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Book Details
Abstract
GI/Liver Secrets Plus, 4th Edition, by Peter R. McNally, DO, FACP, FACG - a volume in the popular Secrets Series® - uses a convenient Q&A approach to provide rapid reference and review of today's most common GI and liver disorders and their management. An expanded size and layout, user-friendly two-color page layout, question-and-answer approach, and list of the "Top 100 GI/Liver Secrets" make it a perfect concise board review tool and a handy clinical reference. Updated coverage throughout equips you with all of the most current and essential knowledge in the field.
- Uses bulleted lists, tables, boxes, short answers, and a highly detailed index to expedite reference.
- Includes Key Points and memory aids in each chapter that make it perfect for board review or clinical reference.
- Covers all of today's most common GI and liver disorders and their management.
- Features the new "Secrets PLUS" format - with an expanded size and layout, more information, and more visual elements - for easier review and an overall enhanced reference experience.
- Contains new images and illustrations to provide more detail and offer a clearer picture of what is seen in practice.
- Incorporates revisions throughout to provide you with an up-to-date overview of gastroenterology and hepatology, including new chapters on Esophageal and Stomach Pathology, Pathology of the Lower GI Tract, Gastroesophageal Reflux and Esophageal Hernias, and Surgery of Achalasia and Esophageal Cancer.
- Offers reorganized and expanded sections covering the bowels and colon for more specific and easier reference: Small and Large Bowel Disorders; Colon Disorders; and General Symptoms and Conditions.
Table of Contents
| Section Title | Page | Action | Price |
|---|---|---|---|
| Front cover | Cover | ||
| Gi/Liversecrets Plus | iii | ||
| Copyright page | iv | ||
| Dedication | v | ||
| Contributors | vii | ||
| Preface | xiii | ||
| Contents | xv | ||
| Top 100 Secrets | 1 | ||
| Chapter 1: Swallowing Disorders and Dysphagia | 7 | ||
| 1. What is the most difficult substance to swallow? | 7 | ||
| 2. What sensory cues elicit swallowing? | 7 | ||
| 3. What is the difference between globus sensation (globus hystericus) and dysphagia? | 7 | ||
| 4. What are common etiologies of globus sensation? | 7 | ||
| 5. Do patients accurately localize the site of dysphagia? | 7 | ||
| 6. What are the differences between esophageal and oropharyngeal dysphagia? | 7 | ||
| 7. What symptoms can be seen in oropharyngeal dysphagia? | 7 | ||
| 8. What are the causes of oropharyngeal dysphagia? | 8 | ||
| 9. What causes oropharyngeal dysphagia in the elderly? | 8 | ||
| 10. Why is a brainstem stroke more likely to cause severe oropharyngeal dysphagia than a hemispheric stroke? | 8 | ||
| 11. When is it appropriate to evaluate stroke-related dysphagia? | 8 | ||
| 12. Is a barium swallow examination adequate to evaluate oropharyngeal dysphagia? | 8 | ||
| 13. What is the characteristic feature of dysphagia in myasthenia gravis? | 8 | ||
| 14. Why is simultaneous involvement of the oropharynx and esophagus extremely unusual for any disease process other than infection? | 9 | ||
| 15. What is Zenker diverticulum? | 9 | ||
| 16. Are Zenker diverticula the result of an obstructive or a propulsive defect? | 9 | ||
| 17. What are the treatment options for Zenker diverticula? | 10 | ||
| 18. How does flexible endoscopic therapy differ from standard surgical therapies? | 10 | ||
| 19. What are the early complications following endoscopy therapy for Zenker diverticulum? | 10 | ||
| 20. What are the indications and late risks of a cricopharyngeal myotomy? | 10 | ||
| 21. When should you consider performing flexible endoscopic therapy for Zenker diverticula? | 10 | ||
| 22. What is the differential diagnosis of dysphagia in a patient who has had surgery, radiation, and chemotherapy for head and neck cancer? | 11 | ||
| 23. Are swallowing disorders related to an increased morbidity and mortality? | 11 | ||
| 24. What therapies can be used to improve swallowing? | 11 | ||
| 25. Which patients are ideal candidates for swallow therapy? | 11 | ||
| 26. What are the etiologies of dysphagia in gastroesophageal reflux disease? | 11 | ||
| 27. What are the common symptoms and causes of xerostomia? | 11 | ||
| 28. Why is cricopharyngeal achalasia a misnomer? How does it differ from classic achalasia? | 11 | ||
| 29. When is botulinum toxin (BTx) used for dysphagia? | 11 | ||
| Websites | 12 | ||
| Bibliography | 12 | ||
| Chapter 2: Gastroesophageal Reflux Disease | 13 | ||
| 1. What is gastroesophageal reflux disease (GERD)? How common is it? | 13 | ||
| 2. What are the typical symptoms of GERD? | 13 | ||
| 3. Is gastrointestinal (GI) hemorrhage a common symptom of GERD? | 13 | ||
| 4. What is odynophagia? Is it a common symptom of GERD? | 13 | ||
| 5. What clues about GERD can be gleaned from the physical exam? | 13 | ||
| 6. Do healthy persons have GERD? | 14 | ||
| 7. How can swallowing and salivary production be associated with GERD? | 14 | ||
| 8. What are the two defective anatomic mechanisms in patients with GERD? | 14 | ||
| 9. What clearance defects are associated with GERD? | 14 | ||
| 10. How may the GE barrier be compromised? | 14 | ||
| 11. What foods and medications influence resting LES pressure? | 14 | ||
| 12. What other medical conditions may mimic symptoms of GERD? | 15 | ||
| 13. What medical condition clinically presents with dysphagia and is often mistaken for GERD? | 15 | ||
| 14. How can GERD be distinguished from coronary artery disease? | 15 | ||
| 15. How should patients with symptoms of GERD be evaluated? | 15 | ||
| 16. Describe a commonly used endoscopic grading system for GERD | 15 | ||
| 17. What are the more sophisticated esophageal function tests? How can they be used appropriately in the evaluation of patients with GERD? | 15 | ||
| 18. Do all patients with GERD need esophageal function testing? | 15 | ||
| 19. What is the use of multichannel intraluminal impedance and pH (MII-pH) technology in the evaluation of GERD? | 15 | ||
| 20. When is ambulatory esophageal pH monitoring helpful? | 16 | ||
| 21. When are esophageal manometry and scintiscanning helpful? | 16 | ||
| 22. Define the various types of medical therapy for GERD and give a logical approach to prescription therapy for patients with longstanding GERD | 16 | ||
| 23. Describe the commonly recommended approach to graded treatment of GERD | 17 | ||
| 24. Do patients scheduled for surgical antireflux procedures need to undergo sophisticated esophageal function testing before surgery? | 17 | ||
| 25. What are some of the new endoscopic treatments for GERD? | 17 | ||
| 26. How should esophageal strictures be managed? | 17 | ||
| 27. What is Barrett’s esophagus? How is it managed? | 17 | ||
| 28. List some of the atypical symptoms and signs of GERD | 17 | ||
| 29. Is there an association between obstructive sleep apnea (OSA) and GERD? | 17 | ||
| 30. Does the presence of heartburn symptoms predict a GERD-related cough etiology? | 17 | ||
| 31. What is the best method to evaluate for possible GERD-related cough? | 18 | ||
| 32. What laryngeal conditions are associated with GERD? | 18 | ||
| 33. How often do people with EPR and hoarseness relate symptoms of heartburn? | 18 | ||
| 34. What is the most efficient, cost-effective method to evaluate hoarse patients for EPR? | 18 | ||
| 35. Can GE reflux worsen asthma? | 18 | ||
| 36. How does GE reflux worsen asthma? | 18 | ||
| 37. What cytochrome P-450 (CYP-450) systems are involved in the metabolism of PPIs? | 18 | ||
| 38. How do esomeprazole (Nexium) and omeprazole (Prilosec) differ? | 18 | ||
| 39. Which patients with GERD should be considered for a surgical antireflux procedure? | 19 | ||
| 40. Which patients are poor candidates for a surgical antireflux procedure? | 19 | ||
| Websites | 19 | ||
| Bibliography | 19 | ||
| Chapter 3: Esophageal Causes Of Chest Pain | 20 | ||
| 1. When should the clinician consider an esophageal cause of chest pain? | 20 | ||
| 2. Does history help to discriminate cardiac from esophageal chest pain? | 20 | ||
| 3. Does a normal coronary angiogram exclude all cardiac diagnoses? | 20 | ||
| 4. What are the noncardiac causes of chest pain? How common are they? | 20 | ||
| 5. Because GERD is the most likely diagnosis, is a trial of acid suppression acceptable? | 20 | ||
| 6. What is the most useful esophageal investigation? | 21 | ||
| 7. How is esophageal pH monitoring performed? | 21 | ||
| 8. What abnormalities may be found with pH monitoring? | 21 | ||
| 9. If reflux has been excluded, which esophageal motility abnormalities may be found in patients with chest pain? | 22 | ||
| 10. How can esophageal motility abnormalities cause chest pain? | 23 | ||
| 11. Can esophageal pain be provoked during testing? | 23 | ||
| 12. How does provocation testing compare with combined ambulatory monitoring of both motility and pH? | 24 | ||
| 13. Are there any emerging technologies for investigation of UCP? | 24 | ||
| 14. What is visceral hypersensitivity? Define the irritable esophagus | 24 | ||
| 15. Does UCP have a psychological component? | 24 | ||
| 16. What are the treatment options for nonreflux esophageal chest pain? | 24 | ||
| 17. Are there any emerging treatment options? | 25 | ||
| 18. Can abnormal belching or aerophagia cause chest pain? | 25 | ||
| 19. What is the prognosis for patients with UCP? | 25 | ||
| Bibliography | 25 | ||
| Chapter 4: Achalasia | 27 | ||
| 1. Define achalasia | 27 | ||
| 2. How common is achalasia? | 27 | ||
| 3. What is vigorous achalasia? | 27 | ||
| 4. What is the relationship between diffuse esophageal spasm (DES) and achalasia? | 27 | ||
| 5. What is the major pathologic lesion in achalasia, and how does it produce the disease? | 27 | ||
| 6. What is the suspected cause of achalasia? | 27 | ||
| 7. Is achalasia an acquired or a congenital disease? | 28 | ||
| 8. Describe the dysphagia associated with achalasia | 28 | ||
| 9. Are there any other symptoms associated with achalasia? | 28 | ||
| 10. Does achalasia involve any other parts of the gastrointestinal tract? | 28 | ||
| 11. What is the best way to diagnose achalasia? | 28 | ||
| 12. What are the characteristic radiologic features of achalasia? | 28 | ||
| 13. What is required for the manometric diagnosis of achalasia? | 28 | ||
| 14. What is the most important potential pitfall in the manometric diagnosis of achalasia? | 28 | ||
| 15. Describe the typical endoscopic features of achalasia | 29 | ||
| 16. What is the difference between secondary achalasia and pseudo-achalasia? | 29 | ||
| 17. How can pseudo-achalasia be diagnosed? | 29 | ||
| 18. Is achalasia a premalignant condition? | 29 | ||
| 19. Should patients undergo periodic endoscopic surveillance? | 29 | ||
| 20. What are the various treatment options available for achalasia? Describe their rationale | 29 | ||
| 21. Discuss the various pharmacologic options available for the palliation of achalasia | 30 | ||
| 22. What does Viagra have to do with achalasia? | 30 | ||
| 23. What is the single most permanent treatment of achalasia? | 30 | ||
| 24. What is the major problem with surgery? | 30 | ||
| 25. How can postoperative GERD be avoided? | 30 | ||
| 26. How is balloon dilation of the LES accomplished? | 30 | ||
| 27. What can be done if symptoms do not respond to the first dilation? | 30 | ||
| 28. What are the results of pneumatic dilation? | 30 | ||
| 29. How does pneumatic dilation compare with surgery? | 31 | ||
| 30. What is the major disadvantage of forceful dilation? How can it be prevented? | 31 | ||
| 31. How is perforation treated in patients with achalasia? | 31 | ||
| 32. Which patients are particularly likely to respond to dilation? | 31 | ||
| 33. What objective parameters should be followed after dilation? | 31 | ||
| 34. How is botulinum toxin type A (BTxA) injection administered? | 31 | ||
| 35. What are the results of BTxA treatment? | 31 | ||
| 36. What are the major drawbacks of BTx treatment? | 31 | ||
| 37. What is the overall best treatment for achalasia? | 32 | ||
| Acknowledgment | 32 | ||
| Websites | 32 | ||
| Bibliogrpahy | 32 | ||
| Chapter 5: Esophageal Cancer | 33 | ||
| 1. What is the incidence of esophageal cancer in the United States and is it changing? | 33 | ||
| 2. What are the risk factors for the development of esophageal cancer? | 33 | ||
| 3. What are the current recommendations for screening and surveillance of esophageal cancer in patients at risk? | 33 | ||
| 4. How is esophageal cancer diagnosed and staged? | 33 | ||
| 5. Discuss the role of endoscopic ultrasound in the diagnosis and staging of esophageal cancer? | 34 | ||
| 6. How is esophageal cancer staged? Why is staging important? | 34 | ||
| 7. What is the prognosis of esophageal cancer? | 35 | ||
| 8. What is the current management of esophageal cancer? | 35 | ||
| Treatment of Limited Disease (Stage I) | 35 | ||
| Treatment of Extensive Disease (Stage IIA–III) | 35 | ||
| Treatment of Distant Metastases (Stage IV) | 35 | ||
| 9. What are the endoscopic methods for the palliation of esophageal cancer? | 35 | ||
| 10. What does the future hold for patients at risk for the development ofesophageal cancer? | 36 | ||
| Websites | 36 | ||
| Bibliography | 36 | ||
| Chapter 6: The Esophagus: Anomalies, Infections, and Nonacid Injuries | 37 | ||
| 1. A patient with iron deficiency anemia and dysphagia is found to have a web by barium studies. What disorder must be considered? | 37 | ||
| 2. What is the best therapy for the dysphagia? | 37 | ||
| 3. What is the best way to confirm a suspected web? | 37 | ||
| 4. For which cancer are patients with esophageal webs reportedly at increased risk? | 37 | ||
| 5. Describe the two types of esophageal rings | 37 | ||
| 6. What causes esophageal A and B rings? | 38 | ||
| 7. Are all Schatzki rings symptomatic? What is the typical history of the symptomatic patient? | 38 | ||
| 8. How are Schatzki rings treated? | 38 | ||
| 9. Describe the three types of esophageal diverticula | 38 | ||
| 10. What is the typical history of Zenker diverticulum? | 38 | ||
| 11. What causes Zenker diverticulum? | 38 | ||
| 12. What is Killian dehiscence? | 39 | ||
| 13. How is Zenker diverticulum treated? | 39 | ||
| 14. Why are midesophageal diverticula called traction diverticula? | 39 | ||
| 15. Should all epiphrenic diverticula be surgically treated? | 39 | ||
| 16. Is surgery required for the cricopharyngeal bar or cricopharyngeal achalasia that radiologists sometimes describe? | 40 | ||
| 17. Define dysphagia lusoria. What is the most common type? | 40 | ||
| 18. What sort of preoperative evaluation should be done in patients with dysphagia lusoria? | 40 | ||
| 19. What causes esophageal atresia with tracheoesophageal fistula? | 40 | ||
| 20. What is the most common type of esophageal atresia with TE fistula? Describe its presentations | 40 | ||
| 21. What is the least common type of esophageal atresia with TE fistula? Describe its presentation | 40 | ||
| 22. How is esophageal atresia with TE fistula treated? | 40 | ||
| 23. What is allergic esophagitis? | 40 | ||
| 24. What is intramural pseudo-diverticulosis? | 41 | ||
| Esophageal Infections | 41 | ||
| 25. What organisms are most commonly identified in esophageal infections? | 41 | ||
| 26. What are the typical presenting symptoms in patients with infectious esophagitis? | 41 | ||
| 27. What is the most common cause of infectious esophagitis in the generalpopulation? | 41 | ||
| 28. List medical conditions known to predispose a person toCandida esophagitis. | 42 | ||
| 29. What commonly used drugs are associated with fungalesophagitis? | 42 | ||
| 30. How is Candida esophagitis treated? | 42 | ||
| 31. Should empiric therapy for Candida esophagitis be considered in an at-risk patientpresenting with typical symptoms of esophageal infection? | 42 | ||
| 32. What is the most common viral pathogen-causing esophagitis? | 42 | ||
| 33. What is the most common cause of viral esophagitis in patients with normalimmunity? | 42 | ||
| 34. How is viral esophagitis diagnosed? | 42 | ||
| 35. Differentiate HSV and CMV esophagitis endoscopically. | 42 | ||
| 36. How is HSV esophagitis treated? | 43 | ||
| 37. Discuss the treatment of CMV esophagitis. | 43 | ||
| 38. Does it make sense to stain for acid-fast organisms in evaluating esophagealulcers? | 43 | ||
| 39. Can the diagnosis of Chagas disease be based on classic manometric findingsand confirmed by histologic evaluation of deep mucosal biopsies from the distalesophagus? | 43 | ||
| Pill And Corrosive Esophageal Injury | 43 | ||
| 40. Who is affected by pill-induced esophageal injury? | 43 | ||
| 41. What factors contribute to esophageal retention of pills? | 43 | ||
| 42. What are the risk factors for pill-induced injury? | 43 | ||
| 43. Describe the typical presentation of patients with pill-induced injury. | 44 | ||
| 44. How is the diagnosis of pill-induced esophageal injurymade? | 44 | ||
| 45. What does the typical pill-induced lesion look like at time of endoscopy? | 44 | ||
| 46. How can you remember the many medications that can cause pill-inducedesophagitis? | 44 | ||
| 47. Where are the areas of physiologic narrowing of the esophagus? | 44 | ||
| 48. What are the options for treating pill-induced esophageal injury? | 45 | ||
| 49. Discuss the epidemiology of caustic ingestion in the United States. | 45 | ||
| 50. What are the common caustic agents? Where are they found? | 45 | ||
| 51. Describe the pathophysiology of acute alkali esophagitis. | 45 | ||
| 52. The severity of caustic injury to the esophagus can be graded as first, second, orthird degree, using the following system. | 45 | ||
| 53. Describe how an endoscopic grading system guides in management and prognosis ofthe patient with corrosive injection. | 45 | ||
| 54. What is the cancer risk to a patient with stricture after lye ingestion? | 45 | ||
| 55. Describe the emergency department management of a patientwith caustic ingestion. | 46 | ||
| 56. What is the role of endoscopic evaluation in patients withcaustic ingestion? | 46 | ||
| Websites | 46 | ||
| Bibliography | 46 | ||
| Chapter 7: Barrett’s Esophagus | 48 | ||
| 1. What is Barrett’s esophagus? | 48 | ||
| 2. How is Barrett’s esophagus diagnosed? | 48 | ||
| 3. Why is Barrett’s esophagus important? | 48 | ||
| 4. Does short-segment Barrett’s esophagus need to be identified? | 48 | ||
| 5. What is the risk of cancer associated with Barrett’s esophagus? | 48 | ||
| 6. Who should be screened for Barrett’s esophagus? | 48 | ||
| 7. What is the therapy for Barrett’s esophagus? | 48 | ||
| Goals of Therapy for Barrett’s Esophagus | 49 | ||
| 8. Does Barrett’s esophagus reverse with medical therapy? | 49 | ||
| 9. Does Barrett’s esophagus reverse with surgical therapy? | 49 | ||
| 10. What is the appropriate surveillance of patients with Barrett’s esophagus? | 49 | ||
| 11. Summarize the evolution of Barrett’s esophagus to adenocarcinoma. | 49 | ||
| 12. Describe the management of HGD. | 49 | ||
| 13. Can the development of adenocarcinoma of the esophagus be prevented in patientswith Barrett’s esophagus? | 49 | ||
| 14. What advantages can we anticipate in the management of Barrett’s esophagus? | 50 | ||
| Websites | 50 | ||
| Bibliography | 50 | ||
| Chapter 8: Esophageal and Stomach Pathology | 51 | ||
| Esophagus | 51 | ||
| 1. Describe a normal esophagus lining. | 51 | ||
| 2. What are the histologic features of gastroesophageal reflux disease (GERD) andeosinophilic esophagitis (EE)? | 51 | ||
| 3. Discuss the infectious causes of esophagitis. | 52 | ||
| 4. What is the most important differential to beconsidered in biopsy samples to evaluategraft-versus-host disease (GVHD)? | 53 | ||
| 5. What is the histologic prevalence of esophageal Crohn’s disease in endoscopicallynormal studies? | 53 | ||
| 6. What are other miscellaneous esophageal conditions? | 53 | ||
| 7. List the dermatologic conditions that can affect the esophagus. | 53 | ||
| 8. Discuss the histology of Barrett’s esophagus and the grading of dysplasia. | 53 | ||
| 9. What histologic patterns can be seen in the biopsy samples from the GE junctionthat do not show typical endoscopic findings of Barrett’s esophagus? | 54 | ||
| 10. What is the differential diagnosis of esophageal polypoid lesions? | 54 | ||
| 11. What are the histologic features of the mucosal lining in different parts of the stomach? | 56 | ||
| 12. What are the histologic patterns of gastritis? | 56 | ||
| 13. What are the various histologic manifestations of Helicobacter pylori–associatedgastritis? | 56 | ||
| 14. What is Helicobacter heilmannii–associatedgastritis? | 57 | ||
| 15. What are the types of chronic atrophicgastritis, and how do these differ histologically? | 57 | ||
| 16. What are the salient histologic features of chemical/reactive gastropathy? | 57 | ||
| 17. What is lymphocytic gastritis, and with which disease processes is it associated? | 57 | ||
| 18. What is the differential diagnosis ofgranulomatous gastritis? | 58 | ||
| 19. What are the histologic featuressuggestive of gastric Crohn’s disease? | 58 | ||
| 20. Histologically, how do you differentiategastric antral vascular ectasia (GAVE),portal hypertensive gastropathy,Dieulafoy lesion, and radiation injury? | 58 | ||
| 21. What are the histologic features of giant mucosal folds seen in Ménétrier diseaseand Zöllinger-Ellison syndrome? | 58 | ||
| 22. What are the histologic features of gastricpolyps/polypoid lesions? | 59 | ||
| 23. Compare gastric dysplasia and adenoma. | 59 | ||
| 24. What are the histologic types ofgastric adenocarcinoma? | 60 | ||
| 25. What is the histologic classification of neuroendocrine neoplasms of the stomach? | 60 | ||
| 26. What is the differential diagnosis of gastric stromal tumors? | 61 | ||
| 27. What are the different types of gastric lymphoma? | 61 | ||
| Acknowledgments | 61 | ||
| Websites | 61 | ||
| Bibliography | 61 | ||
| Chapter 9: Gastritis | 63 | ||
| 1. What is gastritis? | 63 | ||
| 2. What are the symptoms of gastritis? | 63 | ||
| 3. How is gastritis classified? | 63 | ||
| 4. What is the endoscopic and histologic appearance of reactive and chronic gastritis? | 63 | ||
| 5. How do we treat reactive gastritis, and what can be done to prevent it? | 64 | ||
| 6. What are the characteristics of stress gastritis, and how should it be treated? | 64 | ||
| 7. What is the most common etiology of chronic gastritis? | 64 | ||
| 8. How is chronic gastritis secondary to H. pylori infection diagnosed? | 64 | ||
| 9. How is chronic gastritis secondary to H. pylori infection treated? | 65 | ||
| 10. What are the long-term implications of H. pylori infection? | 65 | ||
| 11. What are the other types of chronic gastritis? | 65 | ||
| 12. What is autoimmune gastritis? | 65 | ||
| 13. What is lymphocytic gastritis? | 65 | ||
| 14. What is chronic nonspecific gastritis? | 65 | ||
| 15. What is Ménétrier disease, and how does it differ from the other special forms of chronic gastritis? | 65 | ||
| 16. Describe bile reflux gastritis | 66 | ||
| 17. In what circumstances do granulomatous and eosinophilic gastritis occur? | 66 | ||
| Bibliography | 66 | ||
| Chapter 10: Gastric Cancer | 68 | ||
| 1. What are the histologic types of gastric cancer? | 68 | ||
| 2. What is a signet ring cell carcinoma? | 68 | ||
| 3. What is the ethnic and geographic distribution of distal gastric adenocarcinoma? | 68 | ||
| 4. What is the role of diet in the development of gastric cancer? | 68 | ||
| 5. What inherited genetic alterations are associated with gastric adenocarcinoma? | 68 | ||
| 6. What is the role of H. pylori in gastric adenocarcinoma? | 68 | ||
| 7. What mechanism is proposed for H. pylori causing an increased risk of gastric cancer? | 69 | ||
| 8. What is the role of achlorhydria in gastric cancer? | 69 | ||
| 9. Should H. pylori infection be eradicated to prevent gastric cancer from occurring? | 69 | ||
| 10. Who should be screened for gastric cancer? | 69 | ||
| 11. What is gastric stump cancer? | 69 | ||
| 12. What is early gastric cancer? | 69 | ||
| 13. How is the incidence of gastric adenocarcinoma changing? | 69 | ||
| 14. What is the staging scheme for gastric adenocarcinoma? | 70 | ||
| 15. How does staging help in treating gastric cancer? | 70 | ||
| 16. What is the role of endoscopic ultrasonography in staging gastric cancer? | 70 | ||
| 17. What is the role of endoscopy in the treatment of early gastric cancer? | 70 | ||
| 18. What is the role of surgery in treating localized gastric adenocarcinoma? | 70 | ||
| 19. What is the role of neoadjuvant therapy in gastric adenocarcinoma? | 70 | ||
| 20. What is the role of adjuvant therapy in gastric adenocarcinoma? | 71 | ||
| 21. What is the usual therapy for metastatic gastric adenocarcinoma? | 71 | ||
| 22. What is a MALT lymphoma? | 71 | ||
| 23. What is special about gastric MALT lymphomas? | 71 | ||
| 24. What is the role of antibiotic therapy in gastric MALT lymphomas? | 71 | ||
| 25. Describe the staging scheme for gastric lymphoma. | 71 | ||
| 26. What is the best therapy for aggressive (non-MALT) gastric lymphoma? | 71 | ||
| 27. What are gastric carcinoid tumors? | 71 | ||
| 28. What causes gastric carcinoid tumors? | 71 | ||
| 29. What should be done when a gastric carcinoid has been identified? | 71 | ||
| 30. What is a gastric GIST? | 72 | ||
| Websites | 72 | ||
| Bibliography | 72 | ||
| Chapter 11: Helicobacter Pylori andPeptic Ulcer Disease | 73 | ||
| 1. Why is Helicobacter pylori a unique bacterium? | 73 | ||
| 2. What is the prevalence of H. pylori? | 73 | ||
