Topics in Gastroenterology

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1. Topics in Gastroenterology Melissa (Moe) Hagman, MD, FACP Assistant Professor, Internal Medicine University of Washington [email protected] September 18, 2008

2. In Memory of David Saunders, MD University of Washington Former Chairman of Gastroenterology Chair of Medical Student Gut Course for 33 years Teacher Superior in Perpetuity Died January 22, 2008 of non-Hodkin’s lymphoma Wife Donna Sons – John, Richard, Michael, Brian Died January 22, 2008 of non-Hodkin’s lymphoma Wife Donna Sons – John, Richard, Michael, Brian

3. Outline Case-based parade from esophagus to rectum What are the life-threatening diagnoses on the differential? What are the other diagnoses on the differential? How can I go about a thoughtful and efficient work-up to generate a treatment plan that will benefit the patient?

4. Ms. A 50 yo woman with acute onset of severe mid-sternal chest pain while eating <1 hr ago. For >6 months she reports that solid food has tended to “get stuck” in her mid-chest. She usually avoids the medical establishment and has no known PMH. Clinical Question: What is your differential diagnosis? Chest Pain – MI Thoracic aortic aneurysm, ruptured/dissecting PE Esophageal ruptureChest Pain – MI Thoracic aortic aneurysm, ruptured/dissecting PE Esophageal rupture

5. Assess First for Life-Threatening Diagnoses Aortic dissection or rupture Risk factors, BP on both UE, aortic insufficiency on exam, consider CXR/CT Myocardial infarction Risk factors, ECG Pulmonary embolism Risk factors, LE exam, consider ABG and VQ scan or CT chest Esophageal rupture Risk factors, pleuritic chest pain

6. Ms. A T 37.0C, BP 133/72, HR 105, O2 sat 97% RA Clinical Question: What else do you notice on physical exam? Sclerodactyly Raynaud phenomenon Digital ulcers Pitting at the fingertips Telangiectasia Calcinosis cutis Sclerodactyly Raynaud phenomenon Digital ulcers Pitting at the fingertips Telangiectasia Calcinosis cutis

7. Scleroderma and the Esophagus Smooth muscle atrophy and fibrosis of distal 2/3rd of esophagus with low LES pressure Esophageal dysmotility Esophageal stricture – 17-29% GERD with Barrett’s esophagus – 0-39% Esophageal cancer Also - scleroderma can affect any part of GI tract – SB overgrowth with malabsorption, vascular ectasia of stomach (watermelon stomach) esophagitis J Clin Gastroenterol. 2006 Oct;40(9):769-75. Links Esophageal disease in scleroderma. Ebert EC. Progressive systemic sclerosis (PSS) causes smooth muscle atrophy and fibrosis of the distal two-thirds of the esophagus. Motility studies show reduced-amplitude or absent peristaltic contractions in this region and normal or decreased lower esophageal sphincter pressure. Patients complain of dysphagia, heartburn, and regurgitation due to reflux and dysmotility. Complications include strictures found in 17% to 29% of patients and Barrett esophagus is 0% to 37%. Candida esophagitis is a complication of PSS not seen with non-PSS reflux. Esophageal disease correlates with pulmonary involvement but not with disease in the stomach or intestines. Whether reflux contributes to the pulmonary disease is an open question. Although manometry is the gold standard for diagnosis, cine-esophagram and scintography are only slightly less sensitive and should be considered for following the patients. Symptoms correlate poorly with evidence of esophagitis or abnormal 24-hour pH recordings. As a result, it is unclear which patients should receive acid-reducing or prokinetic medications and which medication to use. Aspiration precautions are important in those with severe esophageal dysmotility. This review of the literature highlights many areas of uncertainty in the diagnosis and treatment of esophageal disease in PSS that can be addressed in clinical studies. Pericarditis Pneumothorax with possible pneumomediastinum Costocondritis Also - scleroderma can affect any part of GI tract – SB overgrowth with malabsorption, vascular ectasia of stomach (watermelon stomach) esophagitis J Clin Gastroenterol. 2006 Oct;40(9):769-75. Links Esophageal disease in scleroderma. Ebert EC. Progressive systemic sclerosis (PSS) causes smooth muscle atrophy and fibrosis of the distal two-thirds of the esophagus. Motility studies show reduced-amplitude or absent peristaltic contractions in this region and normal or decreased lower esophageal sphincter pressure. Patients complain of dysphagia, heartburn, and regurgitation due to reflux and dysmotility. Complications include strictures found in 17% to 29% of patients and Barrett esophagus is 0% to 37%. Candida esophagitis is a complication of PSS not seen with non-PSS reflux. Esophageal disease correlates with pulmonary involvement but not with disease in the stomach or intestines. Whether reflux contributes to the pulmonary disease is an open question. Although manometry is the gold standard for diagnosis, cine-esophagram and scintography are only slightly less sensitive and should be considered for following the patients. Symptoms correlate poorly with evidence of esophagitis or abnormal 24-hour pH recordings. As a result, it is unclear which patients should receive acid-reducing or prokinetic medications and which medication to use. Aspiration precautions are important in those with severe esophageal dysmotility. This review of the literature highlights many areas of uncertainty in the diagnosis and treatment of esophageal disease in PSS that can be addressed in clinical studies. Pericarditis Pneumothorax with possible pneumomediastinum Costocondritis

8. Esophageal Motility Disorders Achalasia Loss of relaxing neurons in myenteric plexus Usually idiopathic Solid and liquid dysphagia Regurgitation Wt loss Chagas’ disease (Trypanosoma cruzi) can cause achalasia.Chagas’ disease (Trypanosoma cruzi) can cause achalasia.

