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GI Board Review Esophagus GERD Middle aged overweight male with retrosternal burning and regurgitation worse with citrus and smoking. GERD Symptoms Retrosternal burning – post prandial/recumbant Regurgitation Dysphagia Water Brash Chronic Cough Historical clues: Pregnancy, Scleroderma, Obesity, hiatal hernia Gold standard – 24 hour pH probe GERD Complications Barrett’s Adenocarcinoma Strictures/Rings Hoarseness/Asthma Empiric treatment – Sensitivity of 80% When refer for endoscopy? Evaluate for Barrett’s/anatomy Don’t respond to therapy Alarm symptoms – dysphagia, bleeding, weight loss, anemia, odynophagia Chronic GERD - treatment On the Boards, remember to be cost effective Lifestyle modification (Weight loss most important and avoidance of foods that cause LES relaxation i.e. peppermint, chocolate, alcohol, fatty foods) Acid suppression Promotility – Reglan/Cisapride (Minimal Data) Surgery – Nissen Fundoplication PPI > H2 blocker(80% control symptoms) PPI better in endoscopically proven esophagitis Equivalent to PPI therapy – 0.2% mortality 2/3 will be on acid suppression in 5 years No evidence that prevents Barrett's or CA Endoscopic Therapy (Stretta, Endocinch, etc) Rarely performed. Barrett’s Esophagus 55 year old white male with 10 years of pyrosis, mildly improved over past year, on PPI daily. Barrett’s Esophagus Middle aged and older, M>F (2:1) Whites and Hispanics predominantly About 5-10% of patients with GERD (though in multiple studies, also present in 0%-25% of asymptomatic patients) Defining characteristic: Change in squamous esophageal epithelium to intestinal metaplasia 0.5% per person per year chance of developing adenocarcinoma Treatment Control GERD Symptoms – PPI vs. surgery No therapy definitively shown to reduce risk of progression to malignancy Surveillance endoscopy Esophageal Cancer 75 year old female with history of tobacco use and alcohol use with progressive solid food dysphagia and 15 pound weight loss over past year. Esophageal Cancer Essentially equal prevalence in United States of esophageal SCC and adenocarcinoma Squamous Cell – proximal esophagus Smoking Tylosis Achalasia Plummer-Vinson Lye Ethanol Sprue/Scleroderma Adenocarcinoma – Distal esophagus GERD/Barrett’s, Obesity, Tobacco Esophageal Cancer Symptoms Progressive Solid Food Dysphagia 75% also weight loss/anorexia Endoscopy with Biopsy – Diagnostic Staging 1. CT chest/abd/pelvis vs. PET for Mets 2. EUS for T and N staging Dysphagia Dysphagia Solids Solids/liquids Intermittent Progressive Intermittent Progressive Ring or Stricture Esophageal CA DES Achalasia / Scleroderma Dysphagia History and Physical Solid vs. liquid Intermittent vs. progressive Oropharyngeal vs. Esophageal Barium swallow (13mm pill) EGD (with possible dilation) Esophageal manometry Peptic Stricture Progressive solid food dysphagia History of GERD No weight loss Patients have normal appetite Majority (60-70%) are peptic in origin Result of chronic esophageal inflammation Esophageal Ring 38 year old female with frequent heartburn, controlled on PPI, with intermittent solid food dysphagia. Achalasia 35 year old male with progressive solid and liquid food dysphagia and fatigue, with regurgitation of undigested food. Achalasia “failure to relax” 1/100,000 M:F 1:1 Age 25-60 (If older>60, think pseudoachalasia especially gastric cancer) Increased risk for squamous cell cancer Hallmarks: Aperistalsis Failure of LES to relax Dysphagia to solid and liquid Postural changes to help swallowing Regurgitation of undigested food Autoimmune vs. Viral Chagas Disease (Trypanosoma cruzei) Achalasia - diagnosis Barium Swallow – Dilated esophagus with column of barium and “Birds Beak” taper. Test of choice if suspected Endoscopy – rule out pseudoachalasia Manometry (Used to confirm diagnosis) (1)Loss of peristalsis, (2)failure of LES to relax, (3)possibly LES high pressure Chest X-ray – wide mediastinum and air fluid level Eosinophilic Esophagitis 20 year old male with history of asthma