| 3. How is infection transmitted? | 73 | ||
| 4. Where in the gastrointestinal (GI) tract does H. pylori live? | 74 | ||
| 5. How does H. pylori produce mucosal damage? | 74 | ||
| 6. What endoscopy-based (invasive) tests can be used to diagnose H. pylori infection? | 74 | ||
| 7. How is H. pylori diagnosed noninvasively? | 74 | ||
| 8. What is the association of H. pylori with histologic gastritis? | 75 | ||
| 9. What is the association of H. pylori with peptic ulcer disease? | 75 | ||
| 10. What may cause ulcers besides H. pylori? | 75 | ||
| 11. Does H. pylori cause symptoms in patients with functional dyspepsia? | 75 | ||
| 12. Does H. pylori play a role in gastric cancer? | 76 | ||
| 13. In what situation is it appropriate to eradicate H. pylori infection? | 76 | ||
| 14. What treatment regimens have been used to eradicate H. pylori? | 76 | ||
| 15. Is reinfection a common problem? | 77 | ||
| 16. What is the role of vaccination in the prevention of H. pylori? | 77 | ||
| 17. What role does H. pylori play in gastroesophageal reflux disease (GERD)? | 77 | ||
| 18. Is H. pylori associated with any diseases outside the GI tract in humans? | 77 | ||
| Websites | 78 | ||
| Bibliography | 78 | ||
| Chapter 12: Gastric Polyps and Thickened Gastric Folds | 79 | ||
| 1. What are gastric polyps, and what are the most commonly observed types of gastric polyps? | 79 | ||
| 2. Describe the endoscopic features typical of each type of gastric polyp. | 79 | ||
| 3. Describe the histologic features of each type of gastric polyp. | 79 | ||
| 4. What is the risk of malignancy associated with gastric polyps? | 79 | ||
| 5. How should gastric polyps be managed? | 80 | ||
| 6. Is surveillance indicated for patients with gastric polyps? | 80 | ||
| 7. Describe the relationships between gastric polyps and other conditions. | 80 | ||
| 8. What is meant by thickened gastric folds? | 80 | ||
| 9. List the differential diagnosis for intrinsic causes of thickened gastric folds. | 80 | ||
| 10. What systemic diseases may be associated with thickened gastric folds or granulomatous gastritis? | 80 | ||
| 11. Endoscopic ultrasound (EUS) displays the gastric wall in five alternating hyperechoic and hypoechoic bands. Histologi ... | 81 | ||
| 12. Describe the role of EUS in the evaluation of thickened gastric folds. | 81 | ||
| 13. What are the clinical features of high-grade non-Hodgkin’s gastric lymphoma? | 81 | ||
| 14. Define MALToma. | 81 | ||
| 15. How are MALTomas managed? | 82 | ||
| 16. Define Ménétrier disease. | 82 | ||
| 17. How is Ménétrier disease different in children and adults? | 83 | ||
| 18. What is the differential diagnosis for a subepithelial mass seen on endoscopy? | 83 | ||
| 19. What role does EUS play in evaluating submucosal lesions? | 83 | ||
| 20. What is a GIST? | 84 | ||
| 21. A 65-year-old woman presents with self-limited, coffee-grounds emesis. Endoscopy reveals a single, pedunculated, 1-cm ... | 84 | ||
| 22. A patient with FAP has multiple gastric polyps on surveillance endoscopy. What is the most likely histology of such p ... | 84 | ||
| 23. Describe the manifestations of gastric polyps in the other hereditary GI polyposis syndromes. | 84 | ||
| 24. A 40-year-old man has a history of chronic pancreatitis complicated by pseudocysts requiring drainage. He presents wi ... | 84 | ||
| 25. A 65-year-old woman is referred for evaluation of chronic iron deficiency anemia and hemoccult-positive stool. Colono ... | 84 | ||
| Bibliography | 85 | ||
| Chapter 13: Gastroparesis | 86 | ||
| 1. Define gastroparesis. | 86 | ||
| 2. What are the factors that determine gastric motility and emptying? | 86 | ||
| 3. Describe the electric pacesetter in the stomach. | 86 | ||
| 4. What is the migrating motor complex? | 87 | ||
| 5. Describe gastric motility and emptying. | 87 | ||
| 6. What is idiopathic gastroparesis? | 87 | ||
| 7. What is diabetic gastroparesis? | 87 | ||
| 8. What is the pathogenesis of diabetic gastroparesis? | 88 | ||
| 9. What surgical procedures are associated with postoperative gastroparesis? | 88 | ||
| 10. What conditions cause selective gastric motor dysfunction leading to gastroparesis? | 88 | ||
| 11. Which disorders with diffuse abnormalities of gastrointestinal motor activity cause gastroparesis? | 88 | ||
| 12. Which drugs affect gastric emptying? | 89 | ||
| 13. List the conditions that have an established association with delayed gastric emptying. | 89 | ||
| 14. What associations are likely to be important in gastroparesis? | 89 | ||
| 15. Which part of the history and physical exam is important in establishing a diagnosis of gastroparesis? | 90 | ||
| 16. What modalities are available for diagnosing gastroparesis? | 90 | ||
| 17. Outline an approach to the diagnosis of gastroparesis. | 90 | ||
| 18. Once gastroparesis is diagnosed, how should it be treated? | 91 | ||
| 19. What are the complications of gastroparesis? | 91 | ||
| 20. What is the surgical management for medically refractory gastroparesis? | 91 | ||
| 21. What is the role of botulinum toxin injection in refractory gastroparesis? | 91 | ||
| 22. What is gastric electrical stimulation? | 92 | ||
| 23. What is the role of gastric electrical stimulation in refractory gastroparesis? | 92 | ||
| Websites | 92 | ||
| Bibliography | 92 | ||
| Chapter 14: Evaluation of Abnormal Liver Tests | 94 | ||
| 1. What are liver tests? | 94 | ||
| 2. What are the true liver function tests? | 94 | ||
| 3. What is the difference between cholestatic and hepatocellular injury? | 94 | ||
| 4. What is the most specific test for hepatocellular damage? | 94 | ||
| 5. How is cholestatic injury best diagnosed? | 94 | ||
| 6. What are serum transaminases? | 94 | ||
| 7. How is ALT assessed? | 95 | ||
| 8. How are normal and abnormal levels of ALT determined? | 95 | ||
| 9. What makes the AP level rise? | 95 | ||
| 10. What does an elevated bilirubin mean? | 96 | ||
| 11. How is bilirubin level determined? | 96 | ||
| 12. What tests are used to evaluate hemochromatosis? | 96 | ||
| 13. Describe the role of a1-antitrypsin. | 96 | ||
| 14. What three tests are used to diagnose a1-antitrypsin deficiency? | 96 | ||
| 15. What is Wilson’s disease? | 97 | ||
| 16. How is Wilson’s disease diagnosed? | 97 | ||
| 17. Summarize the tests for common metabolic disorders of the liver. | 97 | ||
| 18. What are autoimmune markers? | 97 | ||
| 19. How are the common antibody tests performed and interpreted? | 97 | ||
| 20. When should screening or diagnostic tests be ordered for patients with suspected liver disease? | 98 | ||
| 21. What are noninvasive markers of fibrosis, and what is their utility? | 98 | ||
| 22. What is the role of liver biopsy? | 98 | ||
| Websites | 98 | ||
| Bibliography | 98 | ||
| Chapter 15: Viral Hepatitis | 100 | ||
| 1. What are the types of hepatitis viruses? | 100 | ||
| 2. What is the difference between acute and chronic hepatitis? | 100 | ||
| 3. How common is chronicity in hepatitis B? | 100 | ||
| 4. When does chronic hepatitis D develop? | 100 | ||
| 5. How common is chronic hepatitis C? | 100 | ||
| 6. How are hepatitis viruses transmitted? | 100 | ||
| 7. Describe the symptoms of hepatitis. | 101 | ||
| 8. What biochemical abnormalities are associated with viral hepatitis? | 101 | ||
| 9. What biochemical findings indicate chronic infection? | 101 | ||
| 10. How is hepatitis A diagnosed? | 101 | ||
| 11. How is hepatitis B diagnosed? | 101 | ||
| 12. Describe the HBsAg and HBsAb tests. | 102 | ||
| 13. How is the HBcAb test interpreted? | 102 | ||
| 14. What do the HBeAg and HBeAb tests indicate? | 102 | ||
| 15. Describe the bDNA assay. | 102 | ||
| 16. What are HBV PCR assays? | 102 | ||
| 17. How is hepatitis C diagnosed? | 102 | ||
| 18. How is a positive result on the ELISA confirmed? | 103 | ||
| 19. What nucleic acid assays are available for hepatitis C? | 103 | ||
| 20. How is hepatitis D diagnosed? | 103 | ||
| 21. How is hepatitis E diagnosed? | 103 | ||
| 22. Are there other hepatitis viruses not yet discovered? | 103 | ||
| 23. What is the treatment of acute hepatitis B and hepatitis D? | 103 | ||
| 24. What is the treatment of acute hepatitis C? | 103 | ||
| 25. Is chronic viral hepatitis treatable? | 104 | ||
| 26. Does lamivudine have any clinical relevance in this day and age? | 104 | ||
| 27. Which patients with chronic hepatitis B are candidates for therapy? | 104 | ||
| 28. Describe the standard treatment and its side effects. | 104 | ||
| 29. What is the response rate to treatment of chronic hepatitis B? | 104 | ||
| 30. Describe the treatment of chronic hepatitis C. How effective is it? | 104 | ||
| 31. Describe the side effects of ribavirin. | 104 | ||
| 32. What is PEG-interferon? | 105 | ||
| 33. What happens if the patient fails to clear the hepatitis C virus? | 105 | ||
| 34. What alternative therapies for hepatitis C are under investigation? | 105 | ||
| 35. How is hepatitis D treated? | 105 | ||
| 36. Can hepatitis C be prevented? | 105 | ||
| Controversy | 105 | ||
| 37. Should all patients with hepatitis C undergo liver biopsy? | 105 | ||
| Website | 105 | ||
| Bibliography | 106 | ||
| Chapter 16: Antiviral Therapy For Hepatitis C Infection | 107 | ||
| 1. What are the indications for antiviral therapy in patients with chronic hepatitis C? | 107 | ||
| 2. What is the recommended evaluation of patients with chronic hepatitis C before therapy is begun? | 107 | ||
| 3. Should hepatitis C genotype testing be performed before initiation of therapy? | 108 | ||
| 4. Is a liver biopsy mandatory before initiation of antiviral therapy? | 108 | ||
| 5. What are the treatment options for hepatitis C infection? | 108 | ||
| 6. How are the antiviral agents dosed? | 108 | ||
| 7. How is response to antiviral therapy assessed? | 108 | ||
| 8. How often should viral load be measured during treatment? | 109 | ||
| 9. What pretreatment characteristics predict a favorable response to antiviral therapy? | 109 | ||
| 10. What is the efficacy of combination peginterferon and ribavirin? | 109 | ||
| 11. How can response to antiviral therapy be maximized? | 109 | ||
| 12. What are the side effects of IFN therapy? How should the patient be monitored? | 109 | ||
| 13. What are the side effects of ribavirin therapy? How should the patient be monitored? | 110 | ||
| 14. What are the contraindications to IFN therapy? | 110 | ||
| 15. What are the contraindications to ribavirin therapy? | 110 | ||
| 16. Should patients with cirrhosis secondary to hepatitis C infection be treated with antiviral therapy? | 110 | ||
| 17. Should patients with hepatitis C and normal liver enzyme levels be treated with antiviral therapy? | 111 | ||
| 18. Should patients with HCV/HIV coinfection receive antiviral therapy for hepatitis C infection? | 111 | ||
| 19. How should patients with HCV/HBV coinfection be treated? | 111 | ||
| 20. What are the options for patients who did not respond to combination therapy with nonpegylated IFN and ribavirin? | 111 | ||
| 21. What is the role of antiviral therapy in acute hepatitis C? | 111 | ||
| 22. Are there new treatments on the horizon for hepatitis C? | 112 | ||
| Websites | 112 | ||
| Bibliography | 112 | ||
| Chapter 17: Antiviral Therapy For Hepatitis B | 113 | ||
| 1. Is antiviral therapy recommended for acute hepatitis B? | 113 | ||
| 2. Do all patients with chronic hepatitis B benefit from therapy? | 113 | ||
| 3. How should the HBV-DNA PCR assay results be used to make therapy decisions? | 113 | ||
| 4. Is liver biopsy required before therapy is started? | 114 | ||
| 5. What are the options for treating chronic hepatitis B infection? | 114 | ||
| 6. What are the endpoints of antiviral therapy? | 114 | ||
| 7. What is the expected response to interferon therapy? | 115 | ||
| 8. What is the expected response to oral nucleoside/nucleotide therapy? | 115 | ||
| 9. What are the advantages of interferon therapy for chronic hepatitis B infection? | 115 | ||
| 10. What are the disadvantages of interferon therapy? | 115 | ||
| 11. Which parameters predict a good response to interferon therapy? | 115 | ||
| 12. What are the advantages of oral nucleoside/nucleotide therapy? | 116 | ||
| 13. What are the disadvantages of oral nucleoside/nucleotide therapy? | 116 | ||
| 14. Should patients with advanced, decompensated cirrhosis secondary to hepatitis B receive antiviral therapy or be referred for liver transplantation without a trial of therapy? | 116 | ||
| 15. How should response to therapy be monitored? | 116 | ||
| 16. How is resistance diagnosed and how should it be managed? | 116 | ||
| 17. Should patients with chronic hepatitis B be treated if they are to undergo immune suppression? | 117 | ||
| 18. How should HBV infection be treated in patients coinfected with the human immunodeficiency virus (HIV)? | 117 | ||
| 19. Should hepatitis B be treated during pregnancy? | 117 | ||
| Websites | 118 | ||
| Bibliography | 118 | ||
| Chapter 18: Autoimmune Hepatitis: Diagnosis And Pathogenesis | 119 | ||
| 1. What is autoimmune hepatitis? | 119 | ||
| 2. What are its predominant features? | 119 | ||
| 3. What are the symptoms of autoimmune hepatitis? | 120 | ||
| 4. What are the characteristic histologic findings in autoimmune hepatitis? | 120 | ||
| 5. Can autoimmune hepatitis have a fulminant presentation? | 121 | ||
| 6. Are there patients who may be underdiagnosed? | 121 | ||
| 7. What are the different types of autoimmune hepatitis? | 122 | ||
| 8. What are the clinical criteria for diagnosis? | 122 | ||
| 9. What are the diagnostic scoring systems and how are they used? | 123 | ||
| 10. What is the standard serologic battery for diagnosis? | 124 | ||
| 11. What serologic assays are best for detecting the standard autoantibodies? | 125 | ||
| 12. What other autoantibodies may have diagnostic and prognostic importance? | 125 | ||
| 13. What investigational antibodies have promise as clinical tools? | 126 | ||
| 14. What is the significance of antimitochondrial antibodies in autoimmune hepatitis? | 126 | ||
| 15. Can autoimmune hepatitis exist in the absence of conventional autoantibodies? | 126 | ||
| 16. What is the appropriate testing sequence for the autoantibody determinations? | 127 | ||
| 17. In what other clinical situation should autoimmune hepatitis be considered? | 127 | ||
| 18. What are the variant (overlap) syndromes of autoimmune hepatitis? | 127 | ||
| 19. Is autoimmune hepatitis in children different from that of adults? | 128 | ||
| 20. What are the pathogenic mechanisms? | 128 | ||
| 21. What are the autoantigens? | 129 | ||
| 22. Can viruses cause autoimmune hepatitis? | 129 | ||
| 23. Can drugs cause autoimmune hepatitis? | 129 | ||
| 24. Are there genetic predispositions for autoimmune hepatitis? | 129 | ||
| 25. Does autoimmune hepatitis have a Mendelian pattern of inheritance? | 129 | ||
| 26. What are the susceptibility alleles? | 129 | ||
| 27. How do different susceptibility alleles produce the same disease? | 130 | ||
| 28. How do regional factors affect disease occurrence? | 130 | ||
| 29. Why do patients with the same HLA have different clinical phenotypes? | 130 | ||
| 30. Do the HLA phenotypes influence disease expression and outcome? | 130 | ||
| 31. Should HLA typing be part of the standard diagnostic algorithm? | 130 | ||
| Website | 131 | ||
| Bibliography | 131 | ||
| Chapter 19: Autoimmune Hepatitis: Treatment | 132 | ||
| 1. What therapies are effective for patients with autoimmune hepatitis? | 132 | ||
| 2. How do the medications work? | 133 | ||
| 3. What are the side effects of the medication? | 133 | ||
| 4. Can azathioprine be used during pregnancy? | 134 | ||
| 5. What are the indications for treatment? | 134 | ||
| 6. What are the indices that reflect disease severity? | 134 | ||
| 7. Are there any predictors of response to treatment? | 135 | ||
| 8. Does the rapidity of the response to treatment have prognostic value? | 135 | ||
| 9. What are the results of therapy? | 135 | ||
| 10. What are the endpoints of treatment? | 136 | ||
| 11. When should a liver biopsy be performed? | 136 | ||
| 12. Does corticosteroid treatment prevent or reverse fibrosis? | 136 | ||
| 13. What precautions can be undertaken to reduce the frequency side effects? | 136 | ||
| 14. What is the most common treatment problem? | 136 | ||
| 15. What are the consequences of relapse and retreatment? | 136 | ||
| 16. Does determination of serum thiopurine methyltransferase activity predict azathioprine toxicity? | 136 | ||
| 17. How should relapse be managed? | 137 | ||
| 18. Do patients receiving azathioprine maintenance therapy ever get off treatment? | 137 | ||
| 19. How should treatment failure be managed? | 137 | ||
| 20. How effective is liver transplantation for decompensated disease? | 138 | ||
| 21. What strategy is best for patients with drug toxicity or incomplete response? | 139 | ||
| 22. Does hepatocellular carcinoma occur? | 139 | ||
| 23. How are variant syndromes managed? | 139 | ||
| 24. How are patients with mixed autoimmune and viral features managed? | 139 | ||
| 25. What new drug therapies are promising? | 140 | ||
| 26. What new site-specific molecular interventions are promising? | 140 | ||
| Website | 141 | ||
| Bibliography | 141 | ||
| Chapter 20: Primary Biliary Cirrhosis and Primary Sclerosing Cholangitis | 142 | ||
| 1. Define primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) | 142 | ||
| 2. Is PBC an autoimmune disorder? | 142 | ||
| 3. Is PSC an autoimmune disorder? | 142 | ||
| 4. Do viral infections have a role in the development of PSC? | 142 | ||
| 5. What are the clinical features of PBC and PSC? | 142 | ||
| 6. What are the common findings on physical examination? | 143 | ||
| 7. What diseases are associated with PBC? | 143 | ||
| 8. What diseases are associated with PSC? | 143 | ||
| 9. What important biochemical abnormalities are associated with PBC and PSC? | 143 | ||
| 10. What is the lipid profile in patients with PBC? Are they at increased risk for developing coronary artery disease? | 143 | ||
| 11. What serum autoantibodies are associated with PBC? | 143 | ||
| 12. What serum autoantibodies are associated with PSC? | 143 | ||
| 13. What are the cholangiographic features of the biliary tree in PSC? | 144 | ||
| 14. Is it important to evaluate the biliary tree in PBC? | 144 | ||
| 15. What are the hepatic histologic features of PBC and PSC? | 144 | ||
| 16. Do asymptomatic patients with PBC have a normal life expectancy? | 145 | ||
| 17. Do asymptomatic patients with PSC have a normal life expectancy? | 145 | ||
| 18. What is the role of mathematical models in estimating survival for PBC and PSC? | 145 | ||
| 19. What vitamin deficiencies are associated with PBC and PSC? | 145 | ||
| 20. What bone disease is associated with PBC and PSC? | 145 | ||
| 21. What liver-related complications are specific to PSC? | 146 | ||
| 22. What is the differential diagnosis of PBC and PSC? | 146 | ||
| 23. Define autoimmune cholangitis. How is it related to PBC? | 146 | ||
| 24. What is meant by an overlap or a variant syndrome in PBC and PSC? | 146 | ||
| 25. What is meant by small duct PSC? | 146 | ||
| 26. Describe the treatment of pruritus in patients with PBC and PSC. | 147 | ||
| 27. How is osteopenia treated in patients with PBC and PSC? | 147 | ||
| 28. Describe the treatment of fat-soluble vitamin deficiency in PBC and PSC. | 147 | ||
| 29. Do lipid-lowering agents have a role in treatment of PBC and PSC? | 147 | ||
| 30. Describe the treatment of bacterial cholangitis in PSC. | 147 | ||
| 31. What are the therapeutic options for biliary strictures in PSC? | 147 | ||
| 32. Describe the role of transjugular intrahepatic portosystemic shunt (TIPS) in PBC and PSC. | 148 | ||
| 33. What medical agents have been tried for the treatment of PBC? | 148 | ||
| 34. What medical agents have been tried for the treatment of PSC? | 148 | ||
| 35. Describe the mechanism of action for UDCA in PBC | 148 | ||
| 36. What is the role of reconstructive biliary tract surgery in PSC? | 148 | ||
| 37. Does proctocolectomy in patients with PSC and CUC favorably affect hepatobiliary disease? | 148 | ||
| 38. Do patients with PBC and PSC have an increased risk for hepatocellular carcinoma (HCC)? | 148 | ||
| 39. What is the role of liver transplantation in PBC and PSC? | 149 | ||
| 40. Do PBC and PSC recur after liver transplantation? | 149 | ||
| 41. What are the complications in PSC patients after liver transplantation? | 149 | ||
| Websites | 149 | ||
| Bibliography | 149 | ||
| Chapter 21: Hepatitis Vaccines and Immunoprophylaxis | 151 | ||
| 1. Discuss the concept of immunization (vaccination) | 151 | ||
| 2. Outline briefly the history of vaccination | 151 | ||
| 3. Distinguish between active and passive immunization | 151 | ||
| 4. What are the major categories of vaccines? | 151 | ||
| 5. Describe the basic characteristics of immunoprophylaxis | 151 | ||
| 6. Which Igs are available for human use? | 151 | ||
| 7. Which viral agents are mainly responsible for acute and chronic viral hepatitis? | 152 | ||
| 8. When should Ig be used? | 152 | ||
| 9. What vaccines are available for hepatitis A? | 152 | ||
| 10. Compare the major characteristics of VAQTA, HAVRIX, and TWINRIX | 153 | ||
| 11. Who should be immunized against hepatitis A? | 153 | ||
| 12. What side effects have been observed with the hepatitis A vaccine? | 153 | ||
| 13. Do nonresponders to hepatitis A vaccine exist? | 154 | ||
| 14. What is the lowest protective anti-HAV serum level after immunization? | 154 | ||
| 15. Does the concurrent administration of hepatitis A vaccine influence the immune response to other traveler’s vaccines? | 154 | ||
| 16. What kind of immunoprophylaxis is available for hepatitis B? | 154 | ||
| 17. What is the recommended dose of HBIG for adults and children? | 154 | ||
| 18. How many hepatitis B vaccines are available in the United States? Are they comparable? | 154 | ||
| 19. What is the immunization schedule for HBV vaccine in adults and children? | 154 | ||
| 20. What is the recommended regimen for infants born to HBsAg-positive mothers? | 155 | ||
| 21. Is a booster needed after immunization? If so, how often? | 155 | ||
| 22. Summarize the evidence for long-term immunization after vaccination. | 155 | ||
| 23. Is it possible that the vaccine will not protect against HBV infection? | 155 | ||
| 24. Is it harmful to give hepatitis B vaccine to known hepatitis B carriers? | 156 | ||
| 25. Is it appropriate to use the therapeutic vaccines to Hepatitis B? | 156 | ||
| 26. Is it possible to immunize people simultaneously against hepatitis A and B? | 156 | ||
| 27. Is immunoprophylaxis advisable for hepatitis C? | 156 | ||
| 28. Is a vaccine available for hepatitis E? | 156 | ||
| 29. Should patients with chronic liver disease be immunized against hepatitis A and hepatitis B? | 156 | ||
| Website | 156 | ||
| Bibliography | 156 | ||
| Chapter 22: Pregnancy and Liver Disease | 158 | ||
| Normal Anatomical And Physiologic Changes During Pregnancy | 158 | ||
| 1. What are the structural and functional hepatic adaptations during pregnancy? | 158 | ||
| 2. Does liver function change during pregnancy? | 158 | ||
| Diseases During Pregnancy | 158 | ||
| 3. Can gestational age differentiate between different liver diseases in pregnancy? | 158 | ||
| Coincident Occurrence | 158 | ||
| 4. Can we assume the presence of chronic liver disease in a pregnant patient withangiomas and palmar erythema on physical examination and small esophagealvarices detected endoscopically? | 158 | ||
| 5. What is the most common cause of jaundice in pregnancy? | 158 | ||
| 6. How severe is the course of viral hepatitis acquired during pregnancy? | 159 | ||
| 7. What signs and symptoms suggest the diagnosis of Budd-Chiari syndrome? | 159 | ||
| 8. Is the serum ceruloplasmin level a good diagnostic marker in pregnant women atterm who are suspected of having Wilson disease? | 159 | ||
| 9. Can we maintain a woman with Wilson disease on therapy duringpregnancy? | 159 | ||
| Intrahepatic Cholestsis Of Pregnancy | 159 | ||
| 10. What is the most common liver disorder unique to pregnancy? | 159 | ||
| 11. What is the major clinical manifestation of IHCP? | 159 | ||
| 12. What biochemical changes are noted in IHCP? | 159 | ||
| 13. What is the expected clinical and biochemical course after delivery for patientswith IHCP? | 159 | ||
| 14. What is a possible cause for abnormal bleeding in a postpartum woman previouslydiagnosed with IHCP? What is the treatment? | 160 | ||
| 15. What is the effect of IHCP on the fetus? | 160 | ||
| 16. What is the therapy for IHCP? | 160 | ||
| 17. Can IHCP recur? | 160 | ||
| 18. What atypical signs and symptoms make the diagnosis of IHCP doubtful? | 160 | ||
| 19. What biochemical changes suggest an alternate diagnosis? | 160 | ||
| Acute Fatty Liver Of Pregnancy | 160 | ||
| 20. What are the clinical and laboratory features of AFLP? | 160 | ||
| 21. How do we diagnose and treat AFLP? | 160 | ||
| 22. Is biopsy pathognomonic for AFLP? | 160 | ||
| 23. Describe the pathogenesis of AFLP. | 161 | ||
| 24. What is the outcome of a child whose mother has AFLP? | 161 | ||
| 25. Does AFLP recur in subsequent pregnancies? | 161 | ||
| 26. Is genetic testing indicated in women diagnosed with AFLP? | 161 | ||
| Hemolysis, Elevated Liver Enzymes, And Low Platelets (Hellp) | 161 | ||
| 27. What is the spectrum of liver involvement in preeclampsia? | 161 | ||
| 28. How common is HELLP syndrome? | 161 | ||
| 29. Describe the incidence and prognosis of spontaneous intrahepatic hemorrhage. | 161 | ||
| 30. What findings typically lead to the diagnosis of HELLP syndrome? | 161 | ||