9. Esophageal Motility Disorders Achalasia Diagnosis Manometry – no peristalsis and high LES pressure UGI – “bird’s beak” Treatment Balloon dilatation Surgical myotomy Botulinum toxin injections into LES Nitrates, calcium channel blockers – do not help much http://www.nextspace.co.uk/lapsurg/images/achalasia-1072346.jpg Messrs Dehn and Booth Nutcracker esophagus – high amplitude long duration waveforms in body of esophagus Diffuse esophageal spasm - Manometry dx with no clear clinical correlation. - 30% of patients with CP have esophageal dysmotility disorder http://www.nextspace.co.uk/lapsurg/images/achalasia-1072346.jpg Messrs Dehn and Booth Nutcracker esophagus – high amplitude long duration waveforms in body of esophagus Diffuse esophageal spasm - Manometry dx with no clear clinical correlation. - 30% of patients with CP have esophageal dysmotility disorder

10. Mr. B 74 yo gentleman with recurrent discomfort in the mid upper abdomen for 3 months. No heartburn. Occasional bloating. No improvement with OTC H2 blocker. Clinical Question: What additional history do you need and what is your differential diagnosis?

11. Dyspepsia – Alarm Features History New onset >55 yo old Dysphagia/odynophagia Early satiety Vomiting Anemia/bleeding Unexplained wt loss PMH PUD Malignancy Gastric surgery Family Hx GI malignancy Exam Lymphadenopathy Sister Mary Joseph sign Abdominal mass Pts with these features need EGD.Pts with these features need EGD.

12. Dyspepsia - Causes GERD Peptic ulcer disease Functional (non-ulcer) – 60% of cases Functional dyspepsia – Rx with acid suppression, or H. pylori Rx, or pro-motility agent, or antidepressantFunctional dyspepsia – Rx with acid suppression, or H. pylori Rx, or pro-motility agent, or antidepressant

13. Dyspepsia - Treatment If alarm features EGD If no alarm features Try to stop any NSAIDS Empiric acid suppression PPI x 4-8 weeks Or, in patient populations with high H. pylori prevalence, test and treat Patients with low incidence of H. pylori include young, socioeconomically privileged individualsPatients with low incidence of H. pylori include young, socioeconomically privileged individuals

14. H. pylori testing Test in pts with Peptic ulcer disease (PUD) Gastric mucosa-associated lymphoid tissue (MALT) lymphoma Treatment leads to tumor regression in 60-90% Uninvestigated dyspepsia without alarm features Am J Gastroenterol. 2007 Aug;102(8):1808-25. Epub 2007 Jun 29. Links American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA. Helicobacter pylori (H. pylori) remains a prevalent, worldwide, chronic infection. Though the prevalence of this infection appears to be decreasing in many parts of the world, H. pylori remains an important factor linked to the development of peptic ulcer disease, gastric malignanc and dyspeptic symptoms. Whether to test for H. pylori in patients with functional dyspepsia, gastroesophageal reflux disease (GERD), patients taking nonsteroidal antiinflammatory drugs, with iron deficiency anemia, or who are at greater risk of developing gastric cancer remains controversial. H. pylori can be diagnosed by endoscopic or nonendoscopic methods. A variety of factors including the need for endoscopy, pretest probability of infection, local availability, and an understanding of the performance characteristics and cost of the individual tests influences choice of evaluation in a given patient. Testing to prove eradication should be performed in patients who receive treatment of H. pylori for peptic ulcer disease, individuals with persistent dyspeptic symptoms despite the test-and-treat strategy, those with H. pylori-associated MALT lymphoma, and individuals who have undergone resection of early gastric cancer. Recent studies suggest that eradication rates achieved by first-line treatment with a proton pump inhibitor (PPI), clarithromycin, and amoxicillin have decreased to 70-85%, in part due to increasing clarithromycin resistance. Eradication rates may also be lower with 7 versus 14-day regimens. Bismuth-containing quadruple regimens for 7-14 days are another first-line treatment option. Sequential therapy for 10 days has shown promise in Europe but requires validation in North America. The most commonly used salvage regimen in patients with persistent H. pylori is bismuth quadruple therapy. Recent data suggest that a PPI, levofloxacin, and amoxicillin for 10 days is more effective and better tolerated than bismuth quadruple therapy for persistent H. pylori infection, though this needs to be validated in the United States. Am J Gastroenterol. 2007 Aug;102(8):1808-25. Epub 2007 Jun 29. Links American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA. Helicobacter pylori (H. pylori) remains a prevalent, worldwide, chronic infection. Though the prevalence of this infection appears to be decreasing in many parts of the world, H. pylori remains an important factor linked to the development of peptic ulcer disease, gastric malignanc and dyspeptic symptoms. Whether to test for H. pylori in patients with functional dyspepsia, gastroesophageal reflux disease (GERD), patients taking nonsteroidal antiinflammatory drugs, with iron deficiency anemia, or who are at greater risk of developing gastric cancer remains controversial. H. pylori can be diagnosed by endoscopic or nonendoscopic methods. A variety of factors including the need for endoscopy, pretest probability of infection, local availability, and an understanding of the performance characteristics and cost of the individual tests influences choice of evaluation in a given patient. Testing to prove eradication should be performed in patients who receive treatment of H. pylori for peptic ulcer disease, individuals with persistent dyspeptic symptoms despite the test-and-treat strategy, those with H. pylori-associated MALT lymphoma, and individuals who have undergone resection of early gastric cancer. Recent studies suggest that eradication rates achieved by first-line treatment with a proton pump inhibitor (PPI), clarithromycin, and amoxicillin have decreased to 70-85%, in part due to increasing clarithromycin resistance. Eradication rates may also be lower with 7 versus 14-day regimens. Bismuth-containing quadruple regimens for 7-14 days are another first-line treatment option. Sequential therapy for 10 days has shown promise in Europe but requires validation in North America. The most commonly used salvage regimen in patients with persistent H. pylori is bismuth quadruple therapy. Recent data suggest that a PPI, levofloxacin, and amoxicillin for 10 days is more effective and better tolerated than bismuth quadruple therapy for persistent H. pylori infection, though this needs to be validated in the United States.