and eczema with recurrent food impactions. Eosinophilic Esophagitis Atopic history and food impactions Ringed esophagus / linear furrows >15 eosinophils per high power field Some (minority) have peripheral eosinophilia Oral fluticasone 220 mcg/puff 2 puffs bid for 6-8 weeks. Recurrence frequent. Other possible treatments: PPI, singulair (large doses up to 100 mg), elimination diets (children predominantly) and dilation Scleroderma Historical Key: 70 year old woman with sclerodactyly telangiectasias, Raynaud’s with GERD, resistant to PPI 75% have esophageal involvement Severe GERD, frequently resistant to PPI Incompetent LES and lack of peristalsis Control GERD with PPI Stomach Upper GI bleed Presentation Hematemesis (Not to be confused with hemoptysis) Melena (Black, Tar-Like – not solid) Nausea/vomiting common with PUD Orthostasis (Bedside orthostatics) Abdominal pain Hematochezia (10% of maroon stool from upper source – On test will be unstable) Upper GI Bleed Peptic Ulcer Disease – 55% Esophageal Varices – 14% AVM’s / GAVE – 6% Mallory-Weiss tear – 5% Dieulafoy’s – 1% Cameron’s lesion Tumors Esophagitis (Most common cause of UGIB in hospitalized patients, likely due to NGT and reflux in supine position) Peptic Ulcer Disease 65 year old female with arthritis, taking ibuprofen, with melena and lightheadedness. Risk Factors for NSAID-induced Ulcers Definite: Prior PUD Advanced age Concomitant use of glucocorticoids Concomitant use of anticoagulants High doses or combinations of NSAIDs, including low-dose aspirin Comorbid illness (RA, CAD, etc) Ethanol use Possible: H. pylori infection smoking Helicobacter pylori Most peptic ulcers caused by Helicobacter pylori 60-80% of GU’s and 90% DU’s 2 clinical presentations of H. pylori Antrum predominant Body predominant Increased acid production, Duodenal Ulcers, no cancer Decreased acid production, Gastric Ulcers, Gastric Cancer (<1% of those infected, Cag A strain) Eradication of Hp dramatically decreases PUD and its complications Tests for H. pylori Serologic Antibody (90% sens / 90% spec) Endoscopy with Histology (95% sens / 98% spec) Endoscopy w/Rapid Urease Test (CLO) (90% /98%) Urease Breath Test (C13 / C14) (95% / 95%) Remains positive for several years Do not use for evaluation for eradication Best test for eradication Stool Antigen (92% / 90%) All tests (except serology) less reliable if on PPI in last 2 weeks, or antibiotics or bismuth in past 4 weeks. Rx of H. pylori Standard : Amoxicillin, Clarithromycin, PPI bid x 14 days 75-80% eradication rate Major antibiotic resistance to clarithromycin and metronidazole. If allergic to PCN, substitute metronidazole for amoxicillin Peptic Ulcer Disease – Rebleed Risk (within 72 hours) Clean Base Pigmented Spot Adherent Clot Visible Vessel Active Bleeding Baseline PPI 3-5% 7-10% 22-30% 43-52% 55-90% ------0% 12% 73% PPI/EGD Tx ------6.7% 6.7% 6.7% Zollinger-Ellison Gastrin producing neuroendocrine tumor 1% of PUD (Never seen clinically but all over board exams) 90% will have PUD (frequently solitary duodenal ulcer but may be multiple and in unusual places i.e. jejunum) Frequently with abdominal pain and chronic secretory diarrhea 70% Duodenum/30% Pancreas 1/3 metastatic at diagnosis Zollinger - Ellison Fasting Gastrin >1000 diagnostic if acidic pH in stomach (separate low acid states (atrophic gastritis and pernicious anemia) from ZE) Secretin Stimulation Test (secretin infusion promotes gastrin release by gastrinoma cells but not gastric G cells) 150-1000 abnormal but can be secondary to meds (PPI) or H pylori causing atrophic gastritis Positive test - Increased Gastrin by at least 120-200 pg/ml within 20 minutes after secretin infusion Localize with octreoscan/EUS of pancreas MEN1 Pancreatic islet cell tumors seen with MEN1 about 80% of time (parathyroid, pituitary, pancreas) 50-60% with MEN1 have gastrinoma, but… About 20% with gastrinoma have MEN1 Most common pancreatic islet cell tumor associated with MEN1 is a “nonfunctioning” islet cell tumor (i.e. releases hormone that does not