| 31. What is the treatment for severe preeclamptic liver disease? | 162 | ||
| 32. Does HELLP recur in subsequent pregnancies? | 162 | ||
| 33. What information helps to differentiate AFLP from HELLP? | 162 | ||
| 34. Is prospective screening necessary in pregnancies complicated by AFLP or HELLP? | 162 | ||
| Care Of Patients With Preexisting Liver Disease | 162 | ||
| 35. What methods of contraception are available for patients with liver disease? | 162 | ||
| Management Of Underlying Liver Disease | 163 | ||
| 36. How should patients with preexisting liver disease be managed if pregnancyoccurs? | 163 | ||
| Management Of Portal Hypertension | 163 | ||
| 37. What are the effects of pregnancy on the mother with portal hypertension? | 163 | ||
| 38. What is the effect of maternal portal hypertension on pregnancy? | 163 | ||
| Management In The Setting Of Orthotopic Liver Transplantation | 163 | ||
| 39. When can a liver transplant recipient actively seek conception? | 163 | ||
| 40. Is pregnancy possible after liver transplantation? | 163 | ||
| 41. What are the possible complications of pregnancies occurring after livertransplantation? | 163 | ||
| 42. What is recomme | 164 | ||
| 43. What are pregnancy safety data regarding maintenance immunosuppressive agentsused in orthotopic liver transplantation (OLT)? | 164 | ||
| 44. Is breastfeeding permitted after delivery in a liver transplant recipient? | 164 | ||
| 45. Are immunosuppressive agents safe during pregnancy? | 164 | ||
| Prevention Of Vertical Transmission | 164 | ||
| 46. How may vertical transmission of viral hepatitis A be prevented? | 164 | ||
| 47. How may vertical transmission of viral hepatitis B be prevented? | 164 | ||
| 48. What about vertical transmission of viral hepatitis C? | 165 | ||
| 49. Is it possible to prevent vertical transmission of viral hepatitis D and G? | 165 | ||
| 50. Are HCV-infected women allowed to breastfeed? | 165 | ||
| 51. Does the mode of delivery influence hepatitis C transmission? | 165 | ||
| 52. How can perinatal HCV infection be diagnosed? | 165 | ||
| Websites | 165 | ||
| Bibliography | 165 | ||
| Chapter 23: Rheumatologic Manifestations of Hepatobiliary Diseases | 167 | ||
| Viral Hepatitis | 167 | ||
| 1. How often is viral hepatitis associated with rheumatic manifestations? | 167 | ||
| 2. What are the most common extrahepatic rheumatologic manifestations of hepatitis Binfection? | 167 | ||
| 3. Describe the clinical characteristics of the polyarthritis-dermatitis syndromeassociated with hepatitis B infection. | 167 | ||
| 4. What is the typical presentation of hepatitis B–associated polyarteritis nodosa (PAN)? | 167 | ||
| 5. How is PAN associated with hepatitis B antigenemia diagnosed? | 167 | ||
| 6. What is the treatment of hepatitis B–associated PAN? | 167 | ||
| 7. What are the most common hepatitis C virus (HCV)-related autoimmune disorders? | 167 | ||
| 8. What is the relationship between viral hepatitis and cryoglobulinemia? | 168 | ||
| 9. Describe the typical clinical features of cryoglobulinemia associated with hepatitisC infection. | 168 | ||
| Autoimmune And Other Liver Diseases | 168 | ||
| 10. What is lupoid hepatitis? | 168 | ||
| 11. To what degree is type I AIH similar to SLE? | 169 | ||
| 12. What is the difference between anti-Sm and anti-SM antibodies? | 169 | ||
| 13. List the common autoimmune diseases associated with primary biliarycirrhosis (PBC). | 169 | ||
| 14. Compare and contrast the arthritis that may occur with PBC and rheumatoidarthritis. | 169 | ||
| 15. What other musculoskeletal manifestations may occur in patients with PBC? | 170 | ||
| 16. What autoantibodies commonly occur in patients with PBC? | 170 | ||
| 17. How commonly does arthritis occur in patients with hereditary hemochromatosis? | 170 | ||
| 18. Describe the radiographic features suggestive of hemochromatotic arthropathy. | 170 | ||
| 19. What is the relationship between calcium pyrophosphate disease and hemochromatosis? | 170 | ||
| 20. Discuss the genetics of hereditary hemochromatosis. | 170 | ||
| 21. Compare and contrast the features of hemochromatotic arthropathy (HA) andrheumatoid arthritis (RA). | 171 | ||
| 22. How effective is phlebotomy in halting the progression of hemochromatoticarthropathy? | 171 | ||
| 23. What is the correlation between the severity of arthropathy and severity of liverdisease in hemochromatosis? | 171 | ||
| 24. Why does hemochromatosis cause a degenerative arthritis? | 171 | ||
| 25. What other musculoskeletal problems may occur in patients with hemochromatosis? | 171 | ||
| Bibliography | 171 | ||
| Chapter 24: Evaluation of Focal Liver Masses | 173 | ||
| 1. Describe the initial workup for a patient with a liver mass | 173 | ||
| 2. What tumor markers are useful in the evaluation of focal liver lesions? | 173 | ||
| 3. What imaging modalities are used in the detection and characterization of focal liver masses? | 174 | ||
| 4. What is the most common benign cause of a focal liver lesion? | 174 | ||
| 5. Why is oral contraceptive use important in the differential diagnosis of focal liver masses? | 174 | ||
| 6. Why is surgical resection of hepatic adenomas recommended? | 174 | ||
| 7. What is focal nodular hyperplasia (FNH)? | 174 | ||
| 8. List the differences between hepatic adenomas and FNH | 175 | ||
| 9. What is the most frequent malignancy in the liver? | 175 | ||
| 10. What is the most common primary liver cancer? | 175 | ||
| 11. Describe the various presenting forms of HCC | 175 | ||
| 12. What types of cirrhosis are most commonly associated with HCC? | 175 | ||
| 13. What clinical and laboratory findings should raise suspicion for HCC? | 175 | ||
| 14. What primary liver tumor occurs in young adults without underlying cirrhosis? | 176 | ||
| 15. What factors predispose to the development of cholangiocarcinoma? | 176 | ||
| 16. What is a Klatskin tumor? | 176 | ||
| 17. When should liver transplantation be considered in patients with HCC? | 176 | ||
| 18. When should resection be considered in patients with HCC? | 176 | ||
| 19. What palliative therapies are available for the management of HCC? | 176 | ||
| 20. Who should be screened for HCC? Describe a typical screening strategy | 177 | ||
| 21. What benign tissue abnormality may simulate a focal liver mass? | 177 | ||
| 22. What new imaging techniques are under development to evaluate focal liver masses? | 177 | ||
| 23. Why is fine-needle biopsy of hepatic masses controversial? | 177 | ||
| 24. What should be done when small incidental liver lesions are found? | 177 | ||
| 25. Outline a logical approach to the evaluation of a focal hepatic mass. | 178 | ||
| Incidental Lesions | 178 | ||
| Symptomatic Lesions | 178 | ||
| Cirrhosis Or Risk Factors For Cholangiocarcinoma | 178 | ||
| History Of Malignancy | 178 | ||
| Website | 178 | ||
| Bibliography | 178 | ||
| Chapter 25: Drug-Induced Liver Disease | 180 | ||
| 1. How common is drug-induced liver disease? | 180 | ||
| 2. How are the three patterns of drug-induced liver injury distinguished? | 180 | ||
| 3. Describe the typical chronologic association between drug exposure and onset of hepatitis or cholestasis. | 180 | ||
| 4. What is the differential diagnosis of drug-induced liver disease? | 180 | ||
| 5. Explain the two most common mechanisms of drug-induced liver injury | 180 | ||
| 6. What variables appear to influence susceptibility to drug-induced hepatic injury? | 180 | ||
| 7. Name the two most common causes of drug-induced liver disease | 181 | ||
| 8. How is acetaminophen toxic to the liver? | 181 | ||
| 9. At what dose is acetaminophen toxic? | 181 | ||
| 10. How is acetaminophen toxicity treated? | 181 | ||
| 11. Describe the clinical features of allergic hepatitis. | 181 | ||
| 12. What drugs have been reported to cause chronic hepatitis and cirrhosis? | 181 | ||
| 13. Name the two types of cholestatic drug-induced hepatic injury | 181 | ||
| 14. List the common causes of drug-induced cholestasis | 181 | ||
| 15. List the drugs associated with the mixed cholestatic-hepatitis type of liver injury | 181 | ||
| 16. Which drugs cause the three types of drug-induced steatosis (fatty liver)? | 181 | ||
| 17. Which three vascular injuries to the liver can be caused by drugs? | 182 | ||
| 18. What are the three most common drug-induced hepatic neoplasms? | 182 | ||
| 19. More than 50 drugs have been cited as causing hepatic granulomas. Name the most common | 182 | ||
| 20. What antiarthritic drugs have been reported to cause liver injury? | 182 | ||
| 21. How should patients receiving chronic methotrexate (MTX) be monitored for chronic hepatitis and cirrhosis? | 182 | ||
| 22. What are the histologic grades of MTX liver injury? | 183 | ||
| 23. Outline the recommendations for change in MTX therapy based on liver biopsy findings | 183 | ||
| 24. What are the clinical findings of chlorzoxazone hepatotoxicity? | 183 | ||
| 25. Which drugs commonly used to treat endocrine disease have been reported to cause liver injury? | 183 | ||
| 26. What commonly used cardiovascular drugs have been reported to cause liver injury? | 183 | ||
| 27. What are the clinical features of methyldopa (Aldomet) hepatocellular injury? | 184 | ||
| 28. What commonly used antimicrobial agents have been shown to cause liver injury? | 184 | ||
| 29. Who is at risk for liver toxicity from isoniazid (INH) therapy? | 184 | ||
| 30. How is INH toxicity prevented? | 184 | ||
| 31. What commonly used recreational drugs are associated with hepatotoxicity? | 184 | ||
| 32. What anesthetic agents are associated with hepatocellular injury? | 185 | ||
| 33. Can herbal therapies injure the liver? | 185 | ||
| Websites | 185 | ||
| Bibliography | 185 | ||
| Chapter 26: Alcoholic Liver Disease | 186 | ||
| 1. How does the liver metabolize ethanol? | 186 | ||
| 2. How common is alcohol abuse in the United States? | 186 | ||
| 3. How can I screen a patient for alcoholism during an office visit? | 186 | ||
| 4. What are the signs and symptoms of alcohol withdrawal syndrome? | 187 | ||
| 5. How should I manage alcohol withdrawal in the alcoholic patient? | 187 | ||
| 6. How is alcohol detoxification best managed? | 187 | ||
| 7. What are the usual steps taken for in-hospital treatment of withdrawal? | 187 | ||
| 8. What treatments help in the long term for alcohol dependency? | 188 | ||
| 9. What are the different types of alcoholic liver disease (ALD)? | 188 | ||
| 10. How does ALD differ from nonalcoholic fatty liver disease? | 188 | ||
| 11. What is the natural history of ALD? | 188 | ||
| 12. What is the epidemiology of ALD? | 189 | ||
| 13. What is the pathogenesis of ALD? | 189 | ||
| 14. What are the clinical findings in the patient with ALD? | 190 | ||
| 15. What are the laboratory findings in patients with ALD? | 190 | ||
| 16. Patients with alcoholic fatty liver may lack any laboratory signs, although aminotransferase levels and GGT can be elevated | 190 | ||
| 17. How does radiographic imaging help in evaluation of the patient with ALD? | 190 | ||
| 18. What are the characteristic histologic features of ALD? | 190 | ||
| 19. What is the treatment for ALD? | 191 | ||
| 20. What is the prognosis of patients with ALD? | 191 | ||
| 21. Does HCV infection increase the risk of cirrhosis in the alcoholic? | 192 | ||
| 22. Does alcoholic cirrhosis predispose a patient to development of HCC? | 192 | ||
| 23. How should I screen patients with alcoholic cirrhosis for HCC? | 192 | ||
| 24. Can the patient with end-stage ALD undergo liver transplantation? | 192 | ||
| Websites | 193 | ||
| Bibliography | 193 | ||
| Chapter 27: Vascular Liver Disease | 194 | ||
| 1. Describe the principal vascular anatomy of the liver. | 194 | ||
| 2. Describe the microcirculation of the liver. | 194 | ||
| 3. What makes the liver resistant to ischemic and vascular disease? | 195 | ||
| 4. What is Budd-Chiari syndrome? | 195 | ||
| 5. How is BCS diagnosed? | 196 | ||
| 6. Why do some patients with BCS have an enlarged caudate lobe? | 196 | ||
| 7. What are the histopathologic findings in BCS? | 196 | ||
| 8. What is the treatment for BCS? | 196 | ||
| 9. Which patients with BCS should be considered for liver transplantation? | 197 | ||
| 10. What is the pathogenesis of hepatic veno-occlusive disease (VOD)? | 197 | ||
| 11. What are the clinical features of VOD? | 197 | ||
| 12. How is VOD diagnosed? | 197 | ||
| 13. Describe the clinical features of ischemic hepatitis | 197 | ||
| 14. What is the pathogenesis of ischemic hepatitis? | 197 | ||
| 15. What are the clinical manifestations of congestive hepatopathy? | 197 | ||
| 16. What liver chemistry abnormalities are found in congestive hepatopathy? | 198 | ||
| 17. Describe the pathologic changes associated with congestive hepatopathy | 198 | ||
| 18. What is the most frequent vascular complication following liver transplantation? | 198 | ||
| 19. What are the risk factors for portal vein thrombosis (PVT)? | 198 | ||
| 20. What treatments options are available for PVT? | 198 | ||
| 21. What is the most common vascular tumor of the liver? | 198 | ||
| 22. What is hepatic hemangioendothelioma? | 198 | ||
| Bibliography | 199 | ||
| Chapter 28: Nonalcoholic Fatty Liver Disease and Nonalcoholic steatohepatitis | 201 | ||
| 1. What is the difference between nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)? | 201 | ||
| 2. How do patients with NAFLD present? | 201 | ||
| 3. Describe the typical NAFLD patient | 201 | ||
| 4. What is the prevalence of NAFLD and NASH? | 202 | ||
| 5. How can you distinguish between NAFLD and NASH? | 202 | ||
| 6. How is the severity of disease determined in patients with NASH? | 203 | ||
| 7. Are there other causes of fatty liver beside insulin resistance/obesity/metabolic syndrome? | 203 | ||
| 8. What is the relationship between hepatic steatosis and hepatitis C virus infection? | 203 | ||
| 9. What is the cause (pathogenesis) of NAFLD, in particular NASH? | 203 | ||
| 10. How do you treat patients with isolated fatty liver (i.e., NAFLD patients without histologic evidence of NASH)? | 204 | ||
| 11. What is the optimal treatment of patients with biopsy-proved NASH? | 204 | ||
| 12. How many patients diagnosed with NASH go on to require liver transplants? | 205 | ||
| 13. What is the role of hepatic steatosis in liver transplant donors? | 205 | ||
| 14. Does NAFLD/NASH recur after liver transplant? | 205 | ||
| Websites | 205 | ||
| Bibliography | 206 | ||
| Chapter 29: Liver Transplantation | 207 | ||
| 1. What is the current basis for prioritizing patients for cadaveric transplantation? | 207 | ||
| 2. Why was the MELD score developed? | 207 | ||
| 3. For patients with chronic liver disease, when is the appropriate time to refer for liver transplantation? | 207 | ||
| 4. Which patients with HCC are considered and prioritized for transplantation? | 207 | ||
| 5. What can be done to improve the availability of donor organs? | 208 | ||
| 6. Given the high waiting list mortality, is living donor liver transplantation (LDLT) an option? | 208 | ||
| 7. What are the advantages and disadvantages of LDLT? | 208 | ||
| 8. Who are potential recipients for LDLT? | 208 | ||
| 9. List the diseases for which liver transplantation is performed | 208 | ||
| 10. A 33-year-old man was diagnosed with acute hepatitis A 3 weeks ago. His jaundice has progressively worsened since then. Today, his wife found him to be mildly confused and brought him to the emergency department. What is the definition of acute liver fa | 209 | ||
| 11. A 21-year-old woman is admitted following an overdose of acetaminophen. How do you determine whether she should be referred for liver transplantation? | 209 | ||
| 12. Is human immunodeficiency virus (HIV) infection a contraindication to liver transplantation? | 209 | ||
| 13. What conditions are considered contraindications to liver transplantation? | 209 | ||
| 14. A 45-year-old man with end-stage liver disease is evaluated for liver transplantation. Which features of the patient’s psychosocial profile connote a good prognosis for continued abstinence from alcohol? | 210 | ||
| 15. Which factors measured in the recipient prior to transplantation correlate with reduced postoperative survival? | 210 | ||
| 16. Which immunosuppressants are used in liver transplantation? What are their mechanisms of action and side effects? | 210 | ||
| 17. What is the typical immunosuppressive regimen? | 211 | ||
| 18. A liver transplant patient has just sustained a grand mal seizure 36 hours post transplantation. The cyclosporine level is within acceptable limits. The patient is in a postictal state but has no obvious focal neurologic deficits. Which factors contribu | 211 | ||
| 19. A patient, 3 weeks post transplantation, receives erythromycin for atypical pneumonia. Does this drug affect immunosuppressive therapy? | 211 | ||
| 20. A patient who had an uncomplicated transplantation is noted to have rising liver enzyme levels on day 10 after transplantation. What is the differential diagnosis, and which tests should be obtained? | 211 | ||
| 21. A patient with cirrhosis from chronic hepatitis C undergoes liver transplantation. Ten days later his liver enzymes increase. What are the histologic findings of acute rejection versus post-transplantation hepatitis C on liver biopsy? | 212 | ||
| 22. Describe the other post-transplantation complications manifested by elevated liver enzymes | 212 | ||
| 23. A patient having early allograft rejection is treated with a 7-day course of OKT3 returns 1 week later with headache, mild fatigue, low-grade fever, and increased liver enzymes. Is this OKT3 toxicity? | 213 | ||
| 24. If the patient does not have OKT3 toxicity, what is the most likely diagnosis? | 213 | ||
| 25. What are the clinical, biochemical, and histologic features of chronic rejection? | 213 | ||
| 26. How often is it necessary to perform a second liver transplantation, and for what reasons are retransplantations performed? | 213 | ||
| 27. Describe the long-term metabolic complications that occur in the liver transplant recipient | 213 | ||
| 28. Are liver transplant recipients at increased risk to develop cancer? | 214 | ||
| 29. A liver transplant patient comes to the emergency department complaining of cough and shortness of breath. How does one suspect, diagnose, and treat Pneumocystis jiroveci (carinii) pneumonia? | 214 | ||
| 30. What factors contribute to metabolic bone disease after transplantation? | 214 | ||
| 31. A patient who underwent liver transplantation for cirrhosis due to hepatitis C returns with persistently elevated liver enzymes. Liver biopsy reveals chronic active hepatitis but no cirrhosis. Should he be treated with interferon a and/or ribavirin? | 214 | ||
| 32. Is retransplantation for recurrent hepatitis C recommended? | 215 | ||
| Bibliography | 215 | ||
| Chapter 30: Ascites | 217 | ||
| 1. What are the most common causes of ascites? | 217 | ||
| 2. Should a diagnostic tap be performed routinely on all patients with ascites at the time of admission to the hospital? | 217 | ||
| 3. How should a diagnostic paracentesis be performed? | 217 | ||
| 4. What tests should be routinely ordered on ascitic fluid? | 218 | ||
| 5. Should a diagnostic thoracocentesis be performed in patients with cirrhosis and pleural hydrothorax? | 218 | ||
| 6. Why is it useful to measure serum-ascites albumin gradient? | 218 | ||
| 7. What are the causes of high (i.e., ≥1.1 g/dL) serum-ascites albumin gradients? | 219 | ||
| 8. What are the causes of low (i.e., <1.1g/dL) serum-ascites albumin gradients? | 219 | ||
| 9. What are the variants of ascitic fluid infection? | 219 | ||
| 10. What is the diagnostic criterion of spontaneous bacterial empyema? | 219 | ||
| 11. How do you differentiate spontaneous from secondary peritonitis? | 219 | ||
| 12. Who is at high risk of developing SBP? | 220 | ||
| 13. What is the pathogenesis of SBP? | 220 | ||
| 14. What single test provides early information about possible ascitic fluid infection? | 220 | ||
| 15. What is the treatment of choice for suspected SBP? | 220 | ||
| 16. When should antibiotic treatment be started in a patient with cirrhosis and suspected ascitic fluid infection? | 221 | ||
| 17. Should the PMN cell count in ascitic fluid be monitored during treatment of SBP? | 221 | ||
| 18. Does bacterascites represent a real peritoneal infection? Should it be treated? | 221 | ||
| 19. What does the presence of bacterial DNA in blood and ascitic fluid represent in cirrhotic patients? | 222 | ||
| 20. Which subgroups of patients with liver disease should receive treatment to prevent bacterial infection? | 222 | ||
| 21. Are there alternative prophylactic treatments to quinolones for preventing bacterial infections in cirrhosis? | 222 | ||
| 22. What is the treatment of spontaneous bacterial empyema? | 222 | ||
| 23. Why is it important to know the sodium balance in patients with cirrhosis and ascites? | 223 | ||
| 24. Describe the initial treatment of patients with cirrhosis and ascites | 223 | ||
| 25. What is refractory ascites? | 223 | ||
| 26. Which patients should be treated with large-volume paracentesis? | 224 | ||
| 27. Should volume expanders be infused after large-volume paracentesis? | 224 | ||
| 28. Is there currently any indication for peritoneovenous shunt? | 224 | ||
| 29. Which patients with cirrhosis and ascites should be considered for TIPS? | 224 | ||
| 30. Which patients with cirrhosis and ascites should be evaluated for liver transplantation? | 224 | ||
| 31. What is the treatment of hepatic hydrothorax? | 225 | ||
| 32. What is dilutional hyponatremia in patients with cirrhosis? | 225 | ||
| 33. What is the treatment of dilutional hyponatremia? | 225 | ||
| 34. What is the hepatorenal syndrome? | 225 | ||
| 35. What are the criteria of hepatorenal syndrome? | 225 | ||
| 36. Describe the treatment of patients with hepatorenal syndrome | 225 | ||
| 37. Is it possible to prevent hepatorenal syndrome? | 226 | ||
| Website | 226 | ||
| Bibliography | 226 | ||
| Chapter 31: Liver Abscess | 228 | ||
| 1. What are the two major categories of liver abscess? | 228 | ||
| 2. Describe the clinical features of pyogenic liver abscess | 228 | ||
| 3. What are the clinical features of amebic liver abscess? | 228 | ||
| 4. What laboratory features are distinctive in patients with liver abscess? | 228 | ||
| 5. What are the most common sources of pyogenic liver abscess? | 228 | ||
| 6. List the organisms that commonly cause pyogenic liver abscess | 229 | ||
| 7. Do negative cultures from an abscess aspirate indicate a nonpyogenic abscess? | 229 | ||
| 8. What abnormalities can be detected on standard radiologic studies of patients with liver abscess? | 229 | ||
| 9. Which imaging studies should be obtained in evaluating a suspected liver abscess? | 229 | ||
| 10. What areas of the liver are usually affected by hepatic abscess? | 229 | ||
| 11. How can the location, size, and number of liver abscesses help to determine the source? | 230 | ||
| 12. When should a hepatic abscess be aspirated? | 230 | ||
| 13. In what situation should an amebic liver abscess be treated by open surgical drainage? | 230 | ||
| 14. Does aspiration of an amebic hepatic abscess yield diagnostic material in most patients? | 230 | ||
| 15. How often is the biliary tree involved in patients with amebic liver abscess? | 230 | ||
| 16. How can the diagnosis of an amebic abscess be confirmed? | 230 | ||
| 17. Describe the treatment for pyogenic liver abscess | 230 | ||
| 18. Describe the treatment for amebic liver abscess | 231 | ||
| 19. List the potential complications of pyogenic liver abscess | 231 | ||
| 20. List the potential complications of amebic liver abscess | 231 | ||
| 21. What is the prognosis for patients with liver abscess? | 231 | ||
| 22. Is a vaccine against amebiasis feasible? | 231 | ||
| Website | 231 | ||
| Bibliography | 232 | ||
| Chapter 32: Inheritable Forms Of Liver Disease | 233 | ||
| Hemochromatosis | 233 | ||
| 1. How do we classify the various iron-loading disorders in humans? | 233 | ||
| 2. What are neonatal iron overload and African iron overload? | 233 | ||
| 3. How much iron is usually absorbed per day? | 233 | ||
| 4. Where is iron normally found in the body? | 233 | ||
| 5. Discuss the genetic defect in patients with HH. | 234 | ||
| 6. What are the usual toxic manifestations of iron overload? | 234 | ||
| 7. What are the most common symptoms in patients with HH? | 234 | ||
| 8. Describe the most common physical findings in patients with HH. | 234 | ||
| 9. How is the diagnosis of hemochromatosis established? | 234 | ||
| 10. How commonly do abnormal iron studies occur in other types of liver disease? | 235 | ||
| 11. Is computed tomography (CT) or magnetic resonance imaging (MRI) useful indiagnosing hemochromatosis? | 235 | ||
| 12. On liver biopsy, what is the typical cellular and lobular distribution of iron in HH? | 235 | ||
| 13. How useful is HIC? | 235 | ||
| 14. How is the HII used in diagnosing HH? | 235 | ||
| 15. How do you treat a patient with HH? | 235 | ||
| 16. What kind of a response to treatment can you expect? | 235 | ||
| 17. What is the prognosis for a patient with hemochromatosis? | 236 | ||
| 18. Because hemochromatosis is an inherited disorder, what is my responsibility tofamily members once a patient has been identified? | 236 | ||
| 19. Should general population screening be done to evaluate for hemochromatosis? | 236 | ||
| a1-Antitrypsin Deficiency | 236 | ||
| 20. What is the function of a1-AT in healthy people? | 236 | ||
| 21. How common is a1-AT deficiency? | 236 | ||
| 22. Where is the abnormal gene located? | 236 | ||
