A 65-year-old man presents to your office for evaluation of abdominal pain. The patient states that he has epigastric pain that radiates to his back. The pain is worse with eating and improves with fasting. The pain has been present for 6 months and is gradually worsening. The patient has lost 15 lbs but feels his oral intake has been adequate. He complains of greasy stools and frequent thirst and urination. Examination reveals a thin male with temporal wasting and oderate abdominal pain with palpation. The patient consumes approximately 1015 beers per day and smokes a pack of cigarettes per day for the past 20 years.
On further evaluation, the patient is found to be diabetic. He has an elevated HgbA1C and fasting hyperglycemia. The patient is sent for diabetic teaching sessions and begun on insulin therapy, but is unable to achieve euglycemia. He experiences frequent bouts of symptomatic hypoglycemia requiring ER visits. What is the most likely cause for these episodes?
A. insulin overdose
B. impaired glucagon production
C. inadequate oral intake
D. vitamin K deficiency
E. vitamin B12 deficiency
Correct Answer: B Section: (none)
Explanation: The patient's history and examination are worrisome for pancreatic disease, and he has strong signs of pancreatic insufficiency. His long history of alcohol use suggests the possibility of chronic pancreatitis or pancreatic cancer. Fecal fat studies would only confirm or quantify his steatorrhea. ACT scan would image the pancreas for changes consistent with chronic pancreatitis (duct dilation, calcifications, pseudocysts) and could look for a neoplasm of the pancreas as well. ERCP is not indicated as a first-line test in patients with abdominal pain given its risk of causing acute pancreatitis. Upper endoscopy would be helpful to rule out peptic ulcer disease and other gastric complaints, but would not provide more global information about the abdomen. The patient has greasy stools and weight loss, findings seen in patients with steatorrhea due to chronic pancreatitis.
Patients with steatorrhea malabsorb fat-soluble vitamins (vitamins A, D, E, and K). "Night blindness" (poor night vision) due to vitamin Adeficiency is common among patients with advanced chronic pancreatitis and likely led to this patient's motor vehicle accident. The patient has DM as a consequence of pancreatic endocrine insufficiency, another feature of chronic pancreatitis. Diabetes develops when greater than 8090% of the gland has been destroyed. Patients with chronic pancreatitis have a coexisting loss of glucagon from islet cells and, thus, often become brittle diabetics, with hypoglycemia seen after insulin administration. Vitamin K and B12 deficiency, which the patient may have, do not cause hypoglycemia. The patient was previously noted to eat well, so inadequate oral intake is unlikely. Diabetic education should decrease the rate of chronic insulin overdosage.
The patient has pancreatic exocrine insufficiency and thus cannot produce enough pancreatic enzymes to digest his food. Pancreatic enzyme replacement therapy in tablet form is a mainstay of therapy for chronic pancreatitis. It can rapidly reverse this problem by providing exogenously produced pancreatic enzymes to break down fats, carbohydrates, and proteins for absorption in the small bowel. The patient would not benefit from additional oral feedings without enzyme supplementation and would only worsen his steatorrhea by doing so. He can take food orally, so feeding via gastrostomy, TPN, or PPN are not indicated. The patient's worsening pain and weight loss despite therapy is worrisome for the development of pancreatic cancer. CA-19-9 is frequently (but not universally) elevated in pancreatic cancers, although it can be elevated in cholangiocarcinoma as well. PSA is associated with prostate cancer. CEA is associated with colon cancer. CA-125 is associated with ovarian cancer. AFP is associated with hepatocellular carcinoma.
Question 792:
A 65-year-old man presents to your office for evaluation of abdominal pain. The patient states that he has epigastric pain that radiates to his back. The pain is worse with eating and improves with fasting. The pain has been present for 6 months and is gradually worsening. The patient has lost 15 lbs but feels his oral intake has been adequate. He complains of greasy stools and frequent thirst and urination. Examination reveals a thin male with temporal wasting and oderate abdominal pain with palpation. The patient consumes approximately 1015 beers per day and smokes a pack of cigarettes per day for the past 20 years. On further questioning, the patient reports that he recently had a motor vehicle accident at night because he felt he could not see clearly. The most likely cause of this symptom is which of the following?