15. H. pylori testing EGD with gastric biopsy Gold standard, associated risks of endoscopy Serology Inexpensive NPV good, PPV depends Remains positive for 6-12 mo after eradication Urea breath test Stool antigen Am J Gastroenterol. 2007 Aug;102(8):1808-25. Epub 2007 Jun 29. Links American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA. Helicobacter pylori (H. pylori) remains a prevalent, worldwide, chronic infection. Though the prevalence of this infection appears to be decreasing in many parts of the world, H. pylori remains an important factor linked to the development of peptic ulcer disease, gastric malignanc and dyspeptic symptoms. Whether to test for H. pylori in patients with functional dyspepsia, gastroesophageal reflux disease (GERD), patients taking nonsteroidal antiinflammatory drugs, with iron deficiency anemia, or who are at greater risk of developing gastric cancer remains controversial. H. pylori can be diagnosed by endoscopic or nonendoscopic methods. A variety of factors including the need for endoscopy, pretest probability of infection, local availability, and an understanding of the performance characteristics and cost of the individual tests influences choice of evaluation in a given patient. Testing to prove eradication should be performed in patients who receive treatment of H. pylori for peptic ulcer disease, individuals with persistent dyspeptic symptoms despite the test-and-treat strategy, those with H. pylori-associated MALT lymphoma, and individuals who have undergone resection of early gastric cancer. Recent studies suggest that eradication rates achieved by first-line treatment with a proton pump inhibitor (PPI), clarithromycin, and amoxicillin have decreased to 70-85%, in part due to increasing clarithromycin resistance. Eradication rates may also be lower with 7 versus 14-day regimens. Bismuth-containing quadruple regimens for 7-14 days are another first-line treatment option. Sequential therapy for 10 days has shown promise in Europe but requires validation in North America. The most commonly used salvage regimen in patients with persistent H. pylori is bismuth quadruple therapy. Recent data suggest that a PPI, levofloxacin, and amoxicillin for 10 days is more effective and better tolerated than bismuth quadruple therapy for persistent H. pylori infection, though this needs to be validated in the United States. Am J Gastroenterol. 2007 Aug;102(8):1808-25. Epub 2007 Jun 29. Links American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA. Helicobacter pylori (H. pylori) remains a prevalent, worldwide, chronic infection. Though the prevalence of this infection appears to be decreasing in many parts of the world, H. pylori remains an important factor linked to the development of peptic ulcer disease, gastric malignanc and dyspeptic symptoms. Whether to test for H. pylori in patients with functional dyspepsia, gastroesophageal reflux disease (GERD), patients taking nonsteroidal antiinflammatory drugs, with iron deficiency anemia, or who are at greater risk of developing gastric cancer remains controversial. H. pylori can be diagnosed by endoscopic or nonendoscopic methods. A variety of factors including the need for endoscopy, pretest probability of infection, local availability, and an understanding of the performance characteristics and cost of the individual tests influences choice of evaluation in a given patient. Testing to prove eradication should be performed in patients who receive treatment of H. pylori for peptic ulcer disease, individuals with persistent dyspeptic symptoms despite the test-and-treat strategy, those with H. pylori-associated MALT lymphoma, and individuals who have undergone resection of early gastric cancer. Recent studies suggest that eradication rates achieved by first-line treatment with a proton pump inhibitor (PPI), clarithromycin, and amoxicillin have decreased to 70-85%, in part due to increasing clarithromycin resistance. Eradication rates may also be lower with 7 versus 14-day regimens. Bismuth-containing quadruple regimens for 7-14 days are another first-line treatment option. Sequential therapy for 10 days has shown promise in Europe but requires validation in North America. The most commonly used salvage regimen in patients with persistent H. pylori is bismuth quadruple therapy. Recent data suggest that a PPI, levofloxacin, and amoxicillin for 10 days is more effective and better tolerated than bismuth quadruple therapy for persistent H. pylori infection, though this needs to be validated in the United States.

16. GERD Symptoms or mucosal damage caused by the abnormal reflux of stomach contents into the esophagus Diagnosis Empiric acid suppression High dose PPI – sensitivity 75%, specificity 55% EGD Ambulatory reflux monitoring Esophageal manometry SNOUT – sensitivity – if negative, rules out disease = true +/ (true + plus false neg) or all persons with disease SPIN – specificity – if positive, rules in disease = true neg/ (true neg plus false +) or all persons without disease Am J Gastroenterol. 2005 Jan;100(1):190-200. Links Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. DeVault KR, Castell DO; American College of Gastroenterology. Department of Medicine, Mayo Clinic College of Medicine, Jacksonville, FL, USA. Guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD) were published in 1995 and updated in 1999. These and other guidelines undergo periodic review. Advances continue to be made in the area of GERD, leading us to review and revise previous guideline statements. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. These guidelines were developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. Diagnostic guidelines address empiric therapy and the use of endoscopy, ambulatory reflux monitoring, and esophageal manometry in GERD. Treatment guidelines address the role of lifestyle changes, patient directed (OTC) therapy, acid suppression, promotility therapy, maintenance therapy, antireflux surgery, and endoscopic therapy in GERD. Finally, there is a discussion of the rare patient with refractory GERD and a list of areas in need of additional study. SNOUT – sensitivity – if negative, rules out disease = true +/ (true + plus false neg) or all persons with disease SPIN – specificity – if positive, rules in disease = true neg/ (true neg plus false +) or all persons without disease Am J Gastroenterol. 2005 Jan;100(1):190-200. Links Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. DeVault KR, Castell DO; American College of Gastroenterology. Department of Medicine, Mayo Clinic College of Medicine, Jacksonville, FL, USA. Guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD) were published in 1995 and updated in 1999. These and other guidelines undergo periodic review. Advances continue to be made in the area of GERD, leading us to review and revise previous guideline statements. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. These guidelines were developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. Diagnostic guidelines address empiric therapy and the use of endoscopy, ambulatory reflux monitoring, and esophageal manometry in GERD. Treatment guidelines address the role of lifestyle changes, patient directed (OTC) therapy, acid suppression, promotility therapy, maintenance therapy, antireflux surgery, and endoscopic therapy in GERD. Finally, there is a discussion of the rare patient with refractory GERD and a list of areas in need of additional study.