| 23. What is the nature of the defect that causes a1-AT deficiency? | 236 | ||
| 24. Describe the common symptoms and physical findings of a1-AT deficiency. | 236 | ||
| 25. How is the diagnosis of a1-AT deficiency established? | 236 | ||
| 26. What histopathologic stain is used to diagnose a1-AT deficiency? | 237 | ||
| 27. How is a1-AT deficiency treated? | 237 | ||
| 28. What is the prognosis for patients with a1-AT deficiency? Should family screening beperformed? | 237 | ||
| Wilson Disease | 237 | ||
| 29. How common is Wilson disease? | 237 | ||
| 30. Where is the Wilson disease gene located? | 237 | ||
| 31. What is the usual age of onset of Wilson disease? | 237 | ||
| 32. Which organ systems are involved in Wilson disease? | 237 | ||
| 33. What are the different types of hepatic manifestations in Wilson disease? | 237 | ||
| 34. How is the diagnosis of Wilson disease established? | 237 | ||
| 35. What forms of treatment are available for patients with Wilson disease? | 238 | ||
| 36. Is it necessary to perform family screening in Wilson disease? | 238 | ||
| 37. Compare Wilson disease and HH. | 238 | ||
| Website | 238 | ||
| Bibliography | 238 | ||
| Chapter 33: Liver Histopathology | 239 | ||
| Liver Microanatomy And Injury Patterns | 239 | ||
| 1. Explain the role of liver biopsy. | 239 | ||
| 2. Many liver biopsy reports say that the basic architecture is intact and then list astring of abnormalities. What is the basic architecture? | 239 | ||
| 3. What are the geographic differences in pathology between portions of hepatic acini? | 239 | ||
| 4. What is meant by distortion of the hepatic architecture? | 239 | ||
| 5. How are degrees of fibrosis designated? | 239 | ||
| 6. What criteria are used to define the presence of cirrhosis? | 239 | ||
| 7. Can cirrhosis be diagnosed on a needle biopsy specimen? | 239 | ||
| 8. What types of liver cell injury are seen on needle specimens? What causes eachtype? | 240 | ||
| Fatty Change And Steatohepatitis | 240 | ||
| 9. Injury from either acute or chronic ethanol ingestion is one of the most commoninsults to the liver. Describe the major characteristics of mild and severe injury. | 240 | ||
| 10. What are Mallory bodies? | 240 | ||
| 11. How does scarring progress with alcoholinjury? | 240 | ||
| 12. Is alcoholic cirrhosis micronodular ormacronodular? | 240 | ||
| 13. Sometimes a biopsy shows alcoholic hepatitis, but the patient denies drinkingethanol. Is the pathologist’s diagnosis incorrect, or is there a differential diagnosisfor alcoholic hepatitis? | 241 | ||
| Viral Hepatitis | 241 | ||
| 14. How can a liver biopsy help in patients with viral hepatitis? | 241 | ||
| 15. When, if ever, is a biopsy ordered for patients with hepatitis A? With hepatitisB and C? | 241 | ||
| 16. Does chronic hepatitis have unique histopathologic features? | 241 | ||
| 17. What features are typical of chronic hepatitis? | 241 | ||
| 18. How is chronic hepatitis graded and staged? | 241 | ||
| 19. What features in the liver biopsy help to predict etiology? | 242 | ||
| 20. Can chronic viral hepatitis be confused with other injuries? | 242 | ||
| Cholestasis | 242 | ||
| 21. In patients with acute or chronic cholestasis, can the liver biopsy distinguish amongthe various differential diagnoses? | 242 | ||
| Drug Injury | 242 | ||
| 22. What histologic changes suggest drug- or toxin-related liver injury? | 242 | ||
| Bile Duct Disorders | 243 | ||
| 23. In a patient with large duct obstruction, conjugated hyperbilirubinemia, anultrasound showing bile duct stones, and clinical cholangitis, what would a biopsyshow? | 243 | ||
| 24. When is PBC diagnosed? | 243 | ||
| 25. How is PBC staged? | 243 | ||
| 26. What are the histologic features of PSC? | 243 | ||
| 27. How is PSC staged? | 244 | ||
| 28. What are the most common biopsy findings in patients with PSC? | 244 | ||
| Granulomatous Inflammation | 244 | ||
| 29. What is a granuloma? | 244 | ||
| 30. How common are granulomas in liver biopsies? | 244 | ||
| 31. What causes granulomas in the liver? | 244 | ||
| 32. In patients with fever of unknown origin, do negative stains for fungi and acid-fastbacilli exclude infection? | 244 | ||
| 33. What are the different types of granulomas? Is the distinction of diagnostic use? | 244 | ||
| 34. How often are liver granulomas secondary to a drug reaction? | 244 | ||
| Inherited Liver Disease | 244 | ||
| 35. What is hematochromatosis? | 244 | ||
| 36. Is a liver biopsy necessary to diagnosis genetic hemachromatosis? | 245 | ||
| 37. What disorders are problematic in the clinical differential diagnosis ofhemochromatosis? | 245 | ||
| 38. What is Wilson disease? Can liver biopsy help to establish the diagnosis? | 245 | ||
| 39. What other tests are helpful in patients with Wilson disease? | 245 | ||
| 40. What are the features of a1-antitrypsin (a1-AT) deficiency on liver biopsy? | 245 | ||
| 41. Is the presence of PAS-positive, diastase-resistant globules diagnostic for a1-ATdeficiency? | 246 | ||
| Neoplasms | 246 | ||
| 42. Discuss the role of liver biopsy in diagnosing metastatic neoplasms. | 246 | ||
| 43. Discuss the role of biopsy in diagnosing primary liver tumors. | 246 | ||
| 44. Can the clinical laboratory help in classifying tumors? | 246 | ||
| Transplantation | 246 | ||
| 45. Describe the role of liver biopsy in the evaluation of transplant recipients withabnormal liver function tests (LFTs) in the early postoperative period. | 246 | ||
| 46. What are the main histologic features ofacute rejection? | 246 | ||
| 47. What criteria help to distinguish recurrent hepatitis C after transplantation fromallograft rejection? | 247 | ||
| 48. Describe the role of liver biopsy in the evaluation of abnormal LFTs in the first yearafter transplantation (and beyond). | 247 | ||
| 49. How can a liver biopsy help in the evaluation of a bone marrow transplant recipientwith elevated LFTs? | 247 | ||
| Websites | 247 | ||
| Bibliography | 247 | ||
| Chapter 34: Hepatobiliary Cystic Disease | 249 | ||
| 1. Describe the five major classes and subtypes of congenital bile duct cysts (Fig. 34-1) | 249 | ||
| 2. Describe the typical clinical presentation of a bile duct cyst | 249 | ||
| 3. Compare the main features of Caroli disease and Caroli syndrome | 249 | ||
| 4. What is the incidence of malignancy within a congenital bile duct cyst? | 250 | ||
| 5. Describe the preferred treatment for patients with bile duct cyst disease | 250 | ||
| 6. What is the role of cholangiopancreatography in patients with bile duct cyst disease? | 250 | ||
| 7. Provide a differential diagnosis for a cystic hepatic lesion | 250 | ||
| 8. What is the significance of a simple hepatic cyst? | 250 | ||
| 9. Describe the ultrasonographic, CT, and magnetic resonance imaging (MRI) characteristics of a simple hepatic cyst | 250 | ||
| 10. What disease commonly is associated with polycystic liver disease (PLD)? | 251 | ||
| 11. What are the risk factors for polycystic liver disease in patients with ADPKD? | 251 | ||
| 12. Describe the clinical manifestations of complicated polycystic liver disease | 251 | ||
| 13. How does the presence of liver cysts affect hepatic function? | 251 | ||
| 14. What are the treatment options for patients with symptomatic polycystic liver disease? | 251 | ||
| 15. What is echinococcosis? | 251 | ||
| 16. Describe the usual life cycle of E. granulosus | 252 | ||
| 17. Where and how does E. granulosus infect humans? | 252 | ||
| 18. Describe the typical clinical presentation of hepatic cystic echinococcosis | 252 | ||
| 19. How is cystic echinococcosis diagnosed? | 253 | ||
| 20. What are the treatment options for hepatic cystic echinococcosis? | 253 | ||
| 21. What hepatobiliary cystic neoplasm with malignant potential can be mistaken for a simple cyst, polycystic liver disease, or a hydatid cyst? | 253 | ||
| Bibliography | 253 | ||
| Chapter 35: Gallbladder: Stones, Sludge, and Polyps | 254 | ||
| 1. How common are gallstones in Western populations? | 254 | ||
| 2. What is the natural history of asymptomatic and symptomatic gallstones? | 254 | ||
| 3. What are the risk factors for gallstones? | 254 | ||
| 4. What are the symptoms of biliary colic? | 254 | ||
| 5. What are the three principal factors involved in gallstone formation? | 254 | ||
| 6. Name some drugs, medical conditions, or medical therapy associated with gallstone/sludge formation | 254 | ||
| 7. What is biliary sludge? | 254 | ||
| 8. Can gallbladder sludge cause symptoms or complications? | 255 | ||
| 9. What is the risk of gallstones in the obese? Why are gallstones more common with obesity? | 255 | ||
| 10. Why is rapid weight loss a risk factor for development of gallstones? Can such gallstones be prevented? | 255 | ||
| 11. How do yellow, black, and brown biliary stones differ clinically? | 255 | ||
| 12. Discuss complications from the migration of gallstones | 255 | ||
| 13. What causes acute cholecystitis in patients with gallstones? | 255 | ||
| 14. What are the symptoms of acute cholecystitis? How should patients with acute cholecystitis be treated? | 255 | ||
| 15. Should patients with asymptomatic stones be treated? What is the treatment of choice for patients with symptomatic stones? | 256 | ||
| 16. What treatment options are available for patients who do not want to undergo cholecystectomy? | 256 | ||
| 17. Who is a candidate for oral bile acid dissolution therapy? | 256 | ||
| 18. What nonsurgical methods are available for stone removal or destruction? | 256 | ||
| 19. How accurate is ultrasonography for detection of cholecystolithiasis? Of choledocholithiasis? | 256 | ||
| 20. What is the role of magnetic resonance cholangiopancreatography in diagnosing common bile duct stones? | 256 | ||
| 21. What is the role of endoscopic ultrasonography in diagnosing common bile duct stones? | 257 | ||
| 22. A 65-year-old woman undergoes transabdominal ultrasonography due to postprandial abdominal pain. A 1-cm polyp is found in the gallbladder. What is the differential diagnosis? | 257 | ||
| 23. What is a porcelain gallbladder? | 257 | ||
| 24. What is Mirizzi syndrome? | 257 | ||
| 25. What is the clinical significance of a low gallbladder ejection fraction? | 257 | ||
| 26. Describe the clinical manifestations and treatment of acute acalculous cholecystitis | 257 | ||
| Bibliography | 257 | ||
| Chapter 36: Sphincter of Oddi Dysfunction | 259 | ||
| 1. What is the sphincter of Oddi? | 259 | ||
| 2. How does the sphincter of Oddi function? | 259 | ||
| 3. What is sphincter of Oddi dysfunction (SOD)? | 259 | ||
| 4. Describe the pathophysiology of SOD | 259 | ||
| 5. Name typical symptoms of SOD | 259 | ||
| 6. Who is at risk for SOD? | 260 | ||
| 7. How common is SOD? | 260 | ||
| 8. What diagnostic evaluation should be considered in a patient presenting with symptoms suggestive of SOD? | 260 | ||
| 9. Are there noninvasive tests that may be used to diagnose SOD? | 260 | ||
| 10. When should you consider endoscopic retrograde cholangiopancreatography (ERCP) with sphincter of Oddi manometry (SOM)? | 260 | ||
| 11. How is SOM performed, and what manometric criteria define SOD? | 260 | ||
| 12. Which medications can interfere with SOM pressure measurements? | 260 | ||
| 13. What are the possible complications of ERCP with SOM? | 260 | ||
| 14. In multivariate analysis, have any preprocedural pharmacologic agents been shown to help reduce post-ERCP pancreatitis in patients with suspected SOD? | 261 | ||
| 15. What is the Milwaukee classification? | 261 | ||
| 16. Does normal SOM on one occasion rule out SOD? | 261 | ||
| 17. Are there medicines to treat SOD? | 261 | ||
| 18. How is SOD treated endoscopically? | 262 | ||
| 19. What is the clinical response rate of sphincterotomy for treatment of SOD? | 262 | ||
| 20. Can pharmacologic agents cause clinical SOD? | 262 | ||
| 21. During manometry, which segment (biliary or pancreatic) should be studied? | 262 | ||
| 22. In SOD patients, when should the pancreatic duct be stented? | 262 | ||
| 23. Why do some patients with documented SOD not respond to biliary sphincter ablation? | 262 | ||
| Websites | 263 | ||
| Bibliography | 263 | ||
| Chapter 37: Acute Pancreatitis | 264 | ||
| 1. What are the causes of acute pancreatitis (AP)? | 264 | ||
| 2. What are the most common causes of AP? | 264 | ||
| 3. Which drugs have been reported to cause AP? | 264 | ||
| 4. How is pregnancy associated with AP? | 265 | ||
| 5. Which infectious agents have been implicated in causing AP? | 265 | ||
| 6. How do parasitic infections caused by C. sinensis and Ascaris lumbricoides cause AP? | 265 | ||
| 7. Is there an increased incidence of AP in patients with AIDS? | 265 | ||
| 8. How does penetrating or blunt trauma cause AP? | 265 | ||
| 9. What is pancreas divisum? Is it associated with an increased incidence of recurrent AP? | 265 | ||
| 10. What is the relationship between hypertriglyceridemia and AP? | 266 | ||
| 11. What is the relationship between hypercalcemia and AP? | 266 | ||
| 12. How is the diagnosis of AP made? | 266 | ||
| 13. How does serum amylase compare to serum lipase in the diagnosis of AP? | 266 | ||
| 14. What are the causes of hyperamylasemia and hyperlipasemia? | 266 | ||
| 15. What are macroamylasemia and macrolipasemia? | 267 | ||
| 16. What cause of AP should be suspected in patients who present with normal serum amylase levels? | 267 | ||
| 17. Does the magnitude of hyperamylasemia or hyperlipasemia correlate with the severity of AP? | 267 | ||
| 18. What is the most reliable serum marker for diagnosing biliary AP? | 267 | ||
| 19. How is AP classified? | 267 | ||
| 20. What prognostic scoring systems are used to assess the severity of AP? | 268 | ||
| 21. What is the role of serum markers in assessing the severity of AP? | 269 | ||
| 22. What are other prognostic indicators in AP? | 269 | ||
| 23. What are the major systemic complications of AP? | 269 | ||
| 24. When is infection of pancreatic necrosis suspected? | 270 | ||
| 25. What is the most common organism isolated in infected pancreatic necrosis? | 270 | ||
| 26. How is AP treated? | 270 | ||
| 27. When and via what route should nutritional support be initiated in patients with AP? | 270 | ||
| 28. When should ERCP be performed in biliary AP? | 271 | ||
| 29. Should patients undergo a cholecystectomy after an episode of biliary AP? | 271 | ||
| 30. How soon should a cholecystectomy be performed after an attack of biliary AP? | 271 | ||
| 31. Should patients with coexisting alcoholism and cholelithiasis undergo cholecystectomy to prevent further attacks of AP? | 271 | ||
| 32. What are acute pancreatic fluid collections? | 271 | ||
| 33. What are pseudocysts? | 271 | ||
| 34. When should a pseudocyst be suspected? | 272 | ||
| 35. What are the indications for pseudocyst drainage? | 272 | ||
| 36. How are pancreatic pseudocysts drained? | 272 | ||
| 37. What are possible complications of an untreated pancreatic pseudocyst? | 272 | ||
| 38. What is a pancreatic abscess? | 272 | ||
| Bibliography | 272 | ||
| Chapter 38: Chronic Pancreatitis | 274 | ||
| 1. What classification system is used for chronic pancreatitis (CP)? | 274 | ||
| 2. What is the most common cause of CP in adults? | 274 | ||
| 3. What are other causes of CP? | 274 | ||
| 4. What is autoimmune pancreatitis? | 274 | ||
| 5. What is tropical or nutritional pancreatitis? | 275 | ||
| 6. What is obstructive CP? | 275 | ||
| 7. What is hereditary pancreatitis? | 275 | ||
| 8. How is cystic fibrosis associated with CP? | 275 | ||
| 9. What is idiopathic CP? | 275 | ||
| 10. What is the most common presenting symptom of CP? | 275 | ||
| 11. What are the causes of weight loss in patients with CP? | 275 | ||
| 12. Is steatorrhea an early symptom of CP? | 275 | ||
| 13. Is diabetes mellitus an early manifestation of CP? | 275 | ||
| 14. Are measurements of serum pancreatic enzymes helpful in the diagnosis of CP? | 276 | ||
| 15. What do elevated levels of bilirubin and alkaline phosphatase suggest in the patient with CP? | 276 | ||
| 16. What specialized test directly measures pancreatic exocrine function? | 276 | ||
| 17. What conditions may be associated with a false-positive secretin stimulation test? | 276 | ||
| 18. What indirect tests of pancreatic exocrine function are used? | 276 | ||
| 19. Are plain abdominal radiographs helpful in the diagnosis of CP? | 276 | ||
| 20. What other imaging modalities are used in the diagnosis of CP? | 276 | ||
| 21. What is the role of endoscopic retrograde cholangiopancreatography (ERCP) in the diagnosis of CP? | 277 | ||
| 22. What is the Cambridge Grading system of CP based on ERCP findings? | 277 | ||
| 23. What is the role of endoscopic ultrasound (EUS) in the diagnosis of CP? | 277 | ||
| 24. What are the EUS criteria for the diagnosis of CP? | 277 | ||
| 25. What is the role of MRCP in the diagnosis of CP? | 277 | ||
| 26. What is the most common complication of CP? | 278 | ||
| 27. How are pseudocysts treated? | 278 | ||
| 28. What are other complications of CP? | 278 | ||
| 29. How is distal CBD obstruction diagnosed and treated? | 278 | ||
| 30. How is duodenal obstruction diagnosed and treated? | 278 | ||
| 31. How are pancreatic fistulas treated? | 279 | ||
| 32. How is pancreatic ascites or pancreatic pleural effusion diagnosed? | 279 | ||
| 33. Why does the presence of gastric varices in the absence of esophageal varices suggest CP? | 279 | ||
| 34. Are signs of fat-soluble vitamin deficiencies highly suggestive of CP? | 279 | ||
| 35. Are patients with CP predisposed to nephrolithiasis? | 279 | ||
| 36. How should hyperoxaluria be treated in patients with CP? | 279 | ||
| 37. Can patients with CP develop vitamin B12 malabsorption? | 279 | ||
| 38. How is steatorrhea from CP treated? | 279 | ||
| 39. What are nonsurgical modalities of pain control in CP? | 280 | ||
| 40. Does endoscopy have a role in pain control in CP? | 280 | ||
| 41. What is the role of surgery in pain control in CP? | 280 | ||
| Websites | 280 | ||
| Bibliography | 281 | ||
| Chapter 39: Pancreatic Cancer | 282 | ||
| 1. How common is pancreatic cancer (PC) and what are the most common types of malignant tumors? | 282 | ||
| 2. What are the common symptoms of PC, and where are the tumors usually located? | 282 | ||
| 3. What is the Courvoisier sign? | 282 | ||
| 4. What is the survival rate for patients with PC? | 282 | ||
| 5. What are the identifiable risk factors for PC? | 282 | ||
| 6. What genetic alterations have been identified to be associated with increased risk for PC? | 283 | ||
| 7. What are the available serum markers for early detection of PC? | 283 | ||
| 8. Are there precursor lesions to PC? | 284 | ||
| 9. What imaging modalities are used to diagnose PC? | 284 | ||
| 10. What is the double-duct sign in patients with PC? | 284 | ||
| 11. Are there high-risk groups for the development of PC that may benefit from CT and or EUS screening? | 284 | ||
| 12. What are the new staging modalities for PC? | 285 | ||
| 13. What are the common biochemical abnormalities in patients with PC? | 285 | ||
| 14. Is chemotherapy effective for patients with advanced PC? | 285 | ||
| 15. What is the median survival after the diagnosis of advanced PC? | 285 | ||
| 16. Describe the role of celiac blockade in patients with PC. | 285 | ||
| 17. What is a Whipple resection? | 285 | ||
| 18. What surgical procedures are used for cancer in the body and tail of the pancreas? | 285 | ||
| 19. When do patients with PC need palliative procedures? | 285 | ||
| Websites | 286 | ||
| Bibliography | 286 | ||
| Chapter 40: Cystic Disease of the Pancreas | 287 | ||
| 1. Provide a differential diagnosis for a cystic pancreatic lesion. | 287 | ||
| 2. What is the difference between a true pancreatic cyst and a pancreatic pseudocyst? | 287 | ||
| 3. Define an acute fluid collection | 287 | ||
| 4. Define an acute pancreatic pseudocyst | 287 | ||
| 5. Define a chronic pancreatic pseudocyst | 287 | ||
| 6. Describe the typical clinical presentation of a pancreatic pseudocyst | 287 | ||
| 7. What criteria suggest that a pseudocyst will not resolve spontaneously? | 287 | ||
| 8. When should a pseudocyst be drained? | 287 | ||
| 9. Compare the three methods for draining a pancreatic pseudocyst | 288 | ||
| 10. What criteria suggest that a pancreatic pseudocyst may undergo successful endoscopic drainage? | 288 | ||
| 11. Describe a pancreatic abscess | 288 | ||
| 12. What clinical criteria suggest the development of a pancreatic abscess? | 288 | ||
| 13. Define hemosuccus pancreaticus | 288 | ||
| 14. When should you suspect that a cystic pancreatic lesion is not a pseudocyst? | 288 | ||
| 15. What is a serous cystadenoma? | 288 | ||
| 16. What disease commonly manifests by retinal and central nervous system (CNS) hemangioblastomas, renal cell carcinoma, pheochromocytoma, and pancreatic cysts? | 289 | ||
| 17. Describe the characteristics of an MCN | 289 | ||
| 18. What is an IPMN? How does it differ from a MCN? | 289 | ||
| 19. How does the surgical management of an IPMN differ from that of a MCN? | 289 | ||
| 20. What is the utility of EUS in the evaluation of a cystic pancreatic lesion? | 289 | ||
| 21. What conditions are most commonly associated with a pancreatic retention cyst? | 289 | ||
| Websites | 290 | ||
| Bibliography | 290 | ||
| Chapter 41: Celiac Disease, Tropical Sprue, Whipple Disease, Lymphangiectasia, Immunoproliferative Small Intestinal Disease, and Nonsteroidal AAnti-Inflammatory Drugs | 291 | ||
| 1. What is the best screening test for fat malabsorption? | 291 | ||
| 2. What is the best quantitative test for fat malabsorption? | 291 | ||
| 3. Under what physiologic conditions is fecal fat excretion increased? | 291 | ||
| 4. What is the gluten-sensitive enteropathy (GSE) panel? | 291 | ||
| 5. What is tissue transglutaminase? | 292 | ||
| 6. Name the conditions to consider in previously responsive patients with celiac sprue who begin to deteriorate (Fig. 41-2) | 292 | ||
| 7. What are the hepatic manifestations of celiac sprue, and how are they managed? | 292 | ||
| 8. Describe the manifestations of Whipple disease | 292 | ||
| 9. What is the differential diagnosis of a macrophage infiltrate of the small bowel lamina propria? | 293 | ||
| 10. What causes Whipple disease? | 293 | ||
| 11. What are the complications of the enteropathy induced by nonsteroidal anti-inflammatory drugs (NSAIDs)? | 293 | ||
| 12. Does scleroderma produce any manifestations in the small bowel? | 293 | ||
| 13. How does octreotide affect intestinal motility and bacterial overgrowth in scleroderma? | 293 | ||
| 14. Describe the different forms of lymphangiectasia | 293 | ||
| 15. What are the clinical manifestations of abetalipoproteinemia? | 293 | ||
| 16. What are the different clinical presentations of eosinophilic gastroenteritis? | 293 | ||
| 17. How are patients with eosinophilic gastroenteritis treated? | 294 | ||
| 18. What are the common causes of diarrhea in a patient with Crohn’s disease and ileal resection? | 294 | ||
| 19. Where are the endemic areas for tropical sprue? | 294 | ||
| 20. How is tropical sprue treated? | 294 | ||
| 21. How is bacterial overgrowth diagnosed? | 294 | ||
| 22. What is the mechanism of hyperoxaluria in short bowel syndrome? | 294 | ||
| 23. What is immunoproliferative small intestinal disease (IPSID)? | 294 | ||
| 24. What causes IPSID and how is it treated? | 295 | ||
| 25. What are the most common clinical manifestations of IPSID? | 295 | ||
| 26. What is video capsule endoscopy, and what are the indications/contraindications for its use? | 295 | ||
| Websites | 295 | ||
| Bibliography | 295 | ||
| Chapter 42: Crohn’S Disease | 297 | ||
| Diagnosis | 297 | ||
| 1. What are the usual symptoms and signs suggestive of Crohn’s disease? | 297 | ||
| 2. How is the diagnosis of Crohn’s disease established? | 297 | ||
| 3. Which diseases can mimic the symptoms and signs of Crohn’s disease? | 298 | ||
| 4. What serologic tests can help established the diagnosis? | 298 | ||
| Etiology | 299 | ||
| 5. Is cigarette smoking associated with Crohn’s disease? | 299 | ||
| 6. What infectious agents might be responsible for Crohn’s disease? | 299 | ||
| 7. Is there a genetic predisposition for developing Crohn’s disease? | 299 | ||
| Natural History | 299 | ||
| 8. Is mortality increased in patients with Crohn’s disease? | 299 | ||
| 9. Are there factors that predict a flare-up of Crohn’s disease activity? | 299 | ||
| 10. Does behavior of disease predict its natural history? | 299 | ||
| 11. Do patients with Crohn’s disease have an excess cancer risk? | 300 | ||
| 12. What are the extraintestinal manifestations of Crohn’s disease? | 300 | ||
| Treatment | 300 | ||
| 13. Which 5-aminosalicylic acid preparations are effective in treating Crohn’s diseasepatients? | 300 | ||
| 14. Should steroids be used in Crohn’s disease? | 300 | ||
| 15. What is the role for immunosuppressive therapy in Crohn’s disease? | 300 | ||
| 16. Which biologic therapies are effective for patients with Crohn’s disease? | 301 | ||
| 17. Which medications are effective in maintaining remission? | 301 | ||
| 18. What are the indications for surgery in Crohn’s disease? | 301 | ||
| 19. What therapeutic regimen is most often effective for stricturing-type Crohn’sdisease? | 302 | ||
| 20. What therapeutic regimen is most often effective for inflammatory-type Crohn’sdisease? | 302 | ||
| 21. What therapeutic regimen is most often effective for fistulizing Crohn’s disease? | 302 | ||
| 22. When should nutritional supportbe used in patients with Crohn’sdisease? | 302 | ||
| Website | 302 | ||
| Bibliography | 302 | ||
| Chapter 43: Ulcerative Colitis | 304 | ||
| 1. What is ulcerative colitis (UC)? | 304 | ||