A. vitamin B12 deficiency
B. vitamin C deficiency
C. vitamin D deficiency
D. vitamin A deficiency
E. vitamin K deficiency
Correct Answer: D Section: (none)
Explanation:
The patient's history and examination are worrisome for pancreatic disease, and he has strong signs of pancreatic insufficiency. His long history of alcohol use suggests the possibility of chronic pancreatitis or pancreatic cancer. Fecal fat studies would only confirm or quantify his steatorrhea. ACT scan would image the pancreas for changes consistent with chronic pancreatitis (duct dilation, calcifications, pseudocysts) and could look for a neoplasm of the pancreas as well. ERCP is not indicated as a first-line test in patients with abdominal pain given its risk of causing acute pancreatitis. Upper endoscopy would be helpful to rule out peptic ulcer disease and other gastric complaints, but would not provide more global information about the abdomen. The patient has greasy stools and weight loss, findings seen in patients with steatorrhea due to chronic pancreatitis.
Patients with steatorrhea malabsorb fat-soluble vitamins (vitamins A, D, E, and K). "Night blindness" (poor night vision) due to vitamin Adeficiency is common among patients with advanced chronic pancreatitis and likely led to this patient's motor vehicle accident. The patient has DM as a consequence of pancreatic endocrine insufficiency, another feature of chronic pancreatitis. Diabetes develops when greater than 8090% of the gland has been destroyed. Patients with chronic pancreatitis have a coexisting loss of glucagon from islet cells and, thus, often become brittle diabetics, with hypoglycemia seen after insulin administration. Vitamin K and B12 deficiency, which the patient may have, do not cause hypoglycemia. The patient was previously noted to eat well, so inadequate oral intake is unlikely. Diabetic education should decrease the rate of chronic insulin overdosage.
The patient has pancreatic exocrine insufficiency and thus cannot produce enough pancreatic enzymes to digest his food. Pancreatic enzyme replacement therapy in tablet form is a mainstay of therapy for chronic pancreatitis. It can rapidly reverse this problem by providing exogenously produced pancreatic enzymes to break down fats, carbohydrates, and proteins for absorption in the small bowel. The patient would not benefit from additional oral feedings without enzyme supplementation and would only worsen his steatorrhea by doing so. He can take food orally, so feeding via gastrostomy, TPN, or PPN are not indicated. The patient's worsening pain and weight loss despite therapy is worrisome for the development of pancreatic cancer. CA-19-9 is frequently (but not universally) elevated in pancreatic cancers, although it can be elevated in cholangiocarcinoma as well. PSA is associated with prostate cancer. CEA is associated with colon cancer. CA-125 is associated with ovarian cancer. AFP is associated with hepatocellular carcinoma.
Question 793:
A 65-year-old man presents to your office for evaluation of abdominal pain. The patient states that he has epigastric pain that radiates to his back. The pain is worse with eating and improves with fasting. The pain has been present for 6 months and is gradually worsening. The patient has lost 15 lbs but feels his oral intake has been adequate. He complains of greasy stools and frequent thirst and urination. Examination reveals a thin male with temporal wasting and oderate abdominal pain with palpation. The patient consumes approximately 1015 beers per day and smokes a pack of cigarettes per day for the past 20 years. What would be the best initial test to do in this patient?
A. spot fecal fat collection
B. 72-hour fecal fat collection
C. CT scan of the abdomen
D. ERCP
E. upper endoscopy
Correct Answer: C Section: (none)
Explanation:
The patient's history and examination are worrisome for pancreatic disease, and he has strong signs of pancreatic insufficiency. His long history of alcohol use suggests the possibility of chronic pancreatitis or pancreatic cancer. Fecal fat studies would only confirm or quantify his steatorrhea. ACT scan would image the pancreas for changes consistent with chronic pancreatitis (duct dilation, calcifications, pseudocysts) and could look for a neoplasm of the pancreas as well. ERCP is not indicated as a first-line test in patients with abdominal pain given its risk of causing acute pancreatitis. Upper endoscopy would be helpful to rule out peptic ulcer disease and other gastric complaints, but would not provide more global information about the abdomen. The patient has greasy stools and weight loss, findings seen in patients with steatorrhea due to chronic pancreatitis.