17. Sensitivity and Specificity Sensitivity (SNOUT) if a test has high sensitivity, a negative result rules out disease Specificity (SPIN) if a test has high specificity, a positive result rules in disease SNOUT – sensitivity – if negative, rules out disease = true +/ (true + plus false neg) or all persons with disease SPIN – specificity – if positive, rules in disease = true neg/ (true neg plus false +) or all persons without diseaseSNOUT – sensitivity – if negative, rules out disease = true +/ (true + plus false neg) or all persons with disease SPIN – specificity – if positive, rules in disease = true neg/ (true neg plus false +) or all persons without disease

18. GERD Symptoms or mucosal damage caused by the abnormal reflux of stomach contents into the esophagus Diagnosis Empiric acid suppression High dose PPI – sensitivity 75%, specificity 55% EGD Ambulatory reflux monitoring EGD may be normal in pts with GERD on 24hr reflux monitoring. Am J Gastroenterol. 2005 Jan;100(1):190-200. Links Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. DeVault KR, Castell DO; American College of Gastroenterology. Department of Medicine, Mayo Clinic College of Medicine, Jacksonville, FL, USA. Guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD) were published in 1995 and updated in 1999. These and other guidelines undergo periodic review. Advances continue to be made in the area of GERD, leading us to review and revise previous guideline statements. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. These guidelines were developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. Diagnostic guidelines address empiric therapy and the use of endoscopy, ambulatory reflux monitoring, and esophageal manometry in GERD. Treatment guidelines address the role of lifestyle changes, patient directed (OTC) therapy, acid suppression, promotility therapy, maintenance therapy, antireflux surgery, and endoscopic therapy in GERD. Finally, there is a discussion of the rare patient with refractory GERD and a list of areas in need of additional study. EGD may be normal in pts with GERD on 24hr reflux monitoring. Am J Gastroenterol. 2005 Jan;100(1):190-200. Links Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. DeVault KR, Castell DO; American College of Gastroenterology. Department of Medicine, Mayo Clinic College of Medicine, Jacksonville, FL, USA. Guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD) were published in 1995 and updated in 1999. These and other guidelines undergo periodic review. Advances continue to be made in the area of GERD, leading us to review and revise previous guideline statements. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. These guidelines were developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. Diagnostic guidelines address empiric therapy and the use of endoscopy, ambulatory reflux monitoring, and esophageal manometry in GERD. Treatment guidelines address the role of lifestyle changes, patient directed (OTC) therapy, acid suppression, promotility therapy, maintenance therapy, antireflux surgery, and endoscopic therapy in GERD. Finally, there is a discussion of the rare patient with refractory GERD and a list of areas in need of additional study.

19. GERD - Treatment Lifestyle changes Elevate head of bed Decrease intake of fat Avoid chocolate, peppermint, ETOH, coffee Quit smoking Avoid recumbency <3hrs after eating RTC data are lacking for lifestyle modifications, but on pH monitoring, these changes decrease reflux. Am J Gastroenterol. 2005 Jan;100(1):190-200. Links Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. DeVault KR, Castell DO; American College of Gastroenterology. Department of Medicine, Mayo Clinic College of Medicine, Jacksonville, FL, USA. Guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD) were published in 1995 and updated in 1999. These and other guidelines undergo periodic review. Advances continue to be made in the area of GERD, leading us to review and revise previous guideline statements. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. These guidelines were developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. Diagnostic guidelines address empiric therapy and the use of endoscopy, ambulatory reflux monitoring, and esophageal manometry in GERD. Treatment guidelines address the role of lifestyle changes, patient directed (OTC) therapy, acid suppression, promotility therapy, maintenance therapy, antireflux surgery, and endoscopic therapy in GERD. Finally, there is a discussion of the rare patient with refractory GERD and a list of areas in need of additional study. RTC data are lacking for lifestyle modifications, but on pH monitoring, these changes decrease reflux. Am J Gastroenterol. 2005 Jan;100(1):190-200. Links Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. DeVault KR, Castell DO; American College of Gastroenterology. Department of Medicine, Mayo Clinic College of Medicine, Jacksonville, FL, USA. Guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD) were published in 1995 and updated in 1999. These and other guidelines undergo periodic review. Advances continue to be made in the area of GERD, leading us to review and revise previous guideline statements. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. These guidelines were developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. Diagnostic guidelines address empiric therapy and the use of endoscopy, ambulatory reflux monitoring, and esophageal manometry in GERD. Treatment guidelines address the role of lifestyle changes, patient directed (OTC) therapy, acid suppression, promotility therapy, maintenance therapy, antireflux surgery, and endoscopic therapy in GERD. Finally, there is a discussion of the rare patient with refractory GERD and a list of areas in need of additional study.