| 2. Define backwash ileitis | 304 | ||
| 3. What is indeterminate colitis? | 304 | ||
| 4. Why is it important to distinguish between UC and Crohn’s disease? | 304 | ||
| 5. What causes UC? | 304 | ||
| 6. Who gets UC? | 304 | ||
| 7. What are the signs and symptoms of UC? | 304 | ||
| 8. How are patients with UC classified? | 305 | ||
| 9. How are the extraintestinal manifestations of UC classified? | 305 | ||
| 10. What is colitic arthritis? | 305 | ||
| 11. Describe the association between UC and ankylosing spondylitis | 305 | ||
| 12. Discuss the hepatic complications of UC | 305 | ||
| 13. What are the ocular complications of UC? | 306 | ||
| 14. Describe the association between UC and thromboembolic events | 306 | ||
| 15. How do I evaluate a patient with UC? | 306 | ||
| 16. What are 5-ASA products? | 306 | ||
| 17. How do I treat proctitis and proctosigmoiditis? | 306 | ||
| 18. How do I treat an exacerbation of UC? | 307 | ||
| 19. What should I do if the disease is severe? | 307 | ||
| 20. Define toxic megacolon | 307 | ||
| 21. How do I prevent a relapse? | 307 | ||
| 22. Are there adjunctive therapies for UC? | 308 | ||
| 23. How often should patients have surveillance colonoscopy? | 308 | ||
| 24. What should be done if a polyp or dysplasia is found? | 308 | ||
| 25. Is surveillance effective? | 308 | ||
| 26. Is there a role for chemoprevention in UC? | 308 | ||
| 27. Is diet important in the management of UC? | 309 | ||
| 28. Does stress exacerbate UC? | 309 | ||
| 29. How does menstruation affect UC? | 309 | ||
| 30. Do patients with UC have problems with fertility and pregnancy? | 309 | ||
| 31. What medications are contraindicated in patients with UC? | 309 | ||
| 32. What are the surgical options for management of UC? | 309 | ||
| Websites | 310 | ||
| Bibliography | 310 | ||
| Chapter 44: Eosinophilic Gastroenteritis | 311 | ||
| 1. How is eosinophilic gastroenteritis (EGE) defined? | 311 | ||
| 2. What is the incidence of EGE? | 311 | ||
| 3. What is the etiology of EGE? | 311 | ||
| 4. What are the clinical features of EGE? | 311 | ||
| 5. What is the Klein classification for EGE? | 311 | ||
| 6. Why does EGE have so many different clinical faces? | 311 | ||
| 7. Is there an increase in the recognition of cases of eosinophilic infiltration of the GI tract? | 313 | ||
| 8. What is hypereosinophilia syndrome (HES)? | 313 | ||
| 9. What is the differential diagnosis of EGE? | 314 | ||
| 10. What are possible radiographic features of EGE? | 315 | ||
| 11. What are rational steps to diagnose EGE? | 315 | ||
| Laboratory Studies | 315 | ||
| 12. What should be excluded in patients with suspected EGE? | 316 | ||
| 13. What are other treatment modalities for EGE? | 316 | ||
| 14. What is the natural history of EGE? | 316 | ||
| Websites | 317 | ||
| Bibliography | 317 | ||
| Chapter 45: Bacterial Overgrowth | 318 | ||
| 1. Define bacterial overgrowth | 318 | ||
| 2. What is the usual bacterial presence in the gastrointestinal tract? | 318 | ||
| 3. What are the natural protective mechanisms against SIBO? | 318 | ||
| 4. What factors influence small intestinal bacterial proliferation? | 318 | ||
| 5. What kind of structural lesions predispose to overgrowth? | 318 | ||
| 6. How do motility disorders cause overgrowth? | 318 | ||
| 7. How can an excessive bacterial load be delivered to the small bowel? | 318 | ||
| 8. Which impairments of host defenses are important? | 318 | ||
| 9. What conditions are associated with small intestinal bacterial overgrowth? | 319 | ||
| 10. What are the other risk factors for bacterial overgrowth? | 319 | ||
| 11. What are the symptoms of overgrowth? | 319 | ||
| 12. Why do patients with bacterial overgrowth develop anemia? | 319 | ||
| 13. What other micronutrient deficiencies are clinically important? | 319 | ||
| 14. What is the association between SIBO and sepsis? | 319 | ||
| 15. How is bacterial overgrowth diagnosed? | 320 | ||
| 16. What indirect testing can be used? | 320 | ||
| 17. What are the limitations of testing? | 320 | ||
| 18. What about other testing methods? | 320 | ||
| 19. What is the treatment for bacterial overgrowth? | 320 | ||
| 20. What are the antibiotic agents used in the treatment of SIBO? | 321 | ||
| 21. Do prokinetic agents help? | 321 | ||
| 22. How long should overgrowth be treated with antibiotics? | 321 | ||
| 23. What about probiotics? | 321 | ||
| Bibliography | 321 | ||
| Chapter 46: Colorectal Cancer And Colon Cancer Screening | 323 | ||
| 1. What is colorectal cancer (CRC)? | 323 | ||
| 2. How does the pathophysiology of rectal cancer differ from cancer elsewhere in the colon? | 323 | ||
| 3. How common is colorectal cancer? | 323 | ||
| 4. Do the genetic defects leading to sporadic CRC differ from those in genetic syndromes associated with colon cancer? | 323 | ||
| 5. Describe the natural sequence from colon adenoma to colon cancer | 323 | ||
| 6. How prevalent are colonic adenomas among the U.S. population? | 324 | ||
| 7. Where in the colon are polyps most commonly located? | 324 | ||
| 8. Give the mean age of onset and describe the anatomic distribution of CRC | 324 | ||
| 9. How are malignant polyps defined? How are they clinically managed? | 324 | ||
| 10. How is colon cancer staged, and how does this affect prognosis? | 324 | ||
| 11. Describe the workup for CRC after the initial diagnosis | 325 | ||
| 12. What surgical margins are recommended? | 325 | ||
| 13. Describe the recommended schedule of colonoscopic follow-up after surgery | 325 | ||
| 14. Are there any effective blood tests to screen for CRC? | 325 | ||
| 15. List the risk factors for developing CRC | 325 | ||
| 16. What is the effect of age on the risk of developing CRC? | 325 | ||
| 17. Discuss the effect of diet on the risk for developing CRC | 325 | ||
| 18. Do environmental factors increase the risk for developing CRC? | 326 | ||
| 19. Which adenoma features are associated with a greater malignant potential? | 326 | ||
| 20. What are the recommendations for CRC screening in people at average risk for CRC? | 326 | ||
| 21. Give the current guidelines for surveillance colonoscopy in patients with a history of adenomatous polyps | 326 | ||
| 22. Who is considered to be at increased risk for developing CRC? | 326 | ||
| 23. Which method of CRC screening is recommended for individuals at increased risk of developing CRC? | 326 | ||
| 24. List the familial colon cancer syndromes | 327 | ||
| 25. What tests are available for hereditary CRC? | 327 | ||
| 26. What is the recommended surveillance for people with a family history of CRC who do not fit the genetic profiles? | 327 | ||
| 27. How do FAP and Gardner syndrome increase the risk of CRC? | 328 | ||
| 28. How are FAP and Gardner syndrome diagnosed? | 328 | ||
| 29. In addition to colonoscopy, what other tests should be considered in FAP? | 328 | ||
| 30. What is the role of NSAIDs in treating FAP? | 328 | ||
| 31. How do hamartomatous polyp syndromes affect the risk of developing CRC? | 328 | ||
| 32. What is HNPCC? | 328 | ||
| 33. How is HNPCC diagnosed? | 328 | ||
| 34. Outline the screening recommendation for patients with HNPCC | 329 | ||
| 35. What is MYH-associated polyposis (MAP)? | 329 | ||
| 36. What is microsatellite instability (MSI)? | 329 | ||
| 37. How does inflammatory bowel disease (IBD) affect the risk of developing CRC? | 329 | ||
| 38. Which two clinical conditions should raise suspicion for the presence of colon cancer? | 329 | ||
| 39. Is FOBT effective in detecting colon polyps and cancer? | 329 | ||
| 40. Does a program of periodic sigmoidoscopy decrease mortality from CRC? | 330 | ||
| 41. What is the sensitivity and specificity of an air contrast barium enema? | 330 | ||
| 42. How effective is CT colonography (CTC) as a screening test? | 330 | ||
| 43. Can CRC be prevented with medicines (chemoprevention)? | 330 | ||
| Bibliography | 330 | ||
| Chapter 47: Constipation And Fecal Incontinence | 332 | ||
| 1. What is constipation? | 332 | ||
| 2. Describe the normal mechanism of stool passage | 332 | ||
| 3. What are the major causes of constipation? | 333 | ||
| 4. Describe the workup for constipation | 333 | ||
| 5. What tests are used in the evaluation of chronic constipation? | 333 | ||
| 6. How can primary constipation be further defined? | 334 | ||
| 7. What causes impaired colonic transit? How is it diagnosed? | 334 | ||
| 8. What causes impaired rectoanal inhibitory reflex? How is it diagnosed? | 334 | ||
| 9. What is dyschezia? | 334 | ||
| 10. What is anorectal dyssyngergia? | 334 | ||
| 11. What other physiologic abnormalities may lead to anorectal dysfunction, and how are they diagnosed? | 335 | ||
| 12. How is constipation due to irritable bowel syndrome diagnosed? | 335 | ||
| 13. Describe the general management of constipation | 335 | ||
| 14. Describe the proper use of dietary fiber | 335 | ||
| 15. How do osmotic laxatives work? | 336 | ||
| 16. How do cathartics work, and are stool softeners effective? | 336 | ||
| 17. What is lubiprostone, and how does it work? | 336 | ||
| 18. Is surgery ever indicated for constipation? | 336 | ||
| 19. Are there other treatments for constipation? | 336 | ||
| 20. What is fecal incontinence? Who is generally affected? | 336 | ||
| 21. Describe the pathophysiology of fecal incontinence | 337 | ||
| 22. What are the risk factors associated with incontinence? | 337 | ||
| 23. Describe the workup for incontinence | 337 | ||
| 24. What specialized tests are available for the evaluation of incontinence? | 338 | ||
| 25. What is medical therapy for incontinence? | 338 | ||
| 26. What is biofeedback and how is it used to treat incontinence? | 338 | ||
| 27. What are surgical options for treating incontinence? | 339 | ||
| Website | 339 | ||
| Bibliography | 339 | ||
| Chapter 48: Diverticulitis | 340 | ||
| 1. What is a diverticulum? What type are colonic diverticula? | 340 | ||
| 2. How common is diverticular disease? What are the most frequent complications? | 340 | ||
| 3. How do diverticula develop? Who is at risk for developing diverticulosis? | 340 | ||
| 4. What is hypersegmentation? | 340 | ||
| 5. What is myochosis? | 340 | ||
| 6. Where are diverticula located? | 340 | ||
| 7. How does diverticulitis develop? | 340 | ||
| 8. How should symptomatic diverticulosis be managed? | 341 | ||
| 9. What is diverticular or segmental colitis? | 341 | ||
| 10. What are the common signs and symptoms of early diverticulitis? | 341 | ||
| 11. What are the signs and symptoms of severe diverticulitis? | 341 | ||
| 12. What is the Hinchey classification system? How does it predict outcome? | 341 | ||
| 13. What is the natural history of diverticulitis? | 341 | ||
| 14. List the common complications of diverticulitis. | 342 | ||
| 15. Between what organs do fistulous communications develop? | 342 | ||
| 16. What techniques are used to diagnose and localize fistulas? | 342 | ||
| 17. How is a diverticular stricture differentiated from strictures of other causes? | 342 | ||
| 18. Which drugs are known to exacerbate diverticulitis? | 342 | ||
| 19. What imaging modalities are available to diagnose diverticulitis? What is the role of each? | 342 | ||
| 20. How is mild diverticulitis defined and treated? | 342 | ||
| 21. What antibiotic regimen is appropriate for moderately severe disease? How is treatment otherwise different? | 343 | ||
| 22. How is the management of severely ill patients different? | 343 | ||
| 23. What are the indications and goals for surgery? | 343 | ||
| 24. What operations are available in the management of diverticulitis? | 344 | ||
| Websites | 345 | ||
| Bibliography | 345 | ||
| Chapter 49: Diseases Of The Appendix | 346 | ||
| 1. Describe the anatomy and function of the human appendix | 346 | ||
| 2. What is the presumed etiology of appendicitis? | 346 | ||
| 3. What are the signs and symptoms of appendicitis? | 346 | ||
| 4. What are the laboratory findings? | 346 | ||
| 5. Where and what is the McBurney point? | 346 | ||
| 6. What are the psoas and obturator signs? | 346 | ||
| 7. What is the Rovsing sign? | 346 | ||
| 8. The peak incidence of acute appendicitis occurs in what age group? | 346 | ||
| 9. The risk of perforation of the appendix is highest in what age groups? | 346 | ||
| 10. What is the surgical mortality rate for nonperforated appendicitis? Perforated appendicitis? | 346 | ||
| 11. List the differential diagnosis for right lower quadrant pain both in women and in children. | 347 | ||
| 12. What is a Meckel’s diverticulum? | 347 | ||
| 13. What is an acceptable incidence rate for negative appendectomy? Has this rate changed with the increasing use of ultra ... | 347 | ||
| 14. In older patients (older than 50 years), what condition may be indistinguishable from acute appendicitis? | 347 | ||
| 15. What features of pelvis inflammatory disease (PID) can help distinguish it from appendicitis? | 347 | ||
| 16. What is the most common malignant tumor of the appendix? Describe its management | 347 | ||
| 17. What is the proper treatment for late/perforated appendicitis that presents as an abscess? | 347 | ||
| 18. What is the most common complication after appendectomy? | 347 | ||
| 19. In what patient population is ultrasound particularly helpful in making the diagnosis of acute appendicitis? | 347 | ||
| 20. What other imaging modality is often used (and abused)? | 348 | ||
| 21. When is laparoscopic appendectomy appropriate? | 348 | ||
| 22. During an abdominal exploration for right lower quadrant pain, is removal of a normal appendix appropriate in patients with Crohn’s disease? | 348 | ||
| 23. Is an appendectomy during pregnancy a safe procedure? | 348 | ||
| 24. If an ovarian tumor is discovered during laparoscopic or open exploration, what steps should be taken? | 348 | ||
| 25. Does nonoperative therapy have any role in treating acute appendicitis? | 348 | ||
| 26. What is a Mitrofanoff procedure? | 348 | ||
| Bibliography | 348 | ||
| Chapter 50: Colitis: Pseudomembranous, Microscopic, and Radiation | 349 | ||
| Pseudomembranous Colitis | 349 | ||
| 1. What is Clostridium difficile? | 349 | ||
| 2. How is CDI defined? | 349 | ||
| 3. What causes PMC? | 349 | ||
| 4. What are the risk factors for CDI? | 349 | ||
| 5. Which antibiotics are most commonly implicated? | 349 | ||
| 6. Why do some people develop C. difficile diarrhea while others are simply colonized? | 349 | ||
| 7. How has the epidemiology of CDI changed over the past decade? | 350 | ||
| 8. What accounts for the changing epidemiology of CDIs? | 350 | ||
| 9. What possible factors mediate the hypervirulence of the BI/NAP1/027 strain? | 350 | ||
| 10. How is the diagnosis of CDI made? | 350 | ||
| 11. What are the typical findings on colonoscopy? | 350 | ||
| 12. What are the hallmarks of severe CDI? | 351 | ||
| 13. When is treatment indicated? What antibiotics are used? | 351 | ||
| 14. When should you expect a response to treatment? | 351 | ||
| 15. What other treatment options are under development and investigation? | 351 | ||
| 16. What should you do if symptoms recur after therapy? | 351 | ||
| 17. How can we control C. difficile epidemics in hospitals? | 351 | ||
| Microscopic Colitis | 352 | ||
| 18. What is microscopic colitis (MC)? | 352 | ||
| 19. What are the features of CC and LC? | 352 | ||
| 20. What are the clinical features of MC? | 352 | ||
| 21. How do you distinguish MC from patients with irritable bowel syndrome (IBS)? | 352 | ||
| 22. Are there any laboratory tests or imaging studies that can help establish thediagnosis of MC? | 352 | ||
| 23. How common is MC? | 352 | ||
| 24. Which parts of the colon are most commonly affected? | 352 | ||
| 25. What agents are associated with the pathogenesis of MC? | 353 | ||
| 26. What are the associated conditions? | 353 | ||
| 27. What is the natural history of MC? | 353 | ||
| 28. What are the treatment options? | 353 | ||
| Radiation Colitis | 353 | ||
| 29. Which part of the gastrointestinal tract is most commonly injured by radiation? | 353 | ||
| 30. What can be done to prevent radiation damage? | 353 | ||
| 31. What symptoms are associated with irradiation? | 353 | ||
| 32. What are effects of localized radiation to the colon? | 353 | ||
| 33. How can radiation colitis and proctitis be managed? | 353 | ||
| 34. What are the endoscopic therapies for chronic bleeding? | 353 | ||
| 35. How are chronic radiation-induced bowel strictures managed? | 354 | ||
| Bibliography | 354 | ||
| Chapter 51: Upper Gastrointestinal Tract Hemorrhage | 355 | ||
| 1. What are the signs and symptoms of upper gastrointestinal (UGI) bleeding? | 355 | ||
| 2. What historic facts will help with determining the source of UGI bleeding? | 355 | ||
| 3. How can the amount of acute blood lost be estimated clinically? | 355 | ||
| 4. How might one distinguish an UGI bleed from a lower GI bleed in a patient who presents with blood per rectum? | 355 | ||
| 5. What are the first steps in managing a patient with UGI bleeding? | 355 | ||
| 6. How does one interpret the Hct values in a patient with acute UGI bleeding? | 355 | ||
| 7. Why place a nasogastric (NG) tube? | 355 | ||
| 8. What types of fluid should be used for resuscitation and when? | 356 | ||
| 9. Does every patient with UGI bleeding need to be hospitalized in the intensive care unit or even hospitalized? | 356 | ||
| 10. What are the common causes of UGI bleeding? And uncommon causes? | 356 | ||
| 11. What are the endoscopic stigmata of bleeding peptic ulcer? How do they help stratify risk for rebleeding and mortality | 356 | ||
| 12. What is the role of NSAIDs in UGI bleeding? | 358 | ||
| 13. How can one preventing bleeding in patients taking NSAIDs? | 358 | ||
| 14. What are the possible sources of bleeding in a patient with cirrhosis who presents with UGI bleeding? | 359 | ||
| 15. How does one diagnose bleeding from a varix? | 359 | ||
| 16. Which patients need endoscopy and when? | 359 | ||
| 17. What techniques are available to the endoscopist for controlling active bleeding? | 359 | ||
| 18. What nonendoscopic therapies can be used to stop variceal bleeding? | 359 | ||
| 19. What endoscopic therapy is available to control variceal hemorrhage? | 359 | ||
| 20. What are the special considerations that need to be addressed in patients with cirrhosis who have acute UGI bleeding? | 359 | ||
| 21. What is a visible vessel, and what is its significance? | 359 | ||
| 22. Is there a role for other diagnostic tests when evaluating patients with UGI bleeding? | 360 | ||
| 23. Which medications, if any, can be used to reduce rebleeding from UGI tract ulcers? | 360 | ||
| 24. When and who should be treated with surgery for continued nonvariceal UGI bleeding? | 361 | ||
| 25. What medications are used for patients who go home after a bleeding episode? | 361 | ||
| 26. When and what should patients receive by mouth after an UGI bleed? | 361 | ||
| 27. When should patients be sent home after a UGI bleed? | 361 | ||
| 28. What should patients avoid once they have had a UGI bleed? | 361 | ||
| 29. How and when should patients be followed up after their episode of UGI bleeding? | 361 | ||
| Websites | 361 | ||
| Bibliography | 361 | ||
| Chapter 52: Lower Gastrointestinal Tract Bleeding | 363 | ||
| 1. Define lower gastrointestinal bleeding (LGIB) | 363 | ||
| 2. How common is LGIB? | 363 | ||
| 3. What populations are at increased risk? | 363 | ||
| 4. How does the risk of LGIB compare to that of upper GI bleed (UGIB)? | 363 | ||
| 5. What is the mortality associated with LGIB? | 363 | ||
| 6. How is history important in assessing a patient with LGIB? | 363 | ||
| 7. What can help differentiate between an upper and a lower source of bleeding? | 363 | ||
| 8. What are the first steps taken in the management of a patient with significant LGIB? | 364 | ||
| 9. How can continued or recurrent LGIB be determined? | 364 | ||
| 10. What are the causes of most common causes of LGIB? | 364 | ||
| 11. Do NSAIDs increase the risk of LGIB? | 365 | ||
| 12. What types of colitis are associated with LGI bleeding? | 365 | ||
| 13. Do all colonic vascular ectasias or angiodysplasia cause LGIB? | 365 | ||
| 14.How is postpolypectomy LGIB best managed? | 365 | ||
| 15. What diagnostic modalities are available for localization of colonic bleeding? | 365 | ||
| 16. What role does urgent colonoscopy have in the diagnosis of LGIB? | 365 | ||
| 17. Discuss how nuclear medicine scintigraphy and angiography are used in the diagnosis and treatment of LGIB | 365 | ||
| 18. What is the natural history of LGI bleeding from diverticulosis? | 366 | ||
| 19. What endoscopic methods are available for hemostasis? | 366 | ||
| 20. What are the more common causes of small intestinal bleeding? | 366 | ||
| 21. What diagnostic modalities are available for small intestinal bleeding? | 366 | ||
| 22. How does double-balloon endoscopy (DBE) compare with video capsule endoscopy? | 366 | ||
| 23. What is the role of surgery in LGIB? | 367 | ||
| Websites | 367 | ||
| Bibliography | 367 | ||
| Chapter 53: Occult and Obscure Gastrointestinal Bleeding | 368 | ||
| 1. What is occult gastrointestinal (GI) bleeding? | 368 | ||
| 2. What physical examination findings might provide a clue about the source of bleeding? | 368 | ||
| 3. What tests are used to identify patients with occult GI bleeding, and which are the best? | 368 | ||
| 4. What are the factors that influence the results of FOB testing besides bleeding from the GI tract? | 368 | ||
| 5. What is the proper procedure for FOB testing? | 368 | ||
| 6. How much blood is needed to cause a positive FOB test? | 368 | ||
| 7. Who should be electively tested for occult blood and how often? | 368 | ||
| 8. What can be expected to be found at colonoscopy in a patient older than 50 years who is FOB negative? Who is FOB positive? | 368 | ||
| 9. How should a patient with a positive FOB test be evaluated? | 369 | ||
| 10. What are some of the signs and symptoms of iron deficiency anemia? | 369 | ||
| 11. How should a patient with a positive FOB and iron deficiency anemia be initially evaluated? | 369 | ||
| 12. What tests would you do in a patient with iron deficiency (microcytic) anemia who does not respond to iron or has recurrence after an initial negative evaluation? | 369 | ||
| 13. How would the evaluation be different if the patient was only iron deficient? | 369 | ||
| 14. What is the yield for combined colonoscopy and EGD in patients who are FOB positive with or without iron deficiency? | 369 | ||
| 15. How is sprue (celiac disease) diagnosed? | 369 | ||
| 16. What is meant by obscure GI bleeding? | 369 | ||
| 17. What endoscopic tests are available for evaluating a patient with obscure GI bleeding, and how useful are they? | 369 | ||
| 18. What radiologic tests are available for evaluating a patient with obscure GI bleeding, and how useful are they? | 370 | ||
| 19. How would you sequence an evaluation of a patient with obscure GI bleeding? | 370 | ||
| 20. Angiodysplasia (vascular malformations) are a common cause of obscure GI bleeding. How are these treated? | 370 | ||
| 21. What other lesions are found to be a cause of obscure GI bleeding? | 370 | ||
| Websites | 371 | ||
| Bibliography | 371 | ||
| Chapter 54: Evaluation of Acute Abdominal Pain | 372 | ||
| 1. Provide a useful clinical definition of an acute abdomen | 372 | ||
| 2. What are the four types of stimuli for abdominal pain? | 372 | ||
| 3. What are the three categories of abdominal pain? | 372 | ||
| 4. How does the character of the abdominal pain help in the evaluation? | 372 | ||
| 5. What are the important components of the physical examination for patients with acute abdominal pain? | 372 | ||
| 6. Which laboratory tests should be obtained in patients with acute abdominal pain? | 373 | ||
| 7. Which radiologic tests should be ordered to evaluate the patient with acute abdominal pain? | 373 | ||
| 8. Pain referred to the abdomen can be confusing. What are the common extra-abdominal causes of referred abdominal pain? | 373 | ||
| 9. List the common causes of acute abdominal pain in gravid women | 374 | ||
| 10. When the appendix is found to be entirely normal during a laparotomy performed for presumed appendicitis in a gravid woman, should the appendix be removed? | 374 | ||
| 11. What is the most common cause of acute abdominal pain in elderly patients? | 374 | ||
| 12. What symptoms are helpful in evaluating for appendicitis? | 374 | ||
| 13. Discuss atypical forms of appendicitis | 374 | ||
| 14. Describe the ultrasound findings of acute appendicitis | 374 | ||
| 15. When laparotomy is performed for presumed appendicitis, what is the acceptable false-negative rate? How often is another cause identified in this setting? | 374 | ||
| 16. What is the single best test to evaluate patients infected with human immunodeficiency virus (HIV) infection who complain of acute abdominal pain? | 375 | ||
| 17. What are the cardinal features of a ruptured tubal pregnancy? | 375 | ||
| 18. What are the characteristics of acute intestinal obstruction? | 375 | ||
| 19. List the clinical characteristics of large bowel obstruction | 375 | ||
| 20. List the clinical characteristics of diverticulitis | 375 | ||
| 21. What are the characteristic CT findings of diverticulitis? | 375 | ||
| 22. List the clinical hallmarks of acute cholecystitis | 375 | ||
| 23. What is the differential diagnosis of acute cholecystitis? | 375 | ||
| 24. When should a patient undergo surgery for an acute abdomen? | 376 | ||
| 25. What conditions can result in an acute abdomen in HIV-infected patients? | 376 | ||
| 26. Are patients with systemic lupus erythematosus (SLE) at increased risk for intra-abdominal catastrophe? | 376 | ||