Patients with steatorrhea malabsorb fat-soluble vitamins (vitamins A, D, E, and K). "Night blindness" (poor night vision) due to vitamin Adeficiency is common among patients with advanced chronic pancreatitis and likely led to this patient's motor vehicle accident. The patient has DM as a consequence of pancreatic endocrine insufficiency, another feature of chronic pancreatitis. Diabetes develops when greater than 8090% of the gland has been destroyed. Patients with chronic pancreatitis have a coexisting loss of glucagon from islet cells and, thus, often become brittle diabetics, with hypoglycemia seen after insulin administration. Vitamin K and B12 deficiency, which the patient may have, do not cause hypoglycemia. The patient was previously noted to eat well, so inadequate oral intake is unlikely. Diabetic education should decrease the rate of chronic insulin overdosage.
The patient has pancreatic exocrine insufficiency and thus cannot produce enough pancreatic enzymes to digest his food. Pancreatic enzyme replacement therapy in tablet form is a mainstay of therapy for chronic pancreatitis. It can rapidly reverse this problem by providing exogenously produced pancreatic enzymes to break down fats, carbohydrates, and proteins for absorption in the small bowel. The patient would not benefit from additional oral feedings without enzyme supplementation and would only worsen his steatorrhea by doing so. He can take food orally, so feeding via gastrostomy, TPN, or PPN are not indicated. The patient's worsening pain and weight loss despite therapy is worrisome for the development of pancreatic cancer. CA-19-9 is frequently (but not universally) elevated in pancreatic cancers, although it can be elevated in cholangiocarcinoma as well. PSA is associated with prostate cancer. CEA is associated with colon cancer. CA-125 is associated with ovarian cancer. AFP is associated with hepatocellular carcinoma.
Question 794:
A 50-year-old female presents to your office for evaluation of solid food dysphagia without weight loss. Symptoms have been present for 6 months and are progressive. The patient has had two episodes of near impaction, but copious water ingestion and repeated swallows allowed the food bolus to pass. She has never had to present to the ER for disimpaction. She drinks five to six beers per day, loves spicy foods, and smokes a pack of cigarettes daily with a total lifetime history of 30 pack-years. She has had intermittent heartburn symptoms for years and has not sought treatment. She takes hydrochlorothiazide for hypertension. Review of symptoms reveals chronic cough. Physical examination is unremarkable. Upper endoscopy reveals a distal esophageal stricture with inflammatory changes. Esophageal biopsies reveal benign mucosa with chronic inflammation. Gastric biopsies are unremarkable. Helicobacter pylori testing is negative.
The patient is at increased risk for which of the following illnesses?
A. esophageal squamous cell cancer
B. esophageal adenocarcinoma
C. gastric cancer
D. gastric lymphoma
E. duodenal adenocarcinoma
Correct Answer: B Section: (none)
Explanation:
The patient has a peptic stricture, seen in the setting of long-standing untreated gastroesophageal reflux with esophagitis. The history of progressive solid food dysphagia without weight loss is typical. Tobacco, alcohol, thiazide diuretics, and spicy foods do not predispose to benign esophageal strictures. The patient has developed a peptic stricture, a serious complication of GERD. The patient needs esophageal dilation (either with mechanical or pneumatic dilators) and maximal acid suppression. PPI therapy is superior to histamine receptor antagonist therapy in terms of healing erosive esophagitis. Patients with long-standing GERD are at increased risk of developing Barrett esophagus, a risk factor for esophageal adenocarcinoma. GERD is not a risk factor for esophageal squamous cell cancer, gastric cancer, or duodenal cancer. Patients with chronic H. pylori infection (which this patient did not have) are at increased risk for a form of gastric lymphoma known as a MALT-oma.
Question 795:
A 50-year-old female presents to your office for evaluation of solid food dysphagia without weight loss. Symptoms have been present for 6 months and are progressive. The patient has had two episodes of near impaction, but copious water ingestion and repeated swallows allowed the food bolus to pass. She has never had to present to the ER for disimpaction. She drinks five to six beers per day, loves spicy foods, and smokes a pack of cigarettes daily with a total lifetime history of 30 pack-years. She has had intermittent heartburn symptoms for years and has not sought treatment. She takes hydrochlorothiazide for hypertension. Review of symptoms reveals chronic cough. Physical examination is unremarkable. Upper endoscopy reveals a distal esophageal stricture with inflammatory changes. Esophageal biopsies reveal benign mucosa with chronic inflammation. Gastric biopsies are unremarkable. Helicobacter pylori testing is negative.
What is the next best step in therapy for this patient?
