomas are subcapsular tumors and grow with exposure to estrogen

762. Hepatic angiosarcoma is a malignant tumor associated with exposure to arsenic and vinyl chloride

763. Cavernous hemangiomas are common benign tumors involving the deeper tissues of the body (ex. liver brain) that typically occur from age 30
- 50 years

764. Cavernous hemangiomas should NOT be biopsied due to risk of fatal hemorrhage

765. Hepatocellular carcinoma (hepatoma) is the most common primary malignant liver tumor in adults

766. Risk factors for hepatocellular carcinoma include chronic hepatitis (e.g. HBV HCV)

767. Risk factors for hepatocellular carcinoma include causes of cirrhosis (e.g. alcohol NAFLD hemochromatosis Wilson disease A1AT deficiency)

768. Risk factors for hepatocellular carcinoma include aflatoxins derived from Aspergillus


769. Hepatocellular carcinoma increases risk for Budd-Chiari syndrome

770. In addition to HCC Budd-Chiari syndrome may also be seen with hypercoaguable and post-partum states

771. What myeloproliferative disorder is associated with Budd-Chiari syndrome? Polycythemia vera

772. Budd-Chiari syndrome is liver infarction secondary to hepatic vein obstruction

773. Budd-Chiari syndrome presents with painful hepatomegaly (painful or painless) ascites varices and liver failure

774. Budd-Chiari syndrome results in congestion and necrosis of the centrilobular zone of the liver

775. Does Budd-Chiari syndrome present with jugular venous distention (JVD)? No

776. Budd-Chiari syndrome is associated with a characteristic "nutmeg" appearance of the liver

777. How does hepatocellular carcinoma spread? Hematogenously

778. What is the serum tumor marker for hepatocellular carcinoma? alpha-fetoprotein

779. Which is more common primary liver tumors or metastasis to the liver? Metastasis

780. Does metastasis to the liver typically present as a single or multiple nodules? Multiple

781. Metastasis to the liver may be detected clinically as hepatomegaly with a nodular free edge of the liver

782. Spontaneous (primary) bacterial peritonitis is a common potentially fatal bacterial infection in patients with cirrhosis and ascites

783. Spontaneous bacterial peritonitis is commonly caused by aerobic gram negative organisms especially E. coli and Klebsiella

784. Spontaneous bacterial peritonitis is diagnosed by paracentesis with ascitic fluid absolute neutrophil count > 250 cells/mm3

785. AST > ALT in nonalcoholic liver disease suggests progression to advanced fibrosis or cirrhosis

786. Which liver enzyme is increased in cholestasis (e.g. biliary obstruction) infiltrative disorders and bone disease? Alkaline phosphatase

787. Which liver enzyme is increased in various liver/biliary diseases but NOT in bone disease? Œ≥-glutamyl transpeptidase (GGT)

788. Œ≥-glutamyl transpeptidase (GGT) is associated with alcohol use

789. How does prothrombin time (PT) change with advanced liver disease? Increased

790. How do platelet levels change with advanced liver disease? Decreased

791. How do platelet levels change with portal hypertension? Decreased

792. The best way to visualize Kayser-Fleisher rings in Wilson disease is via slit-lamp examination

793. Anti-smooth muscle autoantibodies are associated with autoimmune hepatitis type 1

794. Sialolithiasis is the presence of stones in the salivary gland duct

795. In sialolithiasis a single stone is more common in the submandibular gland specifically in the wharton duct

796. Sialolithiasis presents as recurrent pre-/peri-prandial pain and swelling in affected gland

797. Sialolithiasis is typically caused by dehydration or trauma

798. Sialolithiasis is typically treated conservatively with NSAIDs gland massage warm compresses and sialogogues

799. Behcet syndrome has a high incidence in those of Turkish / East Mediterranean descent

800. Flares of Behcet syndrome last 1-4 weeks

801. Abdominal pain in henoch-schonlein purpura is associated with Intussusception

802. Patients who are experiencing intussusception may draw legs to their chest to ease the pain

803. What is the curative treatment for Crigler-Najjar syndrome? Liver transplant

804. Juvenile polyps are benign with some malignant potential

805. Are cavernous hemangiomas typically symptomatic or asymptomatic? Asymptomatic


806. Patients with cavernous hemangiomas in the brain are at risk of developing an intraparenchymal hemorrhage

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