| 27. How common are severe GI manifestations of polyarteritis nodosa (PAN)? | 376 | ||
| 28. What causes of acute abdominal pain should be considered in illicit drug users? | 376 | ||
| Websites | 376 | ||
| Bibliography | 376 | ||
| Chapter 55: Evaluation of Acute Diarrhea | 378 | ||
| 1. What is the definition of acute diarrhea? | 378 | ||
| 2. What is the impact of acute diarrhea in the United States and worldwide? | 378 | ||
| 3. Who should undergo medical evaluation for acute diarrhea? | 378 | ||
| 4. What are the most common causes of acute bloody diarrhea? | 378 | ||
| 5. What is dysentery? | 378 | ||
| 6. Name the common causes of infectious dysentery in the United States | 378 | ||
| 7. What is the significance of stool leukocytes (white blood cells) and how are they detected? | 378 | ||
| 8. If 100 random patients with acute diarrhea underwent evaluation with stool cultures, how many would be positive? Which patients with acute diarrhea should be evaluated with a stool culture? | 378 | ||
| 9. Which patients with acute diarrhea should be evaluated with an endoscopic examination? | 379 | ||
| 10. By what mechanisms do toxigenic organisms produce diarrhea? | 379 | ||
| 11. Which Campylobacter sp. are implicated as causes of dysentery? How is Campylobacter transmitted? | 379 | ||
| 12. Describe the clinical and endoscopic features of Campylobacter diarrhea | 379 | ||
| 13. How are Salmonella organisms classified? | 379 | ||
| 14. How is Salmonella infection acquired? | 379 | ||
| 15. List the types of illnesses that can be caused by Salmonella | 379 | ||
| 16. What is typhoid fever? | 379 | ||
| 17. How is Salmonella infection treated? | 380 | ||
| 18. Describe the characteristics of Shigella infection. How is it treated? | 380 | ||
| 19. What diarrheogenic illnesses are caused by E. coli? | 380 | ||
| 20. What is the therapy for O157:H7-induced diarrhea? | 381 | ||
| 21. Describe the clinical presentation of infection with Yersinia enterocolitica | 381 | ||
| 22. Which organisms are associated with seafood-induced diarrhea? | 381 | ||
| 23. What parasites cause bloody diarrhea? | 381 | ||
| 24. Who is at risk for amebiasis? What are the potential complications of amebic dysentery? | 381 | ||
| 25. Which laboratory studies are useful in the diagnosis of amebic dysentery? | 381 | ||
| 26. Describe the treatment of amebic dysentery. What are the potential side effects? | 381 | ||
| 27. Which parasites typically cause nonbloody diarrhea? What are the risks for acquisition? | 381 | ||
| 28. What is the most common cause of hospital-acquired diarrhea? | 382 | ||
| 29. List the risk factors and therapy for infectious dysentery | 382 | ||
| 30. The use of empiric antibiotics in the treatment of acute diarrhea is potentially detrimental in what ways? | 382 | ||
| 31. Are antimotility agents contraindicated in patients with dysentery? | 382 | ||
| 32. Several members of a family develop nausea, emesis, and watery diarrhea 2 to 6 hours after a picnic. Food at the picnic included ham, rice, and custard pie. What type of bacteria is likely to be the cause? | 383 | ||
| 33. What are the common causes and incidence of travelers’ diarrhea? | 383 | ||
| 34. How can one avoid travelers’ diarrhea? | 383 | ||
| 35. Describe the treatment of travelers’ diarrhea | 383 | ||
| 36. What is cholera? | 383 | ||
| 37. How is cholera treated? | 383 | ||
| 38. What is oral rehydration solution? How does it work? | 383 | ||
| 39. What is a BRAT diet? | 383 | ||
| 40. What viruses cause acute diarrhea? | 384 | ||
| 41. What are the clinical features of rotavirus gastroenteritis? What tests are available for diagnosis? | 384 | ||
| 42. You are on your honeymoon cruise, and 25% (300 people) of the ship’s occupants are afflicted with acute gastroenteritis. What is the most likely causativeagent? | 384 | ||
| 43. A 42-year-old woman is experiencing lower abdominal cramping, bloating, and intermittent diarrhea 6 months following an episode of dysentery that she experienced during a trip to Mexico. What are the possible mechanisms ofher illness? | 384 | ||
| 44. What is Reiter’s syndrome? Which enteric infections are associated with its development? | 384 | ||
| 45. What is toxic megacolon? What are its risk factors? | 384 | ||
| 46. How does one differentiate between acute infectious dysentery and acute onset of inflammatory bowel disease as the cause of bloody diarrhea? | 384 | ||
| 47. How is acute bacterial dysentery differentiated from acute onset of ischemic colitis? | 384 | ||
| Website | 385 | ||
| Bibliography | 385 | ||
| Chapter 56: Chronic Diarrhea | 386 | ||
| 1. Define chronic diarrhea | 386 | ||
| 2. What other disorder may be described as diarrhea? | 386 | ||
| 3. What is the basic mechanism of all diarrheal diseases? | 386 | ||
| 4. What pathologic processes can cause diarrhea? | 386 | ||
| 5. List three classifications of diarrheal diseases | 387 | ||
| 6. What are the likely causes of diarrhea, according to epidemiologic characteristics? | 387 | ||
| 7. What are the likely causes of osmotic watery diarrhea? | 388 | ||
| 8. List the likely causes of secretory watery diarrhea | 388 | ||
| 9. List the likely causes of inflammatory diarrhea | 388 | ||
| 10. List the likely causes of fatty diarrhea | 389 | ||
| 11. Summarize the initial diagnostic scheme for patients with chronic diarrhea? | 389 | ||
| 12. How do you distinguish secretory and osmotic watery diarrhea? | 389 | ||
| 13. How is the fecal osmotic gap calculated? | 390 | ||
| 14. How is the fecal osmotic gap interpreted? | 390 | ||
| 15. What precautions are necessary when measuring fecal osmotic gaps? | 390 | ||
| 16. How does one evaluate osmotic diarrhea? | 390 | ||
| 17. Describe the evaluation of chronic secretory diarrhea | 390 | ||
| 18. When should neuroendocrine tumors be suspected as a cause of chronic secretory diarrhea? | 391 | ||
| 19. What is Bayes theorem? How does it relate to the diagnosis of peptide-secreting tumors? | 391 | ||
| 20. What is the likely outcome in patients with chronic secretory diarrhea in whom a diagnosis cannot be reached? | 392 | ||
| 21. Describe the evaluation of chronic fatty diarrhea | 392 | ||
| 22. How does one make a diagnosis of celiac disease? | 392 | ||
| 23. Describe the further evaluation of chronic inflammatory diarrhea | 392 | ||
| 24. How does one distinguish irritable bowel syndrome from chronic diarrhea? | 392 | ||
| 25. What causes of chronic diarrhea may be difficult to diagnose? | 393 | ||
| 26. What are common causes of iatrogenic diarrhea? | 393 | ||
| 27. What features should suggest surreptitious laxative ingestion? | 393 | ||
| 28. What is microscopic colitis syndrome? | 394 | ||
| 29. Define bile acid diarrhea | 394 | ||
| 30. What is the likely outcome in chronic idiopathic secretory diarrhea? | 394 | ||
| 31. What is the best nonspecific therapy for chronic diarrhea? | 394 | ||
| Websites | 395 | ||
| Bibliography | 395 | ||
| Chapter 57: Aids and the Gastrointestinal Tract | 396 | ||
| 1. What is the role of barium esophagram for patients with AIDS (acquired immunodeficiency syndrome) and esophageal symptoms? | 396 | ||
| 2. What is the role of empiric therapy for new-onset esophageal symptoms in patients with AIDS? | 396 | ||
| 3. What are the most common causes of esophageal ulceration in AIDS? | 396 | ||
| 4. What biopsy technique should be used to sample an esophageal ulcer? | 396 | ||
| 5. What is AIDS-cholangiopathy? How do patients present? | 397 | ||
| 6. What are the most common causes of AIDS-cholangiopathy? How are they diagnosed? | 397 | ||
| 7. What are the most common causes of pancreatitis in HIV-infected patients? | 397 | ||
| 8. How has HAART affected the incidence of opportunistic gastrointestinal (GI) disorders? | 398 | ||
| 9. What is the recommended workup for diarrhea in AIDS? | 398 | ||
| 10. Describe the clinical features of HSV proctitis in AIDS | 398 | ||
| 11. What is the preferred endoscopic procedure for the evaluation of diarrhea in AIDS? | 399 | ||
| 12. What is the most common cause of viral diarrhea in AIDS? | 399 | ||
| 13. What are the treatment options for CMV enterocolitis? | 400 | ||
| 14. Name the parasites that cause diarrhea in AIDS | 400 | ||
| 15. Compare the clinical features and therapies for cryptosporidiosis and microsporidiosis | 400 | ||
| 16. Which bacteria most commonly cause diarrhea in AIDS? | 400 | ||
| 17. What is bacillary peliosis hepatis (BPH)? | 401 | ||
| 18. Describe the management of HIV wasting syndrome | 401 | ||
| 19. When do you initiate hepatitis B virus (HBV) therapy in the setting of HIV? | 401 | ||
| 20. Why is it important to know the HBV treatments that are also active in treating HIV? | 401 | ||
| Bibliography | 401 | ||
| Chapter 58: Ischemic Bowel Disease | 403 | ||
| 1. What is ischemic bowel disease? | 403 | ||
| 2. Describe the gross anatomy of the mesenteric vascular system | 403 | ||
| 3. An extensive collateral circulatory system exists between the systemic and splanchnic vascular networks. Describe this System | 404 | ||
| 4. What is meant by autoregulation? | 404 | ||
| 5. What are the different varieties of ischemic bowel disease? | 405 | ||
| 6. What clinical circumstances predispose to ischemic bowel disease? | 405 | ||
| 7. Describe the pathophysiology of occlusive AMI | 405 | ||
| 8. What is abdominal angina? What is its clinical significance? | 406 | ||
| 9. Describe the pathophysiology of nonocclusive mesenteric ischemia | 406 | ||
| 10. What should I know about mesenteric venous occlusion as a cause of ischemic bowel disease? | 406 | ||
| 11. What is focal segmental (short segment) ischemia? | 406 | ||
| 12. What are the common symptoms of occlusive mesenteric ischemia? | 406 | ||
| 13. What are the physical findings in a patient with mesenteric ischemia? | 406 | ||
| 14. Do laboratory findings help at all? | 407 | ||
| 15. What are the differential diagnostic considerations in a patient with suspected AMI, and how do plain abdominal radiographs help elucidate the disorder? | 407 | ||
| 16. What is the role of magnetic resonance angiography (MRA) in patients with suspected abdominal angina? | 407 | ||
| 17. Describe the role of Doppler ultrasound studies in diagnosis | 408 | ||
| 18. What is the diagnostic role of endoscopy (sigmoidoscopy, colonoscopy, enteroscopy) and laparoscopy? | 408 | ||
| 19. When should you undertake invasive mesenteric angiographic studies? | 408 | ||
| 20. Is there any medical treatment for mesenteric ischemia? | 408 | ||
| 21. What is the role of angioplasty and stenting in the management of ischemic bowel disease? | 408 | ||
| 22. When should a patient with ischemic bowel disease be sent to the operating room? | 408 | ||
| 23. What is meant by a second-look operation? | 409 | ||
| 24. Can ischemia be isolated to the colon? | 409 | ||
| 25. How does ischemic colitis present clinically? | 409 | ||
| 26. How do you confirm a suspected diagnosis of ischemic colitis? | 409 | ||
| 27. What are the sequelae of ischemic colitis? Can anything be done to modify the course of the disease? | 410 | ||
| 28. When is surgery indicated in patients with ischemic colitis? | 410 | ||
| Bibliography | 410 | ||
| Chapter 59: Nutrition, Malnutrition, and Probiotics | 411 | ||
| 1. What is meant by nutritional status? | 411 | ||
| 2. Define malnutrition | 411 | ||
| 3. How do different types of malnutrition affect function and outcome? | 411 | ||
| 4. How do you perform a simple nutritional assessment? | 411 | ||
| 5. Serum proteins are a marker of overall nutritional health. Which plasma proteins will have the most sensitive turnover rate? | 411 | ||
| 6. What simple blood tests offer an instant nutritional assessment? | 411 | ||
| 7. List desirable weights for men and women (according to the 1983 Metropolitan Height and Weight Tables) | 412 | ||
| 8. Describe the types of commonly prescribed oral diets | 413 | ||
| 9. What is a hidden source of calories in the intensive care unit? | 413 | ||
| 10. Summarize the typical findings in deficiency or excess of various micronutrients | 413 | ||
| 11. What are the nutritional concerns in patients with short bowel syndrome? | 413 | ||
| 12. Describe the management of nutritional problems in patients with short bowel syndrome | 413 | ||
| 13. Describe the approach to nutritional support in patients with acute pancreatitis | 413 | ||
| 14. What adverse GI effects may be encountered in a patient using herbal supplements? | 415 | ||
| 15. How is obesity defined, and how common is it among U.S. residents? | 415 | ||
| 16. In 2007, what U.S. state had an obesity rate of less than 20%? | 415 | ||
| 17. Does obesity carry a significant risk for death? | 416 | ||
| 18. What are the medical therapies for obesity? | 416 | ||
| 19. What are the surgical options for obesity? | 416 | ||
| 20. What are the National Institutes of Health consensus criteria thought to be viable indications for bariatric surgery? | 416 | ||
| 21. What is the operative mortality of GBP surgery? | 416 | ||
| 22. What are medical benefits of bariatric surgery? | 417 | ||
| 23. What nutritional deficiencies are seen with bariatric surgery? | 417 | ||
| 24. Is the number of bacteria populating the human intestine greater than the total number of cells in the human body? | 417 | ||
| 25. What value is gut microbiotica to human existence? | 417 | ||
| 26. Is there a link between gut microbiotica and obesity? | 417 | ||
| 27. What is the definition of a probiotic? | 417 | ||
| 28. What are some of the common probiotics? | 417 | ||
| 29. Have probiotics been shown to benefit the treatment of gastrointestinal disorders? | 418 | ||
| 30. How are probiotics believed to exert beneficial effect on the gut? | 418 | ||
| Websites | 418 | ||
| Bibliography | 418 | ||
| Chapter 60: Pathology of the Lower Gastrointestinal Tract | 420 | ||
| Small Intestine | 420 | ||
| 1. What are the morphologic features of celiac disease? | 420 | ||
| 2. What is the differential diagnosis of the biopsy showing villous blunting? | 420 | ||
| 3. What are the complications of celiac sprue? | 421 | ||
| 4. Histologically, what findings suggest peptic duodentitis versus Crohn’s disease? | 421 | ||
| 5. Discuss a few causes of infectious enteritis. | 421 | ||
| 6. Discuss the neuroendocrine tumors. | 423 | ||
| Large Intestine | 424 | ||
| 7. What are the histologic features of idiopathic inflammatory bowel disease (IBD)? | 424 | ||
| 8. Discuss colitis-associated dysplasia in IBD. | 425 | ||
| 9. What is the differential diagnosis of focal active colitis? | 425 | ||
| 10. What is the differential diagnosis of pseudomembranes? | 425 | ||
| 11. Histologically, which findings helpdifferentiate infectious colitis andNSAID-associated colitis? | 425 | ||
| 12. What are the histologic features of microscopic colitis? | 426 | ||
| 13. What is the differential diagnosis of polypoid lesions that can mimic adenoma? | 427 | ||
| Polyps And Neoplasms | 427 | ||
| 14. What are the histologic features of conventional adenomas? | 427 | ||
| 15. What is meant by intramucosal carcinoma in an adenoma? | 428 | ||
| 16. What is meant by the term depressed or flat adenoma? | 428 | ||
| 17. What is the difference between hyperplastic polyp (HP), traditional serrated adenoma(TSA), and sessile serrated adenoma (SSA)? | 428 | ||
| 18. What are the genetic abnormalities in conventional CRCs? | 428 | ||
| 19. What genetic abnormalities point toHNPCC? | 429 | ||
| 20. What histologic features seen in CRCs can predict MSI-H? | 430 | ||
| 21. What is the abnormality in MSI unstable sporadic CRCs? | 430 | ||
| Polyposis Syndromes | 430 | ||
| 22. Name the hamartomatous polyp syndromes. | 430 | ||
| 23. Name the adenomatous polyp syndromes. | 430 | ||
| 24. How are neuroendocrine tumors classified? | 431 | ||
| 25. What are the most common primary tumor sites that can show colon metastases? | 431 | ||
| 26. What is the differential diagnosis of stromal tumors in colon? | 431 | ||
| Diseases Of The Appendix | 432 | ||
| 27. What is the effect of IBD on the appendix? | 432 | ||
| 28. Describe the mucinous lesions of appendix. | 432 | ||
| 29. What is the incidence of carcinoid tumors in appendectomy specimens (performedfor appendicitis)? | 432 | ||
| 30. What are the histologic types of mixed endocrine-exocrine neoplasms? | 433 | ||
| Diseases Of The Anal Canal | 433 | ||
| 31. The typical findings of Hirschsprung disease include absence of ganglion cells.What other stain can help support the diagnosis, and what is the ideal site ofbiopsy? | 433 | ||
| 32. How is anal intraepithelial neoplasia (AIN) graded and what is the risk of progressionto squamous cell carcinoma (SCC)? | 433 | ||
| 33. What are the cells of origin and the immunohistochemical profile of Pagetdisease? | 433 | ||
| Websites | 433 | ||
| Bibliography | 434 | ||
| Chapter 61: Foreign Bodies and the Gastrointestinal Tract | 435 | ||
| 1. How common are foreign bodies in the gastrointestinal (GI) tract? | 435 | ||
| 2. Which populations are at risk for foreign-body ingestion? | 435 | ||
| 3. Which areas of the GI tract lead to problems in the passage of foreign bodies? | 435 | ||
| 4. What objects are commonly ingested? | 435 | ||
| 5. Describe the typical clinical presentation of foreign-body ingestion | 435 | ||
| 6. What is suggested by respiratory symptoms related to foreign-body ingestion? | 435 | ||
| 7. Do ingested sharp objects perforate the intestine? | 435 | ||
| 8. Why is it important to identify the type of foreign body ingested? | 435 | ||
| 9. How urgent is removal of a foreign body after ingestion? | 436 | ||
| 10. Describe the signs and symptoms of a complication related to foreign-body ingestion | 436 | ||
| 11. How should foreign bodies be removed? | 436 | ||
| 12. Which anatomic/functional defects of the GI tract contribute to foreign-body obstruction? | 437 | ||
| Bibliography | 437 | ||
| Chapter 62: Functional Gastrointestinal Disorders and Irritable Bowel Syndrome | 439 | ||
| 1. What are functional gastrointestinal (GI) disorders? | 439 | ||
| 2. Define irritable bowel syndrome (IBS) | 439 | ||
| 3. Discuss the epidemiology of IBS | 439 | ||
| 4. What is the natural history of IBS? | 439 | ||
| 5. Discuss the current pathophysiology of IBS | 439 | ||
| 6. Discuss the interplay of IBS and psychiatric disorders | 440 | ||
| 7. Discuss important aspects in the patient’s history to diagnosing IBS | 440 | ||
| 8. Discuss clinical assessment of psychological disorders | 440 | ||
| 9. List the differential diagnosis for IBS | 441 | ||
| 10. Discuss postinfectious IBS and related pathology | 441 | ||
| 11. Discuss the physical exam pertinent for IBS | 441 | ||
| 12. What is Carnett test? | 441 | ||
| 13. What laboratory studies should be performed in all patients with IBS? | 441 | ||
| 14. What are alarm symptoms that should alert the clinician to investigate further? | 441 | ||
| 15. Should a colonoscopy be performed on all patients with IBS? | 441 | ||
| 16. How is IBS diagnosed? | 441 | ||
| 17. Discuss the general approach to patients with IBS | 442 | ||
| 18. Describe the initial and general treatment of IBS | 442 | ||
| 19. What medical therapies are helpful for diarrhea-predominant IBS? | 442 | ||
| 20. What is the current role for alosetron in IBS? | 442 | ||
| 21. What role do TCAs play in the treatment of IBS? | 443 | ||
| 22. Discuss therapeutic options for constipation-predominant IBS | 443 | ||
| 23. Discuss the controversy behind fiber and IBS | 443 | ||
| 24. What is the current role for tegaserod in IBS? | 443 | ||
| 25. What is the current role for lubiprostone in IBS? | 443 | ||
| 26. What role do SSRIs and serotonin-norepinephrine reuptake inhibitors (SNRIs) have in the treatment of IBS? | 444 | ||
| 27. Discuss the role of CBT and hypnotherapy in treating IBS | 444 | ||
| 28. Do probiotics and antibiotics have a role in the management of IBS? | 444 | ||
| Websites | 444 | ||
| Bibliography | 445 | ||
| Chapter 63: Endoscopic Cancer Screening and Surveillance | 446 | ||
| 1. What is endoscopic cancer screening and surveillance? | 446 | ||
| 2. Why is endoscopic cancer screening and surveillance performed for gastrointestinal (GI) cancers? | 446 | ||
| Esophagus | 446 | ||
| 3. Endoscopic cancer screening of the esophagus is primarily undertaken for what twotypes of esophageal cancer? What risk factors are associated with these two typesof cancer? | 446 | ||
| 4. What is Barrett (metaplasia) esophagus? Why is endoscopic screening andsurveillance for Barrett’s esophagus necessary? | 446 | ||
| 5. Which patients should undergo endoscopic screening for Barrett’s esophagus? | 446 | ||
| 6. What techniques are used to perform endoscopic screening in Barrett’sesophagus? | 446 | ||
| 7. What is the rationale for endoscopic surveillance in Barrett’s esophagus? | 446 | ||
| 8. What techniques are used to perform endoscopic surveillance in Barrett’s esophagus? | 447 | ||
| 9. How often should patients with Barrett’s esophagus undergo endoscopic surveillance? | 447 | ||
| 10. How do you manage low-grade dysplasia (LGD) in patients with Barrett’s esophagus? | 447 | ||
| 11. How do you manage HGD in patients with Barrett’s esophagus? | 447 | ||
| 12. What is the principal role of endoscopic ultrasound (EUS) in evaluating patients with HGD? | 447 | ||
| 13. What is the next step if adenocarcinoma is identified while performing endoscopicsurveillance for Barrett’s esophagus? | 447 | ||
| 14. What new imaging modalities are available for Barrett’s esophagus endoscopicscreening and surveillance? | 448 | ||
| 15. Do patients with achalasia have an increased risk of esophageal cancer? | 448 | ||
| 16. What is the role of endoscopic cancer surveillance in patients with achalasia? | 448 | ||
| 17. Is there a link between caustic ingestion and the development of esophagealcancer? | 448 | ||
| 18. What are the clinical characteristics of patients who develop esophageal cancerafter a caustic injury? | 448 | ||
| 19. How is endoscopic surveillance used in patients with a history of caustic ingestion? | 448 | ||
| 20. What rare genetic disorder is associated with a high incidence of SCC of the esophagus? | 448 | ||
| 21. What type of endoscopic surveillance is recommended in patients with tylosis? | 448 | ||
| 22. Are patients with a history of head and neck, lung, or esophageal SCC at risk forsynchronous or metachronous cancer of the esophagus? | 448 | ||
| 23. Are endoscopic screening and surveillance warranted in patients with aerodigestiveSCC? | 448 | ||
| Stomach And Small Bowel | 449 | ||
| 24. What is the malignant potential of gastric polyps? | 449 | ||
| 25. How are gastric polyps managed when encountered radiographically or endoscopically? | 449 | ||
| 26. Is endoscopic surveillance required after the removal of a gastric polyp? | 449 | ||
| 27. What is gastric intestinal metaplasia (GIM)? | 449 | ||
| 28. How common is GIM? What is its malignant potential? | 449 | ||
| 29. What role does endoscopic surveillance have in GIM? | 449 | ||
| 30. Are patients with pernicious anemia at an increased risk for gastric cancer? Isendoscopic screening or surveillance required? | 449 | ||
| 31. What is the frequency of gastric cancer in patients who have undergone a partialgastrectomy? | 449 | ||
| 32. What are the endoscopic surveillance recommendations for postgastrectomy surgerypatients? | 449 | ||
| 33. Who is at risk for ampullary and nonampullary duodenal adenomas? | 450 | ||
| 34. What is the upper GI tract endoscopic surveillance strategy for patients with FAP? | 450 | ||
| 35. How often is surveillance endoscopy performed on patients who have undergoneendoscopic resection of ampullary adenomas? | 450 | ||
| 36. When should surveillance endoscopy begin for patients with PJS? | 450 | ||
| 37. What is the role of capsule endoscopy in small bowel surveillance for PJS? | 450 | ||
| 38. What are the endoscopic surveillance guidelines for sporadic duodenal adenomas? | 450 | ||
| Pancreas | 450 | ||
| 39. Who should undergo endoscopic screening and surveillance for pancreatic cancer? | 450 | ||
| 40. When should endoscopic screening begin for patients at increased risk forpancreatic neoplasia? | 450 | ||
| 41. What is the recommended endoscopic surveillance interval for patients at high riskfor pancreatic cancer? | 451 | ||
| Colon | 451 | ||
| 42. At what age is CRC screening recommended for average-risk patients? What are thepreferred testing modalities for CRC screening? | 451 | ||
| 43. When should endoscopic screening begin for individuals with a family history ofCRC? How often should endoscopic surveillance be performed in these individuals? | 451 | ||
| 44. What are the endoscopic surveillance guidelines for individuals with a personalhistory of colon cancer? | 451 | ||
| 45. Outline the endoscopic surveillance guidelines for individuals with a personal historyof rectal cancer | 451 | ||
| 46. What is the role of EUS in the endoscopic surveillance of individuals with a personalhistory of rectal cancer? | 451 | ||
| 47. Do individuals with a first-degree relative diagnosed with adenomatous polypsrequire earlier screening for CRC? Do they have an increased risk for CRC? | 451 | ||
| 48. What are the surveillance recommendations for a patient with a previous history ofadenomatous colon polyps? | 451 | ||
| 49. Define familial adenomatous polyposis syndrome. What is the risk of developing CRCin patients with FAP syndrome? | 452 | ||
| 50. When should endoscopic screening begin in patients with FAP? | 452 | ||
| 51. Do patients with PJS require endoscopic screening and surveillance for CRC? | 452 | ||
| 52. What is hereditary nonpolyposis colorectal cancer syndrome (HNPCC)? | 452 | ||