A. esophageal dilation
B. histamine receptor antagonist therapy
C. PPI therapy
D. esophageal dilation with histamine receptor antagonist therapy
E. esophageal dilation with PPI inhibitor therapy
Correct Answer: E Section: (none)
Explanation:
The patient has a peptic stricture, seen in the setting of long-standing untreated gastroesophageal reflux with esophagitis. The history of progressive solid food dysphagia without weight loss is typical. Tobacco, alcohol, thiazide diuretics, and spicy foods do not predispose to benign esophageal strictures. The patient has developed a peptic stricture, a serious complication of GERD. The patient needs esophageal dilation (either with mechanical or pneumatic dilators) and maximal acid suppression. PPI therapy is superior to histamine receptor antagonist therapy in terms of healing erosive esophagitis. Patients with long-standing GERD are at increased risk of developing Barrett esophagus, a risk factor for esophageal adenocarcinoma. GERD is not a risk factor for esophageal squamous cell cancer, gastric cancer, or duodenal cancer. Patients with chronic H. pylori infection (which this patient did not have) are at increased risk for a form of gastric lymphoma known as a MALT-oma.
Question 796:
A 50-year-old female presents to your office for evaluation of solid food dysphagia without weight loss. Symptoms have been present for 6 months and are progressive. The patient has had two episodes of near impaction, but copious water ingestion and repeated swallows allowed the food bolus to pass. She has never had to present to the ER for disimpaction. She drinks five to six beers per day, loves spicy foods, and smokes a pack of cigarettes daily with a total lifetime history of 30 pack-years. She has had intermittent heartburn symptoms for years and has not sought treatment. She takes hydrochlorothiazide for hypertension. Review of symptoms reveals chronic cough. Physical examination is unremarkable. Upper endoscopy reveals a distal esophageal stricture with inflammatory changes. Esophageal biopsies reveal benign mucosa with chronic inflammation. Gastric biopsies are unremarkable. Helicobacter pylori testing is negative.
What is the most likely etiology of the patient's stricture?
A. alcohol ingestion
B. tobacco use
C. gastroesophageal reflux
D. hydrochlorothiazide
E. spicy food ingestion
Correct Answer: C Section: (none)
Explanation:
The patient has a peptic stricture, seen in the setting of long-standing untreated gastroesophageal reflux with esophagitis. The history of progressive solid food dysphagia without weight loss is typical. Tobacco, alcohol, thiazide diuretics, and spicy foods do not predispose to benign esophageal strictures. The patient has developed a peptic stricture, a serious complication of GERD. The patient needs esophageal dilation (either with mechanical or pneumatic dilators) and maximal acid suppression. PPI therapy is superior to histamine receptor antagonist therapy in terms of healing erosive esophagitis. Patients with long-standing GERD are at increased risk of developing Barrett esophagus, a risk factor for esophageal adenocarcinoma. GERD is not a risk factor for esophageal squamous cell cancer, gastric cancer, or duodenal cancer. Patients with chronic H. pylori infection (which this patient did not have) are at increased risk for a form of gastric lymphoma known as a MALT-oma.
Question 797:
A61-year-old man comes to your office for a checkup. He currently feels well and has no focal complaints. He has a past medical history significant for wellcontrolled hypertension, and his gallbladder was removed 3 years ago in the setting of acute cholecystitis. He does not smoke and drinks one to two alcoholic beverages per day. Family history is remarkable for colon cancer in his mother at age 45 and a brother at age 49. He has a sister who developed endometrial cancer at age 53. He has never undergone colon cancer screening and is interested in pursuing this. The patient's family history is strongly suggestive of which of the following?