20. GERD - Treatment Patient-directed (OTC) therapy Acid suppression Promotility agents Antireflux surgery H2 blockers OK for less severe GERD – start raising pH in about 30 minutes. Endoscopic therapy – radiofrequency ablation of LES, endoscopic sewing procedures, injection of polymersH2 blockers OK for less severe GERD – start raising pH in about 30 minutes. Endoscopic therapy – radiofrequency ablation of LES, endoscopic sewing procedures, injection of polymers

21. GERD - Complications Stricture Barrett’s esophagus (premalignant lesion) Consider EGD to assess in pts with uncontrolled GERD symptoms for >5-10yrs Esophageal cancer Asthma • Cough Hoarseness • Chest pain

22. Ms. C 28 yo previously healthy woman presents with 1 wk of nausea, jaundice, fatigue, confusion after treatment 3wks ago for UTI with TMP/SMX No stigmata of chronic liver disease AST 940 U/L Tbili 11.6mg/dL ALT 899 U/L INR 2.3 alb 3.2 Clinical Question: What is differential diagnosis? Conjugated bili (direct) –obstruction Unconjugated bili (indirect) – over production, hemolysisConjugated bili (direct) –obstruction Unconjugated bili (indirect) – over production, hemolysis

23. Fulminant Hepatic Failure Severe impairment of liver function (coagulopathy) associated with encephalopathy within 8-26 weeks of the first symptoms INR is best marker of liver function DfDx for AST and ALT of near 1000 U/L Hypoperfusion Toxins Viruses Viral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.comViral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.com

24. Fulminant Hepatic Failure - Etiology Medications - most common cause in US (> 50%) Acetaminophen (>4g/day) sulfa-containing – phenytoin NSAIDs – valproate halothane – TCN, erythromycin INH – terbinafine MAOI – herbs antabuse – etc., etc., etc. Viral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.comViral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.com

25. Fulminant Hepatic Failure - Etiology Other Toxins mushrooms (amanita phalloides) yellow phosphorus – illicit drugs CCl4 • cocaine • ecstasy Viral Hepatitis ~10-20% in USA A, B, D, E, HSV, EBV worldwide HBV is the leading cause of ALF Viral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.comViral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.com

26. Fulminant Hepatic Failure - Etiology Metabolic Wilson’s disease young age of onset h/o psychiatric d/o, athetoid movements Kayser-Fleischer ring in cornea check serum ceruloplasmin and copper lethal without transplantation if presents with FHF Rx D-penicillamine or trientine in non-FHF Acute fatty liver of pregnancy Viral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.comViral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.com

27. Fulminant Hepatic Failure - Etiology Other Autoimmune hepatitis check ANA Portal vein thrombosis Budd-Chiari syndrome – blockage of venous outflow Ischemic (“shock liver”) Malignant infiltration Viral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.comViral - don’t forget about EBV, CMV, VZV Structural – HCC, Budd-Chiari (occlusion or partial occlusion of one, two, or all three of the major hepatic veins (right, middle, and left) and/or occlusion or partial occlusion of the inferior vein cava; blockage of venous outflow from the liver Genetic – Wilson’s, alpha 1 antitrypsin Photo from Fred Stevens at mushroomexpert.com

28. Fulminant Hepatic Failure - Rx Stop offending drug/toxin Refer to liver transplantation center Improves survival by 20% if pts with fulminant hepatic failure are managed at specialist ICU facilities At least 12 hrs required to do screening and to list patient for transplantation N-acetylcysteine has not been shown to help in non-acetaminophen-induced liver failure. Good data are lacking, but a study is ongoing (per Larson 11/04). In chronic acetaminophen toxicity, level may not reflect ongoing damage. Error on side of giving acetylcysteine is hidtory is unclear. Increased susceptibility to acetaminophen with chronic ETOH use. N-acetylcysteine has not been shown to help in non-acetaminophen-induced liver failure. Good data are lacking, but a study is ongoing (per Larson 11/04). In chronic acetaminophen toxicity, level may not reflect ongoing damage. Error on side of giving acetylcysteine is hidtory is unclear. Increased susceptibility to acetaminophen with chronic ETOH use.

29. Mr. D 45 yo gentleman presents with hematemesis Takes NSAID for arthritis in hands at MCP joints T37.3C, BP 90/52, HR 122 Stigmata of chronic liver disease Clinical Question: What is differential for GIB in this patient?

30. GIB Two large bore IVs Check coagulation studies Call GI to consider endoscopy Esophageal varices due to portal HTN Octreotide EGD with banding Non-selective ß-blocker (propranolol, nadolol)

31. Hemorrhage of Esophageal Varices Risk of death from hemorrhage as high as 20% in 6 months after bleed Secondary prophylaxis after initial hemorrhage - reduces relative risk of bleeding by about 50% Non-selective ß-blockers (propranolol or nadolol) Push dose to maximum tolerated Band ligation Repeat every 1-2 weeks until varices obliterated Nitrates, shunt therapy, sclerotherapy are not first line treatments for varices.Nitrates, shunt therapy, sclerotherapy are not first line treatments for varices.