cause symptoms like PPP) Gastric Cancer Diffuse (Infiltrating cells, i.e. linitis plastica) vs. Intestinal Type (glandular) Most common in Far East (if Japanese or Korean patient with stomach complaint, think of gastric cancer) Risk Factors 1st degree relative (3x) H. pylori – Chronic Atrophic Gastritis Dietary – Nitrates Tobacco Gastric Cancer Epidemiology Pancreas Acute pancreatitis Alcohol or gallstone predominant etiologies Drugs – DDI, diuretics, estrogen, valproic acid, 5-ASA, azathioprine, TCN, sulfa Interstitial (85%) vs. necrotizing (15%) Organ failure in 10% vs. 54% Mortality Rate 3% vs. 17% 33% of patients with sterile necrosis develop infected necrosis 47% mortality with MSOF Interesting fact – Pain radiates to back only about 50% of time. Complications SIRS: ARDS, Shock, ARF, GI Bleed Necrosis: Infection Pseudocyst/Abscess Pancreatic Ascites, Fistula (pleural effusion) Chronic Pancreatitis Splenic Vein Thrombosis, Pseudoaneurysm Treatment Mild – NPO, pain control, fluid resuscitation Severe pancreatitis – Likely ICU Adequate pain relief, Adequate IV fluid replacement, especially initially (decrease Hct over first 24 hours to reduce risk of necrosis) ERCP for gallstone panc (cholangitis/jaundice) (suspect if ALT or AST>3x ULN) Nutritional support Enteral feeding better than TPN due to decreased episodes of hyperglycemia and sepsis Current teaching to place feeding tube beyond Ligament of Treitz (controversial) Enteral Nutrition and Severe Pancreatitis 16 14 12 10 8 Enteral TPN # PTS 6 4 2 0 septic complications *P<0.01 any complication **P<0.05 Kalfarentos et al Br J Surg 1997; 84:1665 Treatment Severe pancreatitis Contrast CT recommended at some point beyond the first 3 days in severe pancreatitis to rule out necrotizing pancreatitis. Otherwise, minimal role for early CT No role for prophylactic antibiotics with sterile necrosis (controversial) If concern for infected necrosis (usually after 7 days), CT guided aspiration. Chronic pancreatitis Chronic Pancreatitis Chronic epigastric pain/maldigestion related to fibrotic pancreas Diagnosis usually made after disease is well established. Most frequently associated with alcohol abuse Maldigestion with steatorrhea/weight loss Fat soluble vitamin and B12 deficiency DM common in advanced disease Chronic Pancreatitis Lipase and amylase normal or only slightly elevated May mimic pancreatic cancer or autoimmune pancreatitis (IgG4, ANA) with duodenal or biliary obstruction Complications: pseudocyst, splenic vein thrombosis, pancreatic cancer (4% lifetime risk) Diagnosis (difficult) Clinically useful tests for CP Function Secretin stim test Bentiromide test Serum trypsinogen Fecal chymotrypsin Fecal fat Structure ERCP/EUS CT scan US KUB Treatment Pain relief Non-enteric coated pancreatic enzymes (Viokase) with PPI Narcotics Celiac plexus block (CT vs. EUS) ERCP with stent or stone removal Surgical resection or Peustow procedure Maldigestion (steatorrhea) Coated Pancreas enzyme (Creon) Pancreatic Cancer 2nd most common GI cancer and 4th most common cancer death in US Rare before age 45, M>F, African Americans>Whites 28,000 cases per year (27,000 deaths) 85-90% originate from pancreatic ductal cells Rarer cancers of acinar cells or neuroendocrine cells Painful or painless jaundice, acholic stool, dark urine, weight loss Elevated CA 19-9 Diabetes frequently diagnosed within past 2 years Treatment Biggest risk factors – Hereditary pancreatitis, smoking, BRCA-2, chronic pancreatitis Only 20% resectable at diagnosis Surgery Head – Whipple procedure Tail – Distal pancreatectomy/Splenectomy Palliation – Intestinal/Biliary bypass ERCP – Biliary/Duodenal Metal Stent Chemo - 5FU and Gemcitabine Role of XRT controversial Pancreatic Neuroendocrine Tumors Insulinoma Glucagonoma Necrolytic migratory erythema, weight loss, diarrhea 75% malignancy rate VIPoma (aka Verner-Morrison Syndrome or WDHA (Watery diarrhea, hypokalemic and achlorhydria) Usually solitary, 5-10% malignancy Hypoglycemia - 48 hour fast Secretory diarrhea, flushing, achlorhydria, hypokalemia