| 53. What are the endoscopic screening and surveillance guidelines for HNPCC? | 452 | ||
| 54. Do patients with ulcerative colitis (US) and Crohn’s disease require endoscopicsurveillance? | 452 | ||
| 55. Which clinical characteristics increase the risk of CRC in patients with UC andCrohn’s disease? | 452 | ||
| 56. How should endoscopic surveillance be performed in patients with UC and Crohn’sdisease? | 452 | ||
| 57. What is the treatment strategy for dysplasia in patients with UC or Crohn’s disease? | 452 | ||
| 58. How are adenomatous-appearing polyps managed in patients with UC and Crohn’sdisease? | 453 | ||
| Websites | 453 | ||
| Bibliography | 453 | ||
| Chapter 64: Rheumatologic Manifestations of Gastrointestinal Diseases | 455 | ||
| Enteropathic Arthritis | 455 | ||
| 1. How often does an inflammatory peripheral or spinal arthritis occur in patients withidiopathic inflammatory bowel disease (IBD)? | 455 | ||
| 2. What are the most common joints involved in ulcerative colitis and Crohn’s diseasepatients with an inflammatory peripheral arthritis? | 455 | ||
| 3. Describe the clinical characteristics of the inflammatory peripheral arthritisassociated with idiopathic IBD. | 455 | ||
| 4. What other extraintestinal manifestations commonly occur in patients with idiopathicIBD and inflammatory peripheral arthritis? | 456 | ||
| 5. Do the extent and activity of IBD correlate with the activity of the peripheralinflammatory arthritis? | 456 | ||
| 6. Which points in the history and physical examination are helpful in separatinginflammatory spinal arthritis from mechanical low back pain in an IBD patient? | 456 | ||
| 7. Does the activity of inflammatory spinal arthritis correlate with the activity of the IBD? | 456 | ||
| 8. What human leukocyte antigen (HLA) occurs more commonly than expected inpatients with inflammatory spinal arthritis associated with IBD? | 456 | ||
| 9. What serologic abnormalities are seen in patients with IBD? | 456 | ||
| 10. Describe the typical radiographic features of inflammatory sacroiliitis and spondylitisin IBD patients. | 457 | ||
| 11. What other rheumatic problems occur with increased frequency in IBD patients? | 457 | ||
| 12. Can treatment alleviate the symptoms of inflammatory peripheral arthritis and/orspinal arthritis in IBD patients? | 458 | ||
| 13. What rheumatic disorders are associated with pouchitis, lymphocytic colitis (LC),and/or collagenous colitis (CC)? | 458 | ||
| 14. Why are patients with IBD more prone to develop an inflammatory arthritis? | 458 | ||
| Reactive Arthritis | 458 | ||
| 15. What is reactive arthritis, and what are the most common GI pathogens that cause it? | 458 | ||
| 16. Which joints are most commonly involved in a reactive arthritis following a bowelinfection (i.e., postenteritic reactive arthritis)? | 459 | ||
| 17. Describe the clinical characteristics of postenteritic reactive arthritis. | 459 | ||
| 18. What extra-articular manifestations can occur in patients with postenteriticreactive arthritis? | 459 | ||
| 19. How commonly do patients with postenteritic reactive arthritis have the clinicalfeatures of Reiter syndrome? | 459 | ||
| 20. How do the radiographic features of inflammatory sacroiliitis and spondylitis due topostenteritic reactive arthritis differ from those in IBD patients? | 459 | ||
| 21. Discuss the relationship of HLA-B27 positivity in patients with postenteritic reactivearthritis compared with a normal healthy population. | 460 | ||
| 22. Explain the current theory for the pathogenesis of a postenteritic reactive arthritis. | 460 | ||
| 23. Is any therapy beneficial for postenteritic reactive arthritis? | 460 | ||
| Whipple Disease | 461 | ||
| 24. Who was Whipple? | 461 | ||
| 25. What are the multisystem manifestations of Whipple disease? | 461 | ||
| 26. Describe the clinical characteristics of the arthritis associated with Whippledisease. | 461 | ||
| 27. What is the etiology of Whipple disease? | 461 | ||
| 28. How is Whipple disease best treated? | 461 | ||
| Other Gastrointestinal Diseases | 462 | ||
| 29. What rheumatic manifestations have been described in patients with celiac disease(gluten-sensitive enteropathy)? | 462 | ||
| 30. Describe the intestinal bypass arthritis-dermatitis syndrome. | 462 | ||
| 31. What types of arthritis can be associated with carcinomas of the esophagus and colon? | 462 | ||
| 32. What are the clinical features of the pancreatic panniculitis syndrome? | 462 | ||
| 33. What musculoskeletal problem can occur with pancreatic insufficiency? | 462 | ||
| Bibliography | 462 | ||
| Chapter 65: Dermatologic Manifestations of Gastrointestinal Disease | 464 | ||
| 1. At what serum level of bilirubin do adults and infants develop clinically noticeable jaundice? | 464 | ||
| 2. Where is clinical jaundice first visible? | 464 | ||
| 3. What other conditions produce yellowish discoloration of the skin? | 464 | ||
| 4. What are Terry nails and Muehrcke nails? | 464 | ||
| 5. What gastrointestinal disease is associated with blue lunulae? | 464 | ||
| 6. What are spider angiomas? Why are they associated with liver disease? | 464 | ||
| 7. Do the number of spider angiomas correlate with the severity of alcohol-induced liver disease? | 465 | ||
| 8. Why do many patients with hepatobiliary disease itch? | 465 | ||
| 9. A 64-year-old alcoholic man presents with blisters on the dorsal hands and sclerotic changes of the facial skin. For what chronic liver disease should he screened? | 465 | ||
| 10. A 25-year-old woman presents with painful, tender, red-to-violaceous subcutaneous nodules of the pretibial skin associated with diarrhea. What is the skin lesion? | 465 | ||
| 11. A 22-year-old woman presents with low-grade fever and an expanding oozing ulcer of the hand that is rapidly increasing in size despite aggressive surgical debridement and intravenous antibiotics. What does this patient have? | 465 | ||
| 12. List the GI diseases most commonly associated with pyoderma gangrenosum | 466 | ||
| 13. What are the cutaneous manifestations of pancreatitis? | 466 | ||
| 14. A 32-year-old man presents with a 2-year history of recurrent blisters that are intensely pruritic and have been recalcitrant to antihistamines and topical corticosteroids. They are primarily located on the elbows, knees, and buttocks. What does this pa | 466 | ||
| 15. What GI disease is most commonly associated with dermatitis herpetiformis? | 466 | ||
| 16. A 30-year-old man presents with acute GI bleeding. He has yellowish pebbly papules that coalesce into plaques of the neck, antecubital fossae, and axillae. Similar lesions are also present on his lower lip. What does he have? | 467 | ||
| 17. A 24-year-old man presents with a history of unexplained melena, nose bleeds, and red macular lesions of his lips and fingers. What does he have? | 467 | ||
| 18. During evaluation for GI bleeding, a 25-year-old man is noted to have 2- to 4-mm pigmented macules of the lips and buccal mucosa. What does he most likely have? | 467 | ||
| 19. During evaluation for numerous polyps of the colon, a 19-year-old man is noted to have multiple cysts of the skin and an osteoma. What does he most likely have? | 467 | ||
| 20. A 44-year-old man presents with multiple hamartomatous polyps of the small and large bowel. Cutaneous examination reveals cobblestoning of the oral mucosa and multiple small papules and verrucous papules of this face. What does this patient most likely | 467 | ||
| 21. A 60-year-old man has had multiple keratoacanthomas removed from his skin and recently had a biopsy of a sebaceous adenoma of the cheek. For what syndrome should he be evaluated? | 468 | ||
| 22. What is Trousseau sign? | 468 | ||
| 23. A 50-year-old woman presents with alopecia, unexplained 20-pound weight loss, and very superficial flaccid vesicles and erosions on an erythematous base that preferentially involves the perioral and perianal areas. What does she most likely have? | 468 | ||
| 24. Who was Sister Mary Joseph and what is a Sister Mary Joseph nodule? | 468 | ||
| Website | 468 | ||
| Bibliography | 469 | ||
| Chapter 66: Endocrine Aspects of Gastroenterology | 470 | ||
| 1. What are the etiologies of diabetic gastroparesis? How should it be treated? | 470 | ||
| 2. Describe the mechanisms of chronic diarrhea in diabetes mellitus and their treatments | 470 | ||
| 3. Patients with primary biliary cirrhosis (PBC) are at increased risk for what endocrine disorders? | 470 | ||
| 4. What are the most prominent GI manifestations seen in hyperthyroidism and in hypothyroidism? | 471 | ||
| 5. Name the two metabolic causes of acute pancreatitis. Which diabetic medication may cause acute pancreatitis? | 471 | ||
| 6. Define hypoglycemia and list the counter-regulatory response to hypoglycemia | 471 | ||
| 7. What is Whipple triad? Why is it important? | 472 | ||
| 8. Which GI and hepatic disturbances are associated with hypoglycemia? | 472 | ||
| 9. How does ethanol cause hypoglycemia? | 472 | ||
| 10. Should routine screening for polyps and colorectal cancer be performed in patients with acromegaly? | 472 | ||
| 11. What GI symptoms may be seen with hypercalcemia? | 473 | ||
| 12. What are the National Institutes of Health (NIH) criteria for bariatric surgery? | 473 | ||
| 13. How effective are bariatric surgical procedures for long-term control of morbid obesity? | 473 | ||
| 14. Describe gut hormone changes following Roux-en-Y gastric bypass (RYGB) that theoretically may explain the developmen that theoretically may explain the development of nesidioblastosis | 473 | ||
| 15. What is multiple endocrine neoplasia type 1 (MEN1)? | 474 | ||
| 16. List the order of pancreatic islet cell tumor prevalence in MEN1 and their clinical manifestations | 474 | ||
| 17. Are patients with MEN1 and gastrinomas at greater risk for esophageal complications compared with gastrinoma patient without MEN1? | 474 | ||
| 18. Define carcinoid syndrome | 474 | ||
| 19. How are carcinoid tumors classified? | 474 | ||
| 20. Where do carcinoid tumors occur, and what are the characteristic features of carcinoid tumors by site of origin? | 474 | ||
| 21. How is carcinoid syndrome treated? | 475 | ||
| 22. What hepatic effects are seen in patients with adrenal disorders? | 475 | ||
| Bibliography | 475 | ||
| Chapter 67: Radiography And Radiographic-Fluoroscopic Contrast Examinations | 477 | ||
| 1. When requesting an imaging examination, what information should a clinician provide for a radiologist? | 477 | ||
| Abdominal Radiography | 477 | ||
| 2. Which radiographs should constitute an acute abdominal series? | 477 | ||
| 3. What is the key radiographic finding of bowelobstruction? | 478 | ||
| 4. What are causes of pneumatosis intestinalis? | 478 | ||
| 5. What distinguishes portal venous gas from pneumobilia? | 478 | ||
| Contrast Media | 479 | ||
| 6. When is barium preferable to iodinated contrast media to opacify the lumen of thegastrointestinal (GI) tract? | 479 | ||
| 7. What is the role of iodinated (water-soluble) contrast for opacification of the lumenof the GI tract? | 480 | ||
| 8. Are some iodinated contrast media better than others? | 480 | ||
| Swallowing Studies | 481 | ||
| 9. What is a barium swallow? | 481 | ||
| 10. What can a barium swallow contribute to an evaluation for dysphagia? | 481 | ||
| 11. Which esophageal motility disorders are diagnosable by barium swallow? | 482 | ||
| 12. What may a barium swallow contribute to diagnosis and managementof GERD? | 482 | ||
| 13. How can a barium swallowdistinguish achalasia fromscleroderma? | 482 | ||
| 14. What findings help distinguishachalasia secondary to cancerfrom primary achalasia? | 482 | ||
| Upper Gastrointestinal Series | 483 | ||
| 15. Can benign and malignant gastric ulcers be distinguished? | 483 | ||
| Small Bowel | 483 | ||
| 16. What are advantages and disadvantages of, and indications for, enteroclysis (smallbowel enema)? | 483 | ||
| 17. When information from imaging, beyond that provided by radiographs, is indicatedfor suspected small bowel obstruction, which fluoroscopic-radiographic contrastexamination is best? | 484 | ||
| 18. When is CT preferable to a fluoroscopic-radiographic contrast study for small bowelobstruction? | 484 | ||
| 19. When is a retrograde examination of small bowel indicated? | 485 | ||
| Colon And Rectum | 485 | ||
| 20. What are indications for single-contrast and double-contrast techniques of bariumenema examination? | 485 | ||
| 21. What are advantages and disadvantages of screening for colon cancer with a bariumenema instead of colonoscopy? | 485 | ||
| 22. What is the role of defecography (evacuation proctography)? | 485 | ||
| Cholangiopancreatography | 485 | ||
| 23. What cholangiopancreatographic features distinguish pancreatitis from ductaladenocarcinoma of the pancreatic head? | 485 | ||
| 24. What is the double duct sign of cholangiopancreatography? | 485 | ||
| 25. What pancreatographic features distinguish pancreas divisum from completeobstruction of the main pancreatic duct? | 487 | ||
| Other | 487 | ||
| 26. What are advantages of fistulography? | 487 | ||
| Websites | 487 | ||
| Bibliography | 488 | ||
| Chapter 68: Interventional Radiology: Cross-Sectional Imaging Procedures | 489 | ||
| 1. What common percutaneous procedures are performed using cross-sectional imaging guidance? | 489 | ||
| 2. What materials and equipment are used for FNAs, core biopsies, and percutaneous catheter drainages? | 489 | ||
| 3. What are the indications for percutaneous image-guided biopsy? | 489 | ||
| 4. What four conditions must be satisfied before a percutaneous procedure can be performed? | 489 | ||
| 5. What coagulation parameters are assessed before a percutaneous procedure? | 489 | ||
| 6. Which imaging modalities are used to guide interventional procedures? | 490 | ||
| 7. Summarize the advantages and disadvantages of US | 490 | ||
| 8. Summarize the advantages and disadvantages of CT | 491 | ||
| 9. Summarize the advantages and disadvantages of conventional fluoroscopy | 491 | ||
| 10. Summarize the advantages and disadvantages of MRI | 492 | ||
| 11. What two techniques can be used to drain fluid collections? | 492 | ||
| 12. Which technique is used more often? | 492 | ||
| 13. What pharmacologic agents can be injected into septated or viscous abdominal fluid collections to improve drainage? | 492 | ||
| 14. What should you suspect if the drainage catheter has persistently elevated outputs? | 492 | ||
| 15. When should you remove the drainage catheter? | 492 | ||
| 16. What are the major complications of percutaneous procedures? | 492 | ||
| 17. How common is seeding of the needle tract during routine tumor biopsy? | 493 | ||
| Hepatic Interventions | 493 | ||
| 18. What image-guided procedures are performed in the liver? | 493 | ||
| 19. How is hepatic metastatic disease diagnosed? | 493 | ||
| 20. How is malignant, primary hepatic neoplasm diagnosed? | 493 | ||
| 21. How are pyogenic hepatic or parahepatic abscesses treated? | 493 | ||
| 22. Describe the treatment of simple, benign, epithelialized hepatic cysts | 493 | ||
| 23. Is FNA or core biopsy safe for all hepaticlesions? | 494 | ||
| 24. Describe the percutaneous thermal ablative treatments for HCC? | 495 | ||
| 25. What are the advantages of RFA and other methods of percutaneous thermalablation? | 496 | ||
| 26. What are the contraindications of RFA or percutaneous thermal ablative techniques? | 496 | ||
| 27. Describe the association of Childs-Pugh score and survival in patients with HCCtreated with RFA. | 496 | ||
| 28. Describe the risks of RFA related to the anatomic location of the tumor? | 496 | ||
| 29. In the treatment of HCC, how do survival outcomes of RFA compare to surgicalresection? | 496 | ||
| 30. Describe the advantages of combining RFA with transcatheter arterialchemoembolization (TACE) in the treatment of HCC? | 496 | ||
| 31. What other liver cancers have been treated with percutaneous thermal ablativetechniques? | 496 | ||
| Splenic Interventions | 497 | ||
| 32. What interventions are possible in the spleen? | 497 | ||
| Pancreatic Procedures | 497 | ||
| 33. What procedures are appropriate for solid pancreatic masses? | 497 | ||
| 34. What procedures are used for pancreatic fluid collections? | 498 | ||
| 35. What precautions apply to percutaneous drainage of pancreatic fluid collections? | 498 | ||
| Adrenal Biopsy | 499 | ||
| 36. What is the role of adrenal gland biopsy? | 499 | ||
| Bibliography | 499 | ||
| Chapter 69: Interventional Radiology: Fluoroscopic and Angiographic Procedures | 500 | ||
| Hepatic Transarterial Chemoembolization | 500 | ||
| 1. Define hepatic transarterial chemoembolization. | 500 | ||
| 2. How safe is hepatic TACE? | 500 | ||
| 3. Why would TACE be used to treat patients with hepatic malignancy? | 500 | ||
| 4. How effective is TACE? | 501 | ||
| Yttrium-90 (90Y)-Radioembolization | 501 | ||
| 5. Describe 90Y-radioembolization. | 501 | ||
| 6. Name the two FDA-approved and commercially available radioactive microspheresand describe their differences. | 501 | ||
| 7. Compare and contrast radioembolization and TACE. | 501 | ||
| 8. What are the contraindications of radioembolization? | 502 | ||
| Biliary Procedures | 502 | ||
| 9. Is percutaneous transhepatic biliary drainage the primary method to treat biliaryobstruction? | 502 | ||
| 10. What are the indications for PTBD? | 502 | ||
| 11. What particular problems are involved in the treatment of hilar obstruction? | 502 | ||
| 12. Why is endoscopic drainage difficult in patients with biliary obstruction afterbiliary-enteric anastomosis? | 502 | ||
| 13. Describe the approach to bile duct injuries due to laparoscopic cholecystectomy. | 502 | ||
| 14. Explain the advantages and disadvantages of using metallic stents for the treatmentof biliary obstruction. | 502 | ||
| 15. What are the indications for percutaneous cholecystostomy? | 503 | ||
| Gastrointestinal Bleeding | 503 | ||
| 16. When do diagnostic angiography and percutaneous transcatheter therapy play a rolein the management of gastrointestinal (GI) bleeding? | 503 | ||
| 17. How important is localization of the bleeding site before angiography? | 503 | ||
| 18. What two types of transcatheter therapy are used for GI bleeding? | 504 | ||
| 19. What agents are used for transcatheter embolization? | 504 | ||
| Transjugular Liver Biopsy | 504 | ||
| 20. What are the specific indications for transjugular liver biopsy? | 504 | ||
| 21. How is it performed? | 504 | ||
| 22. Why is it important to biopsy via the right hepatic vein and not the middlehepatic vein? | 504 | ||
| Transjugular Intrahepatic Portosystemic Shunt | 505 | ||
| 23. What is TIPS? How is it performed? | 505 | ||
| 24. What are the benefits of successful TIPS? | 505 | ||
| 25. What are the indications for TIPS? | 505 | ||
| 26. What are the contraindications to performing the TIPS procedure? | 505 | ||
| 27. What is the technical success rate for TIPS? What are the most common causes of afailed procedure? | 505 | ||
| 28. How effective is the TIPS procedure for controlling variceal hemorrhage? | 505 | ||
| 29. What are the morbidity and mortality rates for TIPS? | 506 | ||
| 30. Describe the major long-term complication of TIPS. How is it treated? | 506 | ||
| 31. How is shunt patency followed? | 506 | ||
| Bibliography | 507 | ||
| Chapter 70: Nonivasive Gastrointestinal Imaging: Ultrasound, Computed Tomography, Magnetic Resonance Imagine | 508 | ||
| Liver Imaging | 508 | ||
| 1. How is segmental liver anatomy defined? | 508 | ||
| 2. How has the advent of multidetector computed tomography (MDCT) changed theevaluation of the liver, pancreas and biliary system? | 508 | ||
| 3. What is CT arterial portography? | 508 | ||
| 4. What causes fatty filtration of the liver? | 508 | ||
| 5. Describe the imaging findings of fatty infiltration of the liver. | 509 | ||
| 6. Describe the imaging findings in cirrhosis. | 509 | ||
| 7. Define primary and secondary hemochromatosis. | 510 | ||
| 8. Which is the most sensitive exam in detecting hemochromatosis? | 510 | ||
| 9. How do liver metastases appear on different imaging modalities? | 510 | ||
| 10. What MRI contrast agents are available for use in hepatobiliary imaging? | 510 | ||
| 11. What are the three growth patterns of HCC? | 512 | ||
| 12. How does HCC appear on different imaging modalities? | 512 | ||
| 13. What is the most common benign neoplasm of the liver? | 513 | ||
| 14. Describe the imaging characteristics of hepatic hemangiomas. | 513 | ||
| 15. Outline the workup for a suspected cavernous hemangioma. | 513 | ||
| 16. How can FNH and hepatocellular adenoma (HCA) be differentiated? | 514 | ||
| 17. Describe the appearance of FNH on imaging modalities. | 514 | ||
| 18. How does HCA appear on imaging modalities? | 515 | ||
| 19. Describe the appearance of a hepatic abscess on imaging. | 515 | ||
| Doppler Imaging Of The Liver | 515 | ||
| 20. What is a normal Doppler waveform? | 515 | ||
| 21. Describe the sonographic findings of portal hypertension on Dopplerwaveforms. | 515 | ||
| 22. How are Doppler waveforms altered inportal vein thrombosis? | 516 | ||
| 23. How does Budd-Chiari syndrome affect Doppler waveforms? | 516 | ||
| 24. Discuss the role of US in the evaluation of transjugular intrahepatic portosystemicshunts (TIPS). | 516 | ||
| Biliary Tract Imaging | 516 | ||
| 25. Describe the sonographic findings in acute cholecystitis | 516 | ||
| 26. What other conditions can result in gallbladder wall thickening? | 516 | ||
| 27. Describe the radiologic workup of suspected biliary tree obstruction. | 517 | ||
| 28. What is MRCP? What advantages does it have compared with ERCP? | 517 | ||
| 29. Describe the differential imaging features seen in the common causes of biliaryobstruction. | 518 | ||
| Pancreatic Imaging | 518 | ||
| 30. How can acute pancreatitis be distinguished from chronic pancreatitis on imaging? | 518 | ||
| 31. Describe the role of CT and US in assessing the complications of pancreatitis. | 519 | ||
| 32. What are the imaging findings of pancreatic ductal adenocarcinoma? | 520 | ||
| 33. Which imaging modality is best for detecting and staging pancreatic cancer? | 520 | ||
| 34. What are the CT criteria for unresectability of pancreatic carcinoma? | 520 | ||
| 35. What are the characteristic features of the major cystic pancreatic neoplasms? | 520 | ||
| Abdominal And Pelvic Imaging | 521 | ||
| 36. How is simple ascites distinguished from complicated ascites? | 521 | ||
| 37. How do you differentiate abdominal fluid from pleural fluid? | 521 | ||
| 38. How has MDCT changed evaluation of the small bowel? | 521 | ||
| 39. How is CT used to evaluate the large bowel? | 523 | ||
| 40. Describe the optimal radiographic workup of diverticulitis. | 523 | ||
| 41. What are the CT and US findings of acuteappendicitis? | 524 | ||
| 42. Which examination is better for diagnosing acute appendicitis? | 524 | ||
| 43. Discuss the role of imaging in the assessment of intra-abdominal abscess | 524 | ||
| 44. What is CT or virtual colonoscopy and how effective is it in screening for polyps? | 524 | ||
| Aids-Related Disorders | 524 | ||
| 45. What characteristic features of AIDS are seen in the biliary system? | 524 | ||
| 46. Describe the imaging features of AIDS in the liver. | 525 | ||
| 47. What extrahepatic manifestations of AIDS in the GI tract can be noted by imaging? | 525 | ||
| Bibliography | 525 | ||
| Chapter 71: Nuclear Imaging | 527 | ||
| 1. Outline the general advantages of nuclear medicine procedures compared with other imaging modalities. | 527 | ||
| 2. What are the disadvantages of nuclear medicine procedures compared with other radiographic studies? | 527 | ||
| 3. What nuclear medicine tests are most helpful in gastrointestinal (GI) medicine? | 527 | ||
| 4. How is cholescintigraphy (hepatobiliary imaging) performed? What is a normal study? | 527 | ||
| 5. How should patients with acute cholecystitis be prepared? What manipulations are used to shorten the study or increase its reliability? | 527 | ||
| 6. How is cholescintigraphy used to diagnose and manage biliary leak? | 528 | ||
| 7. What is the role of cholescintigraphy in diagnosing biliary atresia? | 529 | ||
| 8. What is gallbladder dyskinesia? How does cholescintigraphy evaluate the emptying of the gallbladder? | 530 | ||
| 9. What nuclear medicine esophageal studies are available? How are they used? | 530 | ||
| 10. What is a nuclear medicine gastric emptying study? | 531 | ||
| 11. What is the role for nuclear medicine studies in evaluating hepatic mass lesions? | 531 | ||
| 12. How can nuclear medicine procedures assist in detecting ectopic gastric tissue? | 532 | ||
| 13. Can accessory splenic tissue or splenosis be detected via nuclear medicine procedures? | 532 | ||
| 14. Which nuclear medicine procedures are useful in localizing lower GI bleeding? | 533 | ||
| 15. Are nuclear medicine procedures clinically useful in localizing GI bleeding, or are simpler techniques adequate? | 533 | ||
| 16. Is nuclear medicine helpful in placement of arterial perfusion catheters? | 534 | ||
| 17. Are there additional minimally invasive treatments for unresectable malignant liver masses? | 534 | ||
| 18. Can abdominal malignancies be evaluated with nuclear medicine studies? | 534 | ||
| 19. What is PET and how does it work? | 534 | ||
| 20. What malignancies can PET and PET/CT be used for? | 535 | ||
| Bibliography | 536 | ||
| Chapter 72: Endoscopic Ultrasound | 537 | ||
| 1. When was intraluminal gastrointestinal (GI) ultrasound (US) first performed? | 537 | ||
| 2. How do US waves visualize the GI tract? | 537 | ||