32. Hemorrhage of Esophageal Varices Guidelines recommend screening EGD at time of diagnosis of cirrhosis Primary prophylaxis with ß-blocker or ligation if Medium to large varices (NNT = 10 to prevent 1 bleeding episode) Decompensated cirrhosis and small varices Repeat EGD 2-3 yrs in compensated disease and no varices 1-2 yrs in setting of small varices 1 yr in decompensated liver disease with or without varices

33. Causes of Cirrhosis Chronic viral hepatitis Alcohol Biliary diseases primary biliary cirrhosis primary sclerosing cholangitis Autoimmune hepatitis Venous outflow obstruction Budd-Chiari syndrome veno-occlusive disease chronic heart failure Metabolic diseases hemochromatosis Wilson’s Disease alpha-1 antitrypsin deficiency glycogen storage diseases porphyria Drugs and toxins Sarcoidosis Intestinal bypass for obesity NASH PSC – male>female, dx by ERCP PBC – women >men, age 30-50, +AMA, US and biopsy hemochromatosisPSC – male>female, dx by ERCP PBC – women >men, age 30-50, +AMA, US and biopsy hemochromatosis

34. Causes of Cirrhosis PSC – male>female, dx by ERCP PBC – women >men, age 30-50, +AMA, US and biopsy hemochromatosisPSC – male>female, dx by ERCP PBC – women >men, age 30-50, +AMA, US and biopsy hemochromatosis

35. Causes of Cirrhosis PSC – male>female, dx by ERCP PBC – women >men, age 30-50, +AMA, US and biopsy hemochromatosisPSC – male>female, dx by ERCP PBC – women >men, age 30-50, +AMA, US and biopsy hemochromatosis

36. Cirrhosis - Complications Hepatic encephalopathy Ascites Spontaneous bacterial peritonitis (SBP) Hepatocellular carcinoma Hemorrhage of esophageal varices Hyponatremia Coagulopathy Hepatorenal dysfunction Hepatopulmonary syndrome

37. Hepatic Encephalopathy - Asterixis

38. Number or Figure Connection Test Ammonia level is not necessarily predictive. Normal is 30 secs except in folks with education issues, narcotics, etc. Goal is for a stable of improving time from test to test. Ammonia level is not necessarily predictive. Normal is 30 secs except in folks with education issues, narcotics, etc. Goal is for a stable of improving time from test to test.

39. Physical Exam for Ascites Best findings arguing for ascites Fluid wave; up to 6L of fluid needed before detection possible (+LR 5) LE edema (+LR 3.8) Best findings arguing against ascites Absence of flank dullness; approximately 0.5-1.1L of fluid needed before detection possible (-LR 0.3) Absence of LE edema (-LR 0.2) LR of 2, 5, 10 increase probability 15%, 30%, 45%. LR 0.5, 0.2, 0.1 decrease probability by 15%, 30%, and 45% respectively.LR of 2, 5, 10 increase probability 15%, 30%, 45%. LR 0.5, 0.2, 0.1 decrease probability by 15%, 30%, and 45% respectively.

40. Likelihood Ratios LR of 2, 5, 10 increase probability 15%, 30%, and 45% respectively LR 0.5, 0.2, 0.1 decrease probability 15%, 30%, and 45% respectively

41. Diagnostic Paracentesis (30cc) Albumin SAAG (serum-ascites albumin gradient) >1.1g/dL is consistent with portal HTN Cell count >250 PMN/µL = spontaneous bacterial peritonitis (SBP) Culture into blood culture bottles at the bedside Total protein If <1.5g/dL, start SBP prophylaxis J Hepatol. 2008 May;48(5):774-9. Epub 2008 Feb 14. Links Ciprofloxacin in primary prophylaxis of spontaneous bacterial peritonitis: a randomized, placebo-controlled study. Terg R, Fassio E, Guevara M, Cartier M, Longo C, Lucero R, Landeira C, Romero G, Dominguez N, Muñoz A, Levi D, Miguez C, Abecasis R. Unidad de Hígado, Hospital de Gastroenterología Dr. Bonorino Udaondo, Sección Hepatología, Avenida Caseros 2061, 1264 Buenos Aires, Argentina. [email protected] BACKGROUND/AIMS: Low protein concentration in ascitic fluid has been identified as a risk factor for spontaneous bacterial peritonitis (SBP). Until now, primary prophylaxis has not been recommended in these patients. The aim was to investigate the efficacy of long-term administration of ciprofloxacin to prevent SBP. METHODS: One hundred cirrhotic patients with <1.5 g/dl of total protein in ascitic fluid were randomized prospectively, in a double blind fashion to receive ciprofloxacin 500 mg/day (n=50) or placebo (n=50) for 12 months. RESULTS: Baseline data were similar in both groups. In the ciprofloxacin group, SBP occurred almost four times less frequently than in the placebo group but it was not statistically significant. The probability of survival at 12 months was significantly higher in patients receiving ciprofloxacin (86% versus 66%) (p<0.04). SBP and sepsis were the most frequent causes of death in the placebo group whereas gastrointestinal bleeding was responsible for the most deaths in the ciprofloxacin group. The probability of remaining free of bacterial infections was higher in patients receiving ciprofloxacin (80% versus 55%) (p=0.05). CONCLUSIONS: Patients with cirrhosis and low protein concentration in ascitic fluid are candidates to receive long-term prophylaxis to reduce the risk of infections and improve survival. J Hepatol. 2008 May;48(5):774-9. Epub 2008 Feb 14. Links Ciprofloxacin in primary prophylaxis of spontaneous bacterial peritonitis: a randomized, placebo-controlled study. Terg R, Fassio E, Guevara M, Cartier M, Longo C, Lucero R, Landeira C, Romero G, Dominguez N, Muñoz A, Levi D, Miguez C, Abecasis R. Unidad de Hígado, Hospital de Gastroenterología Dr. Bonorino Udaondo, Sección Hepatología, Avenida Caseros 2061, 1264 Buenos Aires, Argentina. [email protected] BACKGROUND/AIMS: Low protein concentration in ascitic fluid has been identified as a risk factor for spontaneous bacterial peritonitis (SBP). Until now, primary prophylaxis has not been recommended in these patients. The aim was to investigate the efficacy of long-term administration of ciprofloxacin to prevent SBP. METHODS: One hundred cirrhotic patients with <1.5 g/dl of total protein in ascitic fluid were randomized prospectively, in a double blind fashion to receive ciprofloxacin 500 mg/day (n=50) or placebo (n=50) for 12 months. RESULTS: Baseline data were similar in both groups. In the ciprofloxacin group, SBP occurred almost four times less frequently than in the placebo group but it was not statistically significant. The probability of survival at 12 months was significantly higher in patients receiving ciprofloxacin (86% versus 66%) (p<0.04). SBP and sepsis were the most frequent causes of death in the placebo group whereas gastrointestinal bleeding was responsible for the most deaths in the ciprofloxacin group. The probability of remaining free of bacterial infections was higher in patients receiving ciprofloxacin (80% versus 55%) (p=0.05). CONCLUSIONS: Patients with cirrhosis and low protein concentration in ascitic fluid are candidates to receive long-term prophylaxis to reduce the risk of infections and improve survival.