Elevated fasting VIP Level Increased risk of neuorendocrine tumors in MEN1, Von HippelLindau, neurofibromatosis 1, tuberous sclerosis Choledocholithiasis EUS us MRCP IOC ERCP Common Bile Duct stones/Cholangitis Obstructive jaundice WITH pain Rising LFTS after Lap Chole – either retained stone in CBD vs. Bile leak Answer is ERCP Cholangitis Charcot Triad: RUQ Pain, Fever, Jaundice Reynolds Pentad : Shock, MS changes ERCP stone extraction/biliary stent placement IR placed percutaneous GB drain Antibiotics : Floroquinolone or Unasyn/Zosyn Gallstones Presentation: Usually asymptomatic If no symptoms from stones, then no treatment Type: 75-80% cholesterol stones Risk factors: 4F’s - fat, fertile, female, forty Ethnicity, rapid weight loss 20% pigmented stones Biliary colic, acute cholecystitis, CBD obstruction (acute elevation of ALT, AST, Alk phos and TB with direct predominance), pancreatitis Black – hemolysis and cirrhosis (calcium bilirubinate) Brown – Anaerobic bile duct infections (Rare in US) Diagnosis: Ultrasound best, CT, MRCP Treatment – If symptomatic, cholecystectomy. If not surgical candidate, ursodiol. Biliary Tree Tumors Carcinoma of GB is the leading cause of biliary tree tumors. Risks include: Gallstones Choledochal cysts GB polyps (primarily single and >1 cm) Porcelain GB Cholangiocarcinoma-rare but increasing incidence. Risks include: UC PSC Thorotrast Choledochal cysts Clonorchis and Opisthorchis Treatment - Surgery in minority vs. Palliative stent Colon Acute Diarrhea Virus Protozoa Norovirus Rotavirus Adenovirus Giardia Entamoeba histolytica Cryptosporidium (HIV) Cyclospora Toxin mediated Bacteria Salmonella Campylobacter Shigella E.Coli (0157:H7) C. Difficile Yersinia Vibrio Listeria Norovirus Nursing homes, hospitals, cruise ships, restaurants Incubation 24-48 hours (also highest shedding) Abd cramps followed by vomiting and diarrhea Nonbloody watery diarrhea Myalgias and malaise, low grade fever Lasts 48-72 hours Symptomatic treatment Campylobacter Food borne disease – 3 day incubation Typically with fever, severe abdominal pain (may mimic appendicitis) and bloody diarrhea Lasts on average 7 days Associated with Reactive Arthritis, Guillain-Barre Syndrome, and pericarditis Treatment – Mainly supportive as disease usually self limited If severe, use Erythromycin (other possibilities include Flouroquinolones, Macrolides, and Aminoglycosides) Most resistant to septra Salmonella Non-typhoid Salmonella typhimurium and Salmonella enteritidis Largest number of food borne outbreaks in US Eggs, poultry, undercooked beef, and pet reptiles and rodents Nausea, vomiting, diarrhea, fever, abd pain 4-10 days of diarrhea Antibiotics have not been shown to be of benefit in routine cases Flouroquinolones or bactrim in severe cases or comorbidity (HIV) May become chronic carriers EHEC (0157:H7) Enterohemorrhagic Escherichia coli Incubation 3-4 days >90% will have bloody diarrhea Undercooked ground beef, petting zoos, daycare Differ from other E. coli in the production of Shiga Toxins Enter circulation and target endothelial cells causing vascular damage and prothrombotic state Abdominal Pain Often lack a fever HUS: 6-9% --- 50% dialysis, 3-5% mortality Treatment – Supportive Avoid antimotility agents and antibiotics (risk of causing HUS) Shigella Not susceptible to acid, so few organisms cause infection Fever, abdominal cramps, mucoid or bloody diarrhea 3 day incubation, 7 day duration Rare cause of HUS and reactive arthritis Associated with seizures and encephalopathy in children Treatment – antibiotic recommended (FQ) Reduce shedding and person to person transmission Decrease fever and diarrhea by 2 days Clostridium dificile Associated with antibiotic usage, older age, and possibly PPI NAP1/BI/027 strain with larger quantities of toxins A and B, worse outcomes, and associated with leukemoid reaction. Think C diff in inpatient on antibiotics with WBC 20K. Treatment - Fluids, Avoid/Hold antibiotics Metronidazole 500mg TID or 250mg QID Oral Vancomycin 