A. familial adenomatous polyposis (FAP) syndrome
B. hereditary nonpolyposis colorectal cancer (HNPCC) syndrome
C. Peutz-Jeghers syndrome
D. Cronkhite-Canada syndrome
E. Turcot syndrome
Correct Answer: B Section: (none)
Explanation:
The patient should undergo screening colonoscopy, especially with his strongly positive family history of first-degree relatives developing colon cancer before age 50. Colonoscopy is the only test that can directly evaluate the entire colon and rectum. Most polyps can be removed completely at colonoscopy, and large lesions or masses can be directly biopsied. Virtual colonoscopy and barium enema combined with flexible sigmoidoscopy are good tests, but any positive findings on either of these tests would warrant further examination with colonoscopy. Barium enema alone is insufficient for screening. Fecal occult blood testing is helpful as a screening tool, but would be inadequate alone in this patient given his family history. The patient satisfies criteria for HNPCC, a syndrome seen in patients with germline mutations in DNA mismatch repair (MMR) genes. He has three first-degree relatives with cancer of the colorectum, endometrium, small bowel, ureter, or renal pelvis (all of whom are first-degree relatives of each other). The colorectal cancers involve at least two generations and at least one case was diagnosed before age
50. FAP involves a mutation of the APC gene and results in dense colonic polyposis, mandibular osteomas, and universal colon cancer at a young age unless colectomy is performed. Peutz Jeghers syndrome results in hamartomatous polyps of the gut as well as mucocutaneous pigmentation changes. Cronkhite-Canada syndrome manifests as GI polyposis, alopecia, cutaneous hyperpigmentation, malnutrition, and dystrophic fingernails. Turcot syndrome is a variant of FAP in which patients can also develop medulloblastoma, glioblastoma multiforme, and hypertrophy of retinal pigmented epithelium.
Question 798:
A24-year-old male medical student is admitted to the hospital for the evaluation of a 3-month history of bloody stools. The patient has approximately six blood stained or blood streaked stools per day, associated with relatively little, if any, pain. He has not had any weight loss, and he has been able to attend classes without interruption. He denies any fecal incontinence. He has no prior medical history. Review of systems is remarkable only for occasional fevers and the fact that the patient quit smoking approximately 8 months ago. A colonoscopy is performed and reveals a granular, friable colonic mucosal surface with loss of normal vascular pattern from the anal verge to the hepatic flexure of the colon. Biopsies reveal prominent neutrophils in the epithelium and cryptitis with focal crypt abscesses, and no dysplasia. The patient is diagnosed with ulcerative colitis.
In addition to an increased lifetime risk of colon cancer, the patient is also at increased risk for which of the following tumors?
A. hepatocellular carcinoma
B. hepatoblastoma
C. desmoid tumors
D. small bowel lymphoma
E. cholangiocarcinoma
Correct Answer: E Section: (none)
Explanation:
Oral corticosteroids are a mainstay of firstline treatment for moderate-to-severe ulcerative colitis. Starting doses of 40 mg PO daily of prednisone, with a slow taper, are often effective in reducing colonic inflammation, although some patients are unable to wean steroids or maintain remission once achieved. The patient does not have dysplasia in any biopsy specimens, nor does he have signs of systemic toxicity, so a colectomy would be premature. Oral metronidazole is ineffective in ulcerative colitis. Cortisone enemas would be helpful if the patient had isolated left-sided disease, but it is doubtful that enema therapy would reach his hepatic flexure. Intravenous cyclosporine would be used in severe colitis as a last measure before colectomy but this patient is not yet sick enough to warrant such therapy. PSC occurs in approximately 3% of patients with ulcerative colitis and is its major liver complication. It is a chronic inflammatory condition of the biliary tree. It can typically manifest with elevated alkaline phosphatase and bilirubin levels, and results in diffuse stricturing and pruning of the biliary tree. Wilson disease, hereditary hemochromatosis and alpha-1 antitrypsin deficiency are not associated with ulcerative colitis and are not cholestatic liver diseases. Primary biliary cirrhosis could account for these laboratory findings, but is rare in both males and patients with ulcerative colitis. Patients with PSC are at increased risk of developing cholangiocarcinoma but not the other liver tumors mentioned. Patients with celiac sprue are at increased risk for small bowel cancers (adenocarcinoma, lymphoma). Patients with FAP are at increased risk to develop desmoid tumors.
Question 799:
A24-year-old male medical student is admitted to the hospital for the evaluation of a 3-month history of bloody stools. The patient has approximately six blood stained or blood streaked stools per day, associated with relatively little, if any, pain. He has not had any weight loss, and he has been able to attend classes without interruption. He denies any fecal incontinence. He has no prior medical history. Review of systems is remarkable only for occasional fevers and the fact that the patient quit smoking approximately 8 months ago. A colonoscopy is performed and reveals a granular, friable colonic mucosal surface with loss of normal vascular pattern from the anal verge to the hepatic flexure of the colon. Biopsies reveal prominent neutrophils in the epithelium and cryptitis with focal crypt abscesses, and no dysplasia. The patient is diagnosed with ulcerative colitis.