42. SBP Prophylaxis Indications for prophylaxis Prior episode of SBP Ascites protein <1.5g/dL During acute UGIB www.drugstore.comwww.drugstore.com

43. Moderate Volume Ascites - Rx Low sodium diet (90mmol/day) Diuretic Regimen Optimal ratio Furosemide (Lasix) 20mg po qday Spironolactone (Aldactone) 50mg po day Maximum dose Furosemide 160mg/day Spironolactone 400mg/day Goal diuresis 300-500g/day if no peripheral edema 800-1000g/day if peripheral edema

44. Large Volume Ascites - Rx Total paracentesis with IV albumin Albumin 6-8g IV per liter of ascites removed (as long as ?5 liters ascites removed) For example, If 4 liters removed, no albumin If 5 liters removed, give 5 x 6-8g albumin 25% albumin in 50 ml25% albumin in 50 ml

45. Albumin - Large Volume Paracentesis Assists with plasma volume expansion Tries to balance the increased activity of renin-angiotensin-aldosterone system Attempts to prevent renal impairment 20% of pts with circulatory dysfunction after LV paracentesis develop hepatorenal syndrome and/or dilutional hyponatremia Has not been shown to have direct survival benefit 25% albumin in 50 ml25% albumin in 50 ml

46. HCC Surveillance Serum AFP and liver ultrasound Q6 months Initiate surveillance in pts with cirrhosis due to: HCV HBV Primary biliary cirrhosis (PBC) ETOH Hemochromatosis Unclear benefit in pts with cirrhosis due to: Autoimmune hepatitis Alpha-1-antitrypsin Non-alcoholic steatohepatitis

47. HCC Surveillance Serum AFP and liver ultrasound Q6 months Also recommended in HBV carriers without cirrhosis who are: Asian men = 40 yo Asian women = 50 yo African men or women = 20 yo Family history of HCC

48. Surveillance for HCC RCT, >18,000 ESLD pts with HBV Every 6 month serum AFP and hepatic ultrasound vs no surveillance Reduced HBV associated mortality by 37% in surveillance group Find disease early. Once sxs from HCC, 5-yr survival 0-10%. Small HCC disease-free survival (at 5-yrs) is >50%. Surveillance should be offered when incidence of HCC >1.5%/yrFind disease early. Once sxs from HCC, 5-yr survival 0-10%. Small HCC disease-free survival (at 5-yrs) is >50%. Surveillance should be offered when incidence of HCC >1.5%/yr

49. Mr. D 45 year-old gentleman with ESLD secondary to hemochromatosis PE: moderate ascites Labs: bilirubin 3.1mg/dL - INR 1.8 albumin 2.8g/dL - Cr 1.7mg/dL Clinical Question: How can we classify the severity of Mr. D’s liver disease? Asked to see as med consult pre-operatively.Asked to see as med consult pre-operatively.

50. Child-Turcotte-Pugh Class 1 2 3 Albumin >3.5 2.8 - 3.5 <2.8 Bilirubin <2 2 - 3 >3 INR <1.8 1.8 – 2.3 >2.3 Ascites None Mild Mod Encephalopathy None 1 - 2 3 - 4

51. Model for End-Stage Liver Disease (MELD) Score MELD = 9.57 x loge creatinine (mg/dL) + 3.78 x loge bilirubin (mg/dL) + 11.20 x loge INR + 6.43 Predicts risk of death with TIPS Predicts overall risk of death at 3 months & 1 yr Used to prioritize organ allocation for liver transplantation since Feb 2002 MELD adopted Feb 2002. Heuman et al. Persistent ascites and low serum sodium identify patients with cirrhosis and low MELD scores who are at high risk for early death. Hepatology 2004;40:802-810. – MELD-AS (ascites, sodium) TIPS – transjugular intrahepatic portosystemic shunt MELD adopted Feb 2002. Heuman et al. Persistent ascites and low serum sodium identify patients with cirrhosis and low MELD scores who are at high risk for early death. Hepatology 2004;40:802-810. – MELD-AS (ascites, sodium) TIPS – transjugular intrahepatic portosystemic shunt

52. MELD – Overall Mortality Prediction MELD Mortality (3mo) < 9 2% 10-19 6% 20-29 20% 30-39 53% >40 71% Wiesner, et al. Gastro 2003; 124:91 – prospective; 3437 OLT candidates listed for OLT from 12/99-12/01 Wiesner, et al. Gastro 2003; 124:91 – prospective; 3437 OLT candidates listed for OLT from 12/99-12/01

53. Mr. G 68 yo gentleman presents with epigastric pain of 1 day duration h/o HTN Drinks 2 glasses of wine a day Clinical Question: What further history do you want and what is your differential diagnosis?