125 – 250 mg po QID 20% Relapse rate – retreat with Flagyl or Vancomycin Other Infectious Causes Amebiasis (Entamoeba histolytica) Invade and penetrate colonic mucosa Subacute moderate diarrhea with abdominal pain and bloody stools and weight loss Treatment – Metronidazole 500-750 mg tid for 7-10 d Giardia lamblia (Chronic, large volume) Contaminated water source (stream, well), or person to person (daycare, MSM) Watery diarrhea, malaise, steatorrhea, abd cramps and bloating Treatment: Metronidazole 250 mg tid for 5 days Chronic Diarrhea Chronic Diarrhea (>4wks) Diarrhea Watery Osmotic Inflammatory Fatty Secretory Initial Testing: Large Volume (Small Bowel) vs. Small Volume (colon) 1. Stool Osmolar Gap = 290 – 2(Na +K) <50 is secretory >100 osmotic 2. Fecal Occult Blood Testing and Fecal Leukocytes 3. Fecal Fat - >7g over 24 hours with 100 g fat diet (tends to be higher (i.e. 30g/day) with maldigestion than malabsorption) Chronic Diarrhea Osmotic Fatty Mg, PO4, Carb Maldigest Short gut/Resection Bacterial overgrowth Mucosal Disease/Celiac Pancreatic insufficiency Inflammatory Inflammatory Bowel Ischemia Diverticulitis Chronic infection Secretory Non-osmotic laxative Post-cholecystectomy Bile acid malabsorption IBS Gastrinoma VIPoma Mastocytosis Carcinoid syndrome Hyperthyroid Vasculitis Microscopic colitis Lymphoma, colon ca History for Chronic Diarrhea Osmotic gets better with fasting – others don’t Bloody BM’s – Inflammatory (UC) Weight loss – Fatty, Inflammatory RLQ pain – think Crohn’s Iron Deficiency – think Celiac sprue Wakes up at night with symptoms – not IBS Ask about medications or surgeries (cholecystectomy or IC valve resection, etc) Irritable Bowel Syndrome Rome III Criteria Recurrent abdominal pain or discomfort at least 3 days per month in the last 3 months associated with 2 or more of the following Improvement with defecation Onset associated with a change in frequency of stool Onset associated with change in form of stool Criteria fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis Irritable Bowel Syndrome Pain poorly localized and inconsistent and often in BLQ Need to have bowel movement soon after meals (gastro-colic reflex) Symptoms do NOT wake the person from sleep Symptoms worsened with stress Less than age 40 at start of symptoms Depression or Anxiety Often overlap with other functional syndromes (Dyspepsia, FMS, etc) Evaluation for IBS If meet Rome III Criteria then testing has not been shown to be helpful (except for sprue in diarrhea predominant) Celiac Sprue serology has been positive in 5% Sigmoidoscopy/Colonoscopy no benefit ESR, FOBT, Stool Culture, O&P etc. no benefit If they don’t meet the criteria or fit the usual description then testing is indicated For testing purposes, avoid performing diagnostic tests (CT) on patients who meet Rome III criteria Treatment Treat symptoms Most medications have unproven benefit Fiber : Metamucil, Citrucel, Benefiber Antispasmodics: Bentyl, Levsin, Donnatol Tricyclic Antidepressants, SSRI’s Imodium (diarrhea), Miralax (constipation) Stress Reduction Avoid fatty foods, Avoid Dairy Celiac Sprue 40 year old Irish immigrant with history of DM 1 and hypothyroidism with steatorrhea, microcytic anemia and mild elevation of ALT (80). Chronic malabsorption of small intestine secondary to exposure to dietary gluten (gliadin portion) 1:250 in US Symptoms include: Diarrhea or steatorrhea Weight loss Transaminase elevations Anemia (iron deficiency) Vitamin deficiency Asymptomatic Celiac Disease Associated with HLA DQ2 and DQ8 Associated diseases: IBS Osteoporosis IgA nephropathy Dermatitis Herpetiformis - Elbows, knees, buttocks Increased risk of lymphoma (NHL) and GI malignancies DM 1 IgA deficiency Thyroid disease Celiac Sprue Diagnose with endomysial Ab or tissue transglutaminase Ab (both IgA). Confirm diagnosis with small bowel biopsy. Activated T-cells damage villous architecture with inflammatory response (blunted villi, epithelial lymphocytic infiltrate, crypt hyperplasia). All testing improves with treatment