| 3. How does the frequency of the US beam influence the depth of beam penetration and image resolution? | 537 | ||
| 4. What are the ultrasonographic properties of the common structures of the body? | 537 | ||
| Normal Anatomy | 537 | ||
| 5. What determines the thickness of the echosonographic layer visualized? What is thenormal endosonographic anatomy of the intestinal wall? | 537 | ||
| 6. What are the imaging characteristics of normal and malignant lymph nodes on EUS? | 538 | ||
| 7. How are blood vessels distinguished from lymph nodes on EUS? | 538 | ||
| 8. Describe the normal EUS anatomy of the retroperitoneum. What are its major landmarks? | 538 | ||
| 9. What are the indications for EUS examination? | 539 | ||
| 10. How is EUS used in the clinical evaluation of esophageal cancer? | 539 | ||
| 11. How can EUS findings affect clinical management of esophageal carcinoma? | 539 | ||
| 12. What are the problematic areas for EUS in the staging of esophageal cancer? | 539 | ||
| 13. Does EUS have a role in the evaluation of gastric cancer? | 540 | ||
| 14. What are the problematic areas for EUS staging of gastric malignancy? | 540 | ||
| 15. Summarize the TNM staging classification for gastric malignancy. | 540 | ||
| 16. How does staging affect treatment? | 541 | ||
| 17. Is EUS helpful in the evaluation of gastric lymphoma? | 541 | ||
| 18. How is EUS helpful in evaluating pancreatic neoplasms? | 541 | ||
| 19. Neuroendocrine tumors (NETs) of the pancreas and peripancreas are often difficult tolocalize by conventional CT, US, and angiography. Does EUS examination offer anyvalue in localizing these tumors? | 541 | ||
| 20. Describe the use of EUS in the evaluation of colon malignancy. | 541 | ||
| 21. Describe the use of EUS in the evaluation of rectal malignancy. | 541 | ||
| 22. Summarize the EUS characteristics of submucosal tumors (SMTs). | 542 | ||
| 23. Is EUS useful in the evaluation of nonneoplastic disease? | 542 | ||
| 24. How is EUS used in the evaluationof patients with portalhypertension? | 543 | ||
| 25. Does EUS have a role in the evaluation of recurrent idiopathic pancreatitis? | 543 | ||
| 26. What is the stack sign? Does it have clinical significance? | 543 | ||
| 27. Describe the role of EUS in the evaluation of chronic pancreatitis. | 543 | ||
| 28. Summarize the EUS criteria for chronic pancreatitis. | 544 | ||
| 29. What is the role of EUS in the evaluation of autoimmune pancreatitis (AIP)? | 544 | ||
| 30. Discuss the role of EUS in evaluating patients with common bile duct stones. | 544 | ||
| Websites | 544 | ||
| Bibliography | 544 | ||
| Chapter 73: Advanced Therapeutic Endoscopy | 545 | ||
| 1. What is advanced therapeutic endoscopy? | 545 | ||
| 2. What are the major advanced therapeutic endoscopy techniques? | 545 | ||
| 3. What are the applications of EMR and ESD? | 546 | ||
| 4. How is EMR performed? | 547 | ||
| 5. How is ESD performed? | 547 | ||
| 6. What are the differences/limitations of the EMR and ESD? | 547 | ||
| 7. What are the complications of EMR/ESD? | 547 | ||
| 8. What are some investigational applications of EMR/ESD? | 548 | ||
| 9. What are some investigational applications of advanced endoscopic ultrasound? | 548 | ||
| 10. What is the role of EUS-guided fine-needle aspiration (FNA) biopsy in tissue sampling? Sampling of nodes? | 548 | ||
| 11. How is EUS-FNA performed? | 548 | ||
| 12. What are the advantages of EUS-FNA over other sampling modalities? | 548 | ||
| 13. What are the sensitivity and specificity of EUS-FNA for the diagnosis of malignancy? | 549 | ||
| 14. What is the role of EUS-FNA in the evaluation of mediastinal lymphadenopathy? | 549 | ||
| 15. What are the risks of EUS-FNA? | 549 | ||
| 16. What is the role of EUS in sampling pancreatic cystic neoplasms? | 549 | ||
| 17. Is there a risk of biopsy tract seeding when EUS-FNA of a suspected malignancy is sampled? | 549 | ||
| 18. How is EUS-guided transmural pseudocyst drainage performed? | 549 | ||
| 19. What are the indications for EUS-guided celiac plexus block (CPB) and celiac plexus neurolysis (CPN)? What is the difference? Why do they work? | 550 | ||
| 20. How are EUS-guided celiac plexus block and neurolysis performed? | 551 | ||
| 21. What is the success rate of CPN? CPB? | 551 | ||
| 22. What are the potential complications of CPN? | 551 | ||
| 23. Is EUS-guided cholangiography or pancreatography possible? When are they indicated? | 552 | ||
| 24. What is high-frequency US-probe sonography-assisted EMR? | 552 | ||
| Websites | 552 | ||
| Bibliography | 552 | ||
| Chapter 74: Surgery: Gastroesophageal Reflux And Esophageal Hernias | 553 | ||
| Gastroesophageal Reflux Disease | 553 | ||
| 1. Define gastroesophageal reflux disease (GERD). | 553 | ||
| 2. Describe the typical and atypical symptoms of GERD. | 553 | ||
| 3. What factors play a role in altering the gastroesophageal (GE) barrier? | 553 | ||
| 4. Describe the workup of patients with suspected GERD. | 553 | ||
| 5. What is the significance of a defective LES? | 554 | ||
| 6. What is the significance of abnormal esophageal motility in patients with GERD? | 554 | ||
| 7. What is Barrett’s esophagus and what are the risk factors? | 554 | ||
| 8. What are the indications for an antireflux operation? | 554 | ||
| 9. What are the surgical options to relieve GERD? | 554 | ||
| 10. What are the important technical steps of a Nissen fundoplication? | 555 | ||
| 11. What are the predictors of successful antireflux surgery? | 555 | ||
| 12. What are the predictors of poor outcome after antireflux surgery? | 555 | ||
| 13. Explain the benefits of surgical treatment of GERD. | 555 | ||
| 14. What are the complications of laparoscopic fundoplication? | 556 | ||
| Paraesophageal Hernias | 556 | ||
| 15. Define the four types of hernias occurring at the hiatus. | 556 | ||
| 16. What causes a hiatal hernia? | 557 | ||
| 17. What are the signs and symptoms of a paraesophageal hernia? | 557 | ||
| 18. How are hiatal and paraesophageal hernias diagnosed and evaluated? | 557 | ||
| 19. What are the indications for surgical repair of paraesophageal hernias? | 557 | ||
| 20. What is the operative strategy of a paraesophageal hernia repair? | 557 | ||
| Website | 557 | ||
| Bibliography | 558 | ||
| Chapter 75: Surgery: Achalasia and Esophageal Cancer | 559 | ||
| Achalasia | 559 | ||
| 1. Define achalasia. What are the classic findings of esophageal achalasia? | 559 | ||
| 2. What are the most common symptoms of achalasia? | 559 | ||
| 3. What is pseudoachalasia? How is it diagnosed? | 559 | ||
| 4. What is vigorous achalasia? | 559 | ||
| 5. What are the nonsurgical options for treatment of achalasia? | 559 | ||
| 6. What are the basic components of laparoscopic Heller myotomy for achalasia? | 559 | ||
| 7. How do long-term results of Heller myotomy compare with mechanical esophagealdilatation? | 560 | ||
| 8. Describe the complications of Heller myotomy. | 560 | ||
| 9. Summarize the treatment algorithm for patients with achalasia. | 560 | ||
| 10. What is the association between achalasia and esophageal cancer? | 560 | ||
| Esophageal Cancer | 560 | ||
| 11. What is the incidence of esophageal cancer? | 560 | ||
| 12. What are the risk factors of esophageal cancer? | 560 | ||
| 13. Describe the relationship of Barrett’s esophagus to esophageal cancer. | 560 | ||
| 14. Can Barrett’s esophagus regress after antireflux therapy? | 561 | ||
| 15. Discuss the surgical management of patients with high-grade dysplasia. | 561 | ||
| 16. What are the surgical approaches to the patient with esophageal cancer? | 561 | ||
| 17. When is neoadjuvant therapy appropriate in the treatment of patients withesophageal carcinoma? | 561 | ||
| 18. Describe nonsurgical options for treatment of esophageal cancer. | 561 | ||
| 19. What is the survival of patients with esophageal cancer? | 562 | ||
| Bibliography | 562 | ||
| Chapter 76: Surgery For Peptic Ulcer Disease | 563 | ||
| 1. Describe the five types of gastric ulcer in terms of location, gastric acid secretory status, incidence, and complications | 563 | ||
| 2. Describe the classic indications and goals for peptic ulcer surgery | 563 | ||
| 3. What are the three classic operations used for PUD? | 563 | ||
| 4. Describe the truncal vagotomy, selective vagotomy, and highly selective vagotomy | 563 | ||
| 5. Why is an outlet or drainage procedure added to truncal vagotomy? What are the surgical options? | 564 | ||
| 6. What are the relative indications and contraindications to highly selective vagotomy? | 565 | ||
| 7. What are the surgical options for reconstruction after antrectomy? | 565 | ||
| 8. How is the type of reconstruction determined for a given patient? | 565 | ||
| 9. Define intractability in terms of the medical treatment of PUD? | 565 | ||
| 10. Describe the most appropriate elective operative procedure for duodenal ulcers and each type of gastric ulcer | 566 | ||
| 11. Describe the presentation of a patient with a perforated peptic ulcer | 566 | ||
| 12. Why do almost all perforated gastric ulcers require an operation? | 566 | ||
| 13. What are the contraindications to medical management of perforated PUD? | 566 | ||
| 14. What are the three major goals of operation for perforated PUD? | 566 | ||
| 15. What is the preferred operation for treatment of perforated gastric ulcer? | 567 | ||
| 16. What is the preferred operation for treatment of a perforated duodenal ulcer? | 567 | ||
| 17. What are the major risk factors for mortality in the surgical treatment of perforated PUD? | 567 | ||
| 18. Discuss the role for laparoscopy in the management of perforated PUD and the indications for conversion to an open operation | 567 | ||
| 19. In patients with GI bleeding caused by PUD, what are the predictors for rebleeding in the hospital? What is the Forrest classification? | 567 | ||
| 20. What are the classic indications for operation for rebleeding after endoscopic therapy? | 567 | ||
| 21. What are the operative options for control of a bleeding gastric ulcer? | 568 | ||
| 22. What is the most appropriate surgical procedure for a bleeding duodenal ulcer? | 568 | ||
| 23. How is gastric outlet obstruction due to PUD surgically managed? | 568 | ||
| 24. Discuss the role for endoscopic and laparoscopic management of GOO secondary to PUD | 568 | ||
| 25. What are the long-term outcomes and risks for complications after truncal vagotomy and drainage, truncal vagotomy and antrectomy, and highly selective vagotomy? | 568 | ||
| 26. What are the Visick criteria? | 569 | ||
| 27. How should postoperative gastroparesis be managed? | 569 | ||
| 28. Describe the management of duodenal stump disruption (blow-out) after truncal vagotomy, antrectomy, and Billroth II reconstruction | 569 | ||
| 29. What is dumping syndrome? Describe the pathophysiology and treatment | 569 | ||
| 30. Describe the pathophysiology of bile reflux gastritis. How is it managed? | 569 | ||
| 31. What is the presentation of Zöllinger-Ellison syndrome? | 570 | ||
| 32. How is Zöllinger-Ellison syndrome diagnosed? | 570 | ||
| 33. For which patients with Zöllinger-Ellison syndrome is operative intervention indicated? | 570 | ||
| 34. Describe the preoperative evaluation for gastrinoma | 570 | ||
| 35. Where is the gastrinoma triangle? What percentage of tumors occur in this area? | 571 | ||
| 36. Describe the operative scheme for exploration, localization, and removal of gastrinoma | 571 | ||
| 37. Describe the risk of gastric stump cancer after partial gastrectomy for duodenal and gastric ulcer | 571 | ||
| Bibliography | 571 | ||
| Chapter 77: Surgical Approach To The Acute Abdomen | 572 | ||
| 1. What is the significance of the term acute abdomen? | 572 | ||
| 2. What are the critical factors in the history of present illness? | 572 | ||
| 3. Which disorders are associated with specific age groups? | 572 | ||
| 4. Summarize the significance of pain location | 572 | ||
| 5. What associated problems help to pinpoint the diagnosis? | 572 | ||
| 6. What is the peritoneum and its pain innervation, and what are peritoneal signs? | 572 | ||
| 7. What is the significance of rebound pain, and should it be elicited? | 572 | ||
| 8. What is the nature of intestinal pain? | 573 | ||
| 9. How does the duration of pain help in making a diagnosis? | 573 | ||
| 10. Is acute abdomen ruled out by absence of fever or leukocytosis? | 573 | ||
| 11. What is the significance of bowel sounds? | 573 | ||
| 12. What is the most important part of the abdominal examination? | 573 | ||
| 13. What are the psoas and obturator signs? | 573 | ||
| 14. What is Rovsing sign? | 573 | ||
| 15. What is Kehr’s sign? | 573 | ||
| 16. Define mittelschmerz | 573 | ||
| 17. How does urinalysis help in the assessment? | 573 | ||
| 18. What should be the first imaging study obtained? | 573 | ||
| 19. How is ultrasound (US) used? | 573 | ||
| 20. What additional imaging studies may help in the diagnosis? | 573 | ||
| 21. If the diagnosis is in doubt, what other procedure should be done? | 574 | ||
| 22. Is exploratory laparotomy justified, even if it produces no significant findings? | 574 | ||
| 23. Is exploratory laparoscopy useful in the setting of acute abdomen? | 574 | ||
| 24. In blunt trauma, CT scan of the abdomen and pelvis reveals free peritoneal fluid collections. When is observation appropriate instead of immediate surgical exploration? | 574 | ||
| 25. Do all penetrating injuries to the abdomen require laparotomy? | 574 | ||
| 26. What is the role of laparoscopy in trauma? | 574 | ||
| 27. When is surgery indicated for peptic ulcer disease (PUD)? | 574 | ||
| 28. When is cholecystectomy optimal for acute pancreatitis, presumably due to gallstone disease? | 574 | ||
| 29. When is surgery indicated for severe acute pancreatitis? | 574 | ||
| 30. Describe treatment for a pancreatic pseudocyst | 575 | ||
| 31. What is the best method to diagnose pain secondary to mesenteric ischemia? | 575 | ||
| 32. Describe the surgical strategy for the treatment of Crohn’s disease | 575 | ||
| 33. When should surgery be offered for uncomplicated acute diverticulitis? | 575 | ||
| 34. Should elderly patients with sigmoid or cecal volvulus undergo surgery? | 575 | ||
| 35. How should toxic megacolon in the setting of ulcerative colitis be managed? | 575 | ||
| 36. How should Ogilvie’s syndrome be managed? | 575 | ||
| 37. After endoscopic retrograde cholangiopancreatography (ERCP), a patient develops upper abdominal and back pain. What steps should be considered? | 575 | ||
| 38. How should esophageal perforation be managed after endoscopy? What if the patient has achalasia? Esophageal carcinoma? | 575 | ||
| 39. How should colonic perforation be managed after colonoscopy? | 576 | ||
| Bibliography | 576 | ||
| Chapter 78: Colorectal Surgery: Polyposis Syndromes And Inflammatory Bowel Disease | 577 | ||
| 1. Name four different types of intestinal polyps. | 577 | ||
| 2. What is a hamartoma? | 577 | ||
| 3. Which intestinal polyposis syndromes are associated with hamartomatous polyps? | 577 | ||
| 4. How is Peutz-Jeghers syndrome manifest? | 577 | ||
| 5. Describe the manifestation of familial adenomatous polyposis (FAP). | 577 | ||
| 6. What is Gardner syndrome? | 577 | ||
| 7. How does one screen for FAP? | 577 | ||
| 8. What are the surgical indications for ulcerative colitis? | 578 | ||
| 9. What are the elective surgical options for FAP and chronic ulcerative colitis? | 578 | ||
| 10. Can one always tell the difference between Crohn’s disease and ulcerative colitis? | 578 | ||
| 11. What is pouchitis? How is it treated? | 578 | ||
| 12. Does a defunctionalized colon develop colitis? | 578 | ||
| 13. What type of ileal pouches are used? | 578 | ||
| Anorectal Disease | 578 | ||
| 14. What are anal fissures? | 578 | ||
| 15. What disorders should be considered in patients with laterally situated anal fissures? | 578 | ||
| 16. How are acute fissures managed? | 578 | ||
| 17. What are the signs of a chronic anal fissure? What do they imply? | 579 | ||
| 18. Which surgical procedures are available for treatment of a chronic anal fissure? | 579 | ||
| 19. How are hemorrhoids classified? | 579 | ||
| 20. How are acute hemorrhoids treated? | 579 | ||
| 21. List several minimally invasive outpatient treatments of internal hemorrhoids. | 579 | ||
| 22. Who is the patron saint of hemorrhoid sufferers? | 579 | ||
| 23. How is an acute thrombosed external hemorrhoid best treated? | 579 | ||
| 24. Explain the cause of anorectal abscesses andfistulas. | 579 | ||
| 25. List the various types and locations of anorectalabscesses. | 579 | ||
| 26. What is the best treatment for an anorectalabscess? | 579 | ||
| 27. What is the Goodsall rule? | 579 | ||
| 28. What is a seton? | 580 | ||
| 29. What are the common indications for inserting a seton? | 580 | ||
| 30. List new developments for treatment of anorectal fistulas. | 580 | ||
| 31. When is anorectal suppurative disease especially dangerous? | 580 | ||
| 32. What is Fournier gangrene? | 580 | ||
| 33. Describe perianal Paget disease. | 580 | ||
| 34. Which patient characteristics are associated with rectal prolapse? | 580 | ||
| 35. What surgical options are available for rectal prolapse? | 580 | ||
| 36. How is rectal prolapse handled in pediatric patients? | 580 | ||
| Colorectal Malignancies | 580 | ||
| 37. What is the best way to stage rectal cancer? | 580 | ||
| 38. When is endoscopic mucosal resection (EMR) indicated? | 581 | ||
| 39. What are the indications for neoadjuvant (before surgery) and adjuvant (after surgery)therapy? | 581 | ||
| 40. What is an abdominal perineal resection (APR), and when is it indicated? | 581 | ||
| Colon Cancer | 581 | ||
| 41. What are the fundamental principals of colon resection for cancer? | 581 | ||
| 42. Does laparoscopic surgery compromise the chance for a cure? | 581 | ||
| 43. What are the pros and cons of laparoscopic versus open colectomy? | 581 | ||
| 44. What are the findings of sigmoid volvulus on plain abdominal film and contrastenema? | 581 | ||
| 45. How is a nonstrangulated sigmoid volvulus treated? | 581 | ||
| 46. Why should elective surgery be performed after a successful endoscopic detorsionand decompression of a sigmoid volvulus? | 582 | ||
| 47. Do colon perforations from colonoscopy mandate surgical repair? | 582 | ||
| 48. What is Ogilvie syndrome? | 582 | ||
| 49. What does plain radiographic study of the abdomen reveal in large bowel obstruction? | 582 | ||
| 50. What radiologic findings are associated with gallstone ileus? | 582 | ||
| 51. What does endometriosis have to do with the alimentary system? | 582 | ||
| 52. What is a primary bowel obstruction? | 582 | ||
| 53. How is postoperative ileus differentiated from postoperative SBO? | 582 | ||
| 54. Is treatment of postoperative SBO different from treatment of SBO remote from surgery? | 582 | ||
| 55. What is the most common cause of SBO? | 582 | ||
| 56. Can adhesions be prevented? | 582 | ||
| 57. What are the pathologic findings of late radiation enteritis? | 582 | ||
| 58. What are general principles of managing radiation enteritis? | 583 | ||
| 59. What treatments are available for bleeding radiation proctitis? | 583 | ||
| Websites | 583 | ||
| Bibliography | 583 | ||
| Chapter 79: Bariatric Surgery | 584 | ||
| 1. What is the definition of obesity? | 584 | ||
| 2. How is body fat relative to weight usually measured? | 584 | ||
| 3. Describe the BMI classification system | 584 | ||
| 4. What are the limitations of BMI? | 584 | ||
| 5. What proportion of the U.S. adult population is considered overweight? | 584 | ||
| 6. What proportion of the U.S. adult population is considered obese? | 584 | ||
| 7. Are there health implications associated with a BMI of 30 kg/m2? | 584 | ||
| 8. Can obesity lead to premature death? | 584 | ||
| 9. How successful is nonsurgical treatment of obesity? | 584 | ||
| 10. How is obesity best treated? | 584 | ||
| 11. What was the NIH Consensus Statement? | 585 | ||
| 12. List the contraindications to bariatric surgery | 585 | ||
| 13. Categorize the surgical options for weight reduction | 585 | ||
| 14. List the options for restrictive surgery | 585 | ||
| 15. Describe the combined restrictive/malabsorptive option | 585 | ||
| 16. What is the option for malabsorptive surgery? | 586 | ||
| 17. The other category includes which procedures? | 586 | ||
| 18. What are the weight loss expectations after each procedure? | 586 | ||
| 19. Are these just cosmetic operations? | 586 | ||
| 20. Does surgical weight loss translate to improved long-term survival? | 586 | ||
| 21. Which comorbidity can have the most dramatic improvement? | 586 | ||
| 22. How does the gastric bypass and biliopancreatic diversion cure diabetes prior to weight loss? | 586 | ||
| 23. Can these changes in the gut hormonal milieu have a detrimental effect? | 586 | ||
| 24. What are other complications after a gastric bypass? | 586 | ||
| 25. How are anastomotic leaks handled? | 586 | ||
| 26. How is an anastomotic stenosis treated? | 587 | ||
| 27. What is a marginal ulcer, and how is it treated? | 587 | ||
| 28. What are the vitamin/mineral deficiencies and potential long-term risks? | 587 | ||
| 29. What is the most common surgical weight loss procedure in Europe and Australia? | 587 | ||
| 30. Why would someone choose a lap band over a Roux-en-Y gastric bypass? | 587 | ||
| 31. What are the specific complications after a lap band procedure? | 587 | ||
| 32. How does the biliopancreatic diversion work? | 587 | ||
| 33. Is there malnutrition, and how problematic is it? | 587 | ||
| 34. Are there other health risks associated with biliopancreatic diversion? | 587 | ||
| 35. Why would one choose biliopancreatic diversion? | 587 | ||
| 36. What does preoperative surgical counseling entail with any procedure? | 587 | ||
| Bibliography | 588 | ||
| Chapter 80: Laparoscopic Surgery | 589 | ||
| 1. When did laparoscopic surgery become a credible surgical option? | 589 | ||
| 2. What are the advantages of laparoscopic surgery compared with open procedures? | 589 | ||
| 3. What are the contraindications to laparoscopic surgery? | 589 | ||
| 4. Does laparoscopic surgery preserve immune function? | 589 | ||
| 5. What are the respiratory effects of pneumoperitoneum (planned intra-abdominal hypertension)? | 589 | ||
| 6. What are the hemodynamic effects? | 589 | ||
| 7. At 24 hours after open upper abdominal surgery using subcostal incisions, patients show a decrease in pulmonary function tests of nearly 50%. What decreases should be expected at 24 hours after laparoscopic cholecystectomy? | 590 | ||
| 8. Should we routinely use prophylactic antibiotics for laparoscopic cholecystectomy? | 590 | ||
| 9. What is the difference between the hepatocystic triangle and the triangle of Calot? | 590 | ||
| 10. Which alternative gases can be used for laparoscopy? | 590 | ||
| 11. List the advantages and disadvantages of using carbon dioxide (CO2) as an insufflation gas instead of other gases | 591 | ||
| 12. A 9-year-old girl presents with a 2-month history of right upper quadrant abdominal pain that most commonly occurs after eating fatty foods and usually resolves in 30 minutes. She is afebrile, and the physical exam is unremarkable. Laboratory values, in | 591 | ||
| 13. TThe HIDA scan demonstrated rapid filling of the gallbladder and unobstructed flow into the duodenum. Cholecystokinin (CCK) is administered, and the gallbladder ejection fraction (EF) is calculated at 30%. What is the most likely diagnosis? How should t | 591 | ||
| 14. Summarize the key strategies for safe laparoscopic cholecystectomy. | 591 | ||
| 15. Compare the rate of conversion from laparoscopic cholecystectomy to open cholecystectomy in patients with acute versus chronic cholecystitis | 591 | ||
| 16. What pathophysiologic features of acute cholecystitis increase the likelihood of technical difficulties? | 592 | ||
| 17. How does laparoscopic gastric bypass compare to open gastric bypass? | 592 | ||
| 18. Is there any clearly defined benefit to laparoscopic appendectomy? | 592 | ||
| 19. Is gangrenous or perforated appendicitis a contraindication to laparoscopic appendectomy? | 592 | ||
| 20. Is laparoscopic antireflux surgery (LARS) justified for chronic gastroesophageal reflux disease (GERD)? | 592 | ||
| 21. A 46-year-old woman with a BMI of 44 kg/m2 is referred for a laparoscopic antireflux procedure. She has been taking proton pump inhibitors for 20 years. Her symptoms are well controlled with medication; however, she prefers a surgical procedure if it wi | 592 | ||
| 22. What are the benefits and drawbacks of laparoscopic versus open inguinal hernia repair? | 592 | ||
| 23. What is the role of laparoscopic surgery for curable colon cancer? | 592 | ||
| 24. A thin, 68-year-old woman with chronic obstructive pulmonary disease from 52 years of smoking undergoes laparoscopic cholecystectomy for acute cholecystitis. Because she has had a previous lower midline abdominal incision, you choose the open Hasson tec | 593 | ||
| 25. Can laparoscopic cholecystectomy be done safely in the pregnant patient? | 593 | ||
| 26. Can laparoscopic appendectomy be performed safely during pregnancy? | 593 | ||
| 27. What are some technical considerations when performing laparoscopy on the pregnant patient? | 593 | ||
| 28. What percentage of patients have free intra-abdominal air on upright radiograph 24 hours after laparoscopic procedure? | 593 | ||
| 29. What are the indications and contraindications for laparoscopic adrenalectomy? What are the advantages of laparoscopic ... | 594 | ||
| 30. How are bile spills managed? | 594 | ||
| Websites | 594 | ||
| Bibliography | 594 | ||
| Index | 595 |