54. Acute Pancreatitis Etiology Gallstones, ETOH, mass, pancreas divisum, trauma (MVA, ERCP), scorpion bite, autoimmune If young person with pulm or GI disease, think about cystic fibrosis APACHE II score =8 Better predictor of severe pancreatitis than Ranson criteria Complications Necrosis, pseudocyst APACHE II score t, HR, MAP, RR, O2, pH, Na, K, Cr, HCT, WBC, age, glasgow coma scale Ranson criteria to predict severity of acute pancreatitis at 0 and 48hrs 0 hours Age >55 White blood cell count >16,000/mm3 Blood glucose >200 mg/dL (11.1 mmol/L) Lactate dehydrogenase >350 U/L Aspartate aminotransferase (AST) >250 U/L 48 hours Hematocrit Fall by 10 percent Blood urea nitrogen Increase by 5 mg/dL (1.8 mmol/L) despite fluids Serum calcium <8 mg/dL (2 mmol/L) pO2 <60 mmHg Base deficit >4 MEq/L Fluid sequestation >6000 mL The presence of 1 to 3 criteria represents mild pancreatitis; the mortality rate rises significantly with four or more criteria. Adapted from Ranson, JHC, Rifkind, KM, Roses, DF, et al, Surg Gynecol Obstet 1974; 139:69. APACHE II score t, HR, MAP, RR, O2, pH, Na, K, Cr, HCT, WBC, age, glasgow coma scale Ranson criteria to predict severity of acute pancreatitis at 0 and 48hrs 0 hours Age >55 White blood cell count >16,000/mm3 Blood glucose >200 mg/dL (11.1 mmol/L) Lactate dehydrogenase >350 U/L Aspartate aminotransferase (AST) >250 U/L 48 hours Hematocrit Fall by 10 percent Blood urea nitrogen Increase by 5 mg/dL (1.8 mmol/L) despite fluids Serum calcium <8 mg/dL (2 mmol/L) pO2 <60 mmHg Base deficit >4 MEq/L Fluid sequestation >6000 mL The presence of 1 to 3 criteria represents mild pancreatitis; the mortality rate rises significantly with four or more criteria. Adapted from Ranson, JHC, Rifkind, KM, Roses, DF, et al, Surg Gynecol Obstet 1974; 139:69.

55. Chronic Pancreatitis Watch for signs of pancreatic insufficiency DM Treat as for type 1 DM Steatorrhea Treat with pancreatic enzymes Pancreatic calcifications on KUB Amylase/lipase may not rise much with acute on chronic pancreatitis

56. Ms. E 72 yo woman calls with c/o watery loose stools several hours after a picnic. Other family members have similar symptoms. No fever. No blood in stool. Nausea without emesis. Otherwise well. Clinical Question: What work-up is necessary and what treatment would you recommend?

57. Acute Diarrhea Food-borne disease Sxs start within 6 hrs – S. aureus, B. cereus Sxs start within 8-14 hrs – C. perfringens Sxs start >14hrs – viral or E. coli E. coli O157:H7 – 10% of infected pts get HUS or TTP Watch for giardia if unfiltered H2O ingestion

58. Acute Diarrhea Work-up/Treatment Hydration and watchful waiting unless Symptoms >7 days Fever Abdominal pain Hematochezia Avoid antimotility agents with E. coli suspected

59. Mr. F 21 yo gentleman presents with 8-10 bloody bowel movements per day, abd pain, and tenesmus x 3 months. Clinical Question: What additional information do you want? Fam hx negative HIV negativeFam hx negative HIV negative

60. Chronic Diarrhea Is patient immunocompromised? Is diarrhea…? Bloody/Inflammatory Guaiac, fecal leukocytes + Osmotic/Malabsorption Stool osm > 340 mosm/kg Resolves with fasting, no nocturnal symptoms Lactase deficiency most common Secretory Large volume, watery No change with fasting, nocturnal sxs present

61. Inflammatory Bowel Disease

62. IBD – Extra-Intestinal Manifestations Uvetitis, episcleritis Erythema nodosum red nodules most classically on shins Pyoderma gangrenosum erythematous papules or pustules Arthritis Primary sclerosing cholangitis (PSC) Venous thromboembolism

63. Mr. F Colonoscopy and EGD most consistent with Crohn’s disease Started on prednisone and then azathioprine after symptoms improved Develops new vague diffuse abdominal pain that is different than prior symptoms No fever. BP 100/60, HR 90. Mild diffuse TTP. No rebound/guarding. Clinical Question: Why does Mr. F have new pain? Pred to induce remission. Aza to try to hold remission. Pred to induce remission. Aza to try to hold remission.

64. Mr. F

65. Bowel Perforation and Steroids In patients on >20mg/day of prednisone, abdominal tenderness is the only consistent symptom/sign of abdominal perforation Delay in diagnosis up to 8 days from onset of symptoms Mortality approximately 85%

66. Celiac Sprue Symptoms chronic diarrhea, steatorrhea, bloating, wt loss, abd pain PE pruritic papulovesicular rash on extensor surfaces = dermatitis herpetiformis Associated with autoimmune disease (i.e. DM1) Dx IgA anti-tissue transglutaminase IgA anti-endomysial antibody test Biopsy of proximal small bowel Rx - Gluten-free diet

67. Nausea - Pathophysiology

68. Nausea - Pathophysiology

69. Nausea - Pathophysiology

70. Dopamine Antagonists Prochlorperazine (Compazine) Haloperidol Metoclopramide Droperidol Often used empirically as first line drug of choice Can cause drowsiness and extrapyramidal symptoms

71. Nausea - Pathophysiology

72. Nausea – Medication Options Histamine antagonists Can cause sedation Promethazine (Phenergan) Diphenhydramine Meclizine Hydroxyzine Acetylcholine antagonist Scopolamine, hyoscine

73. Nausea - Pathophysiology

74. Nausea - Pathophysiology

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