While on the inpatient service, the patient is noted to have a serum alkaline phosphatase of 380 U/L and a bilirubin of 2.4 mg/dL. An ERCP is performed, and the following cholangiogram is obtained. In addition to ulcerative colitis, the patient likely has what other illness?
A. primary biliary cirrhosis
B. Wilson disease
C. alpha-1 antitrypsin deficiency
D. hereditary hemochromatosis
E. primary sclerosing cholangitis (PSC)
Correct Answer: E Section: (none)
Explanation:
Oral corticosteroids are a mainstay of firstline treatment for moderate-to-severe ulcerative colitis. Starting doses of 40 mg PO daily of prednisone, with a slow taper, are often effective in reducing colonic inflammation, although some patients are unable to wean steroids or maintain remission once achieved. The patient does not have dysplasia in any biopsy specimens, nor does he have signs of systemic toxicity, so a colectomy would be premature. Oral metronidazole is ineffective in ulcerative colitis. Cortisone enemas would be helpful if the patient had isolated left-sided disease, but it is doubtful that enema therapy would reach his hepatic flexure. Intravenous cyclosporine would be used in severe colitis as a last measure before colectomy but this patient is not yet sick enough to warrant such therapy. PSC occurs in approximately 3% of patients with ulcerative colitis and is its major liver complication. It is a chronic inflammatory condition of the biliary tree. It can typically manifest with elevated alkaline phosphatase and bilirubin levels, and results in diffuse stricturing and pruning of the biliary tree. Wilson disease, hereditary hemochromatosis and alpha-1 antitrypsin deficiency are not associated with ulcerative colitis and are not cholestatic liver diseases. Primary biliary cirrhosis could account for these laboratory findings, but is rare in both males and patients with ulcerative colitis. Patients with PSC are at increased risk of developing cholangiocarcinoma but not the other liver tumors mentioned. Patients with celiac sprue are at increased risk for small bowel cancers (adenocarcinoma, lymphoma). Patients with FAP are at increased risk to develop desmoid tumors.
Question 800:
A24-year-old male medical student is admitted to the hospital for the evaluation of a 3-month history of bloody stools. The patient has approximately six blood stained or blood streaked stools per day, associated with relatively little, if any, pain. He has not had any weight loss, and he has been able to attend classes without interruption. He denies any fecal incontinence. He has no prior medical history. Review of systems is remarkable only for occasional fevers and the fact that the patient quit smoking approximately 8 months ago. A colonoscopy is performed and reveals a granular, friable colonic mucosal surface with loss of normal vascular pattern from the anal verge to the hepatic flexure of the colon. Biopsies reveal prominent neutrophils in the epithelium and cryptitis with focal crypt abscesses, and no dysplasia. The patient is diagnosed with ulcerative colitis. Which of the following is the best initial treatment for this patient?
A. colectomy
B. oral prednisone
C. oral metronidazole
D. cortisone enemas
E. intravenous cyclosporine
Correct Answer: B Section: (none)
Explanation:
Oral corticosteroids are a mainstay of firstline treatment for moderate-to-severe ulcerative colitis. Starting doses of 40 mg PO daily of prednisone, with a slow taper, are often effective in reducing colonic inflammation, although some patients are unable to wean steroids or maintain remission once achieved. The patient does not have dysplasia in any biopsy specimens, nor does he have signs of systemic toxicity, so a colectomy would be premature. Oral metronidazole is ineffective in ulcerative colitis. Cortisone enemas would be helpful if the patient had isolated left-sided disease, but it is doubtful that enema therapy would reach his hepatic flexure. Intravenous cyclosporine would be used in severe colitis as a last measure before colectomy but this patient is not yet sick enough to warrant such therapy. PSC occurs in approximately 3% of patients with ulcerative colitis and is its major liver complication. It is a chronic inflammatory condition of the biliary tree. It can typically manifest with elevated alkaline phosphatase and bilirubin levels, and results in diffuse stricturing and pruning of the biliary tree. Wilson disease, hereditary hemochromatosis and alpha-1 antitrypsin deficiency are not associated with ulcerative colitis and are not cholestatic liver diseases. Primary biliary cirrhosis could account for these laboratory findings, but is rare in both males and patients with ulcerative colitis. Patients with PSC are at increased risk of developing cholangiocarcinoma but not the other liver tumors mentioned. Patients with celiac sprue are at increased risk for small bowel cancers (adenocarcinoma, lymphoma). Patients with FAP are at increased risk to develop desmoid tumors.
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