Gluten-free diet No wheat, rye or barley Not in oats, though they are often contaminated with gluten Nonresponsive or relapse likely due to dietary indiscretion Lower GI Bleed Diverticular (Painless) Ischemic Colitis (painful) Angiodysplasia Cancer / Polyps Ulcerative Colitis / Crohn’s Hemorrhoids 10% LGIB is from upper source Diagnose etiology with colonoscopy If unable to find source of bleeding or if unable to tolerate a colonoscopy then: Tagged RBC Scan (Technetium 99m) - Requires .1-.4ml/min of active bleeding Angiography - Requires .5-1ml/min of active bleeding Allows directed therapy with gelfoam etc. Inflammatory Bowel Disease String sign – seen with Crohn’s Ulcerative Colitis Recurring episodes of inflammation limited to the mucosal layer of the colon. Invariably involving the rectum and extends proximally in a continuous fashion. Bloody diarrhea Rectal urgency Abdominal cramps Fever, weight loss, anorexia, N/V UC - Complications Massive hemorrhage Toxic megacolon Colonic perforation (5%) Extraintestinal Manifestations Lead pipe – chronic UC UC - treatment Inducing remission Mild = 5-ASA (mesalamine, sulfasalazine) Moderate = Steroid taper Severe = IV steroids, Cyclosporine, colectomy, TNF alpha antagonists (i.e. Remicade or Humira) Maintenance 5-ASA Azathioprine/6-MP TNF alpha antagonists Crohn’s Disease Chronic recurring transmural inflammation associated with fibrosis and sinus tracts that penetrate serosa giving rise to microperforations and fistulae presenting as skip lesions in any area of the GI tract Mucosal Stricturing Penetrating Based upon location 50% ileocolitis, 30% ileitis, 5% Gastroduodenal Crohn’s complications 74% require surgery Right lower quadrant pain Diarrhea Weight loss/Anorexia Small Bowel Obstruction Fistulas Perirectal Abscess/Intraabdominal abscesses Osteoporosis Extraintestinal Manifestations Enterocolonic fistula and string sign Crohn’s - Treatment Induction of Remission ?5-ASA = target to area of disease Ciprofloxacin / Flagyl Steroids (Prednisone or Budesonide) TNF alpha antagonists Maintenance 5-ASA 6-MP/Azathioprine/MTX TNF alpha antagonists Extraintestinal Manifestations Arthropathy (20%) Large joint – follows disease activity Small joint – independent of disease Ankylosing Spondylitis (10%) Erythema Nodosum (10%) Not associated with disease activity Associated with disease Pyoderma Gangrenosum (10%) Not associated with disease activity Extraintestinal Manifestations Episcleritis / Uveitis – 5% Nephrolithiasis Primary Sclerosing Cholangitis Calcium oxalate stones with ileal Crohn's 5% of UC, 75% of PSC have UC 25% cancer at 10 years after PSC diagnosis Colon Cancer 1% per year after 15 years Start surveillance at 8-10 year after diagnosis in pancolitis and after 15 years in left sided colitis IBD = Indication for surgery UC Toxic megacolon/Perforation Failure to control symptoms Dysplasia on surveillance Crohn’s Strictures with obstruction Complicated fistula Unresponsive inflammatory mass Dermatologic and GI Associations Dermatitis Herpetiformis Chronic, symmetric, intensely pruritic eruption including vesicles, papules and urticarial wheals Celiac Disease Acanthosis Nigricans Diffuse, velvety thickening and hyperpigmentation of skin in axilla and other body folds Gastric Cancer Tricholemmomas Cowden’s Syndrome Cowden’s syndrome more associated with thyroid and breast cancer as well as GI hamartomas Necrolytic Migratory Erythema Superficial migratory necrolytic erythema with central blisters or erosions that crust and heal with hyperpigmentation, a beefy red tongue, and angular cheilitis Glucagonoma Peutz Jeghers Syndrome Intussusceptions and Malignancies Pancreatic Neuroendocrine tumors Neurofibromatosis-1 Tuberous Sclerosis MEN1, And… Von Hippel-Lindau Hemagioblastomas and retinal angiomas Clear cell RCC Pheochromocytoma Endolymphatic sac tumors of middle ear Pancreatic serous cystadenoma or neuroendocrine tumors Papillary cystadenomas of epididymis and broad ligament Questions? 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