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Path GI – Liver – Biliary – Exocrine Pancreas

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Path GI – Liver – Biliary – Exocrine Pancreas CONGENITAL DISEASES OF THE ESOPHAGUS Tracheoesophageal Fistula ‐ Esophagus has both atresia (blind pouch) and fistula (connection to something else) Atresia ‐ Patients have the trachea and esophagus connected o Patients “swallow” food into their lungs = aspiration pneumonia Fistula o Coughing and Cyanosis during feeding o Amniotic fluid cannot be swallowed, causes polyhydramnios ‐ Must be surgically corrected, which is easily done. Most common presentation of o Most common = atresia of upper esophagus and fistula of lower esophagus to trachea atresia/fistula Esophageal Webs ‐ Web‐like projections of esophageal mucosa into the lumen ‐ Food gets stuck in webs, presenting with dysphagia and bad breath ‐ Associated with o Plummer‐Vinson Syndrome = webs, iron deficiency anemia, women, ↑ Risk for sqaumous cell carcinoma o Schacktzi Ring = webs down at the esophageal‐gastric junction Achalasia Esophagus o Inability to relax the Lower Esophageal Sphincter (LES) o Presents with dysphagia or megaesophagus (can’t get food into stomach) Bird’s Beak o Diagnosed with barium swallow revealing “bird’s beak” esophagus Stomach o Caused by death of ganglion cells in the LES o Treated with stenting or surgical resection Pylorus HEMATEMESIS AND BLEEDS Mallory‐Weiss Tear Stomach Lesion Esophagus o Associated with retching or prolonged vomiting = bulimics and alcoholics o Are longitudinal tears, usually at the gastro‐esophageal junction o May cause hematemesis, but bleeding usually spontaneously heals o Lesions may completely heal over time, if retching is discontinued Esophageal Varices o Patients with liver failure develop porto‐caval shunts (Left Gastric Vein Æ Esophageal) o One shunt = esophageal veins giving rise to distending, tortuous veins in esophagus o Varices are prone to rupture producing massive hematemesis and melena o Surgical emergency; these will not spontaneously stop on their own Can do a balloon tamponade to temporarily stop the bleeding Endoscopy with1 |protruding Owl distendedClub veinsReview (arrows) Sheets Path GI – Liver – Biliary – Exocrine Pancreas ESOPHAGITS (Big Robbins 803, Baby Robbins 412) Esophagitis = inflammation of the esophageal mucosa. It has many causes, but here we cover the most common three: Reflux, Barrett’s, and Infectious/Chemical Reflux Esophagitis, aka GERD, aka “Heartburn” ‐ Definition o Reflux or regurgitation of gastric contents through the LES causing caustic damage to the lower esophagus ‐ Causes o ↓ LES Tone allowing gastric contents to come back out the in hole CNS depressants, Pregnancy, Obesity, Alcohol, and Tobacco all ↑ incidence o Presence of a sliding hiatal hernia with subsequent dilation of LES o Inadequate or slowing of gastric emptying with increased volume of stomach Elongation of dermal Action of gastric juices is critical to the development of mucosal injury papillae and basal zone o hyperplasia ‐ Morphology o Dependent on severity and exposure time (two weeks versus seven years) o Simple Hyperemia (“redness”) may be the only indicator o Inflammatory Infiltrate = PMNs, Lymphocytes, and/or Eosinophils Red streaks are hyperemia. o Basal Zone Hyperplasia > 20% of epithelial thickness Endoscopic image. o Elongation of Lamina Propria Papillae ‐ Clinical o Common with increased age (>40) though possible in children through adulthood Minor Eosinophilia in the Esophagus is almost o Severity of symptoms ≠ severity of disease (lots of burning without lots of changes) pathognomonic for Reflux. o Most common complaint is “heartburn,” diffuse burning in the center of the chest LOTS of eosinophils means o If not treated, the burning will stop as metaplastic changes create Barrett’s Esophagus Eosinophilic Esophagitis Barrett Esophagus – this, or cancer, will undoubtedly be on your Tulane exam, Shelf, and on Step 1 ‐ Definition o Long‐term GERD results in a ‘protective’ replacement of distal esophageal sqaumous epithelium by a metaplastic columnar, glandular epithelium resembling the duodenum ‐ Pathogenesis o Long‐standing acidic pH in the lower esophagus induces metaplastic differentiation of pluripotent stem cells into columnar type epithelium with goblet cells o A protective precancerous change to defend against acidic pH ‐ Morphology o Gross = circumferential, red, velvety mucosa at the gastroesophageal junction o Micro = columnar epithelium with glandular differentiation and goblet cells = Dysplasia is not required for diagnosis but is critical for prognosis ‐ Clinical o GERD lasts 20 years before Barrett’s sets in Salmon Velvet appearance o Patient goes from severe heartburn to no pain spontaneously (progressive or acute) on endoscopy o This is precancerous with 30‐40 TIMES risk for adenocarcinoma o Treatment with PPIs can potentially reverse both dysplasia and metaplasia Columnar Epithelium2 | Owl Club Review Sheets with goblet cells = Barrett’s Path GI – Liver – Biliary – Exocrine Pancreas Infectious and Chemical Esophagitis – the “others” ‐ Types o Ingestion of mucosal irritants = alcohol, corrosive acids/alkali (suicide), hot beverages o Infection of any kind such as fungus (candida), bacteria, or virus (Herpes, CMV) o Uremia from Renal Failure ‐ Morphology o Dependent on etiology, Baby Robbins basically says “don’t bother with specifics” o All share acute inflammation, superficial necrosis/ulceration, and eventual granulation/fibrosis Candida esophagitis. This is a fungus Herpes Esophagitis. In the showing pseudohyphae, stained immunocompromised individual, black against a green background. look for Cowdry Type A and Cowdry Candida normally lives in the mouth; Type B. There is typically nuclear you must have invasion to call it molding and inclusions showing candidiasis. Usually occurs in the perinuclear halos. immunocompromised. It is an AIDS defining disease. TUMORS (Big Robbins 806, Baby Robbins 413) Malignant Tumors – Sqaumous Cell Carcinoma ‐ Definition o Dysplastic carcinoma of the sqaumous cells of the esophagus ‐ Etiology and Pathogenesis o Obvious impact of various environmental factors combined with genetic predisposition o Chronic esophagitis, Alcohol, or Tobacco contribute to ↑ risk o Most common esophageal tumor worldwide GERD Æ Barrett’s ÆAdenocarcinoma equal to or more common in US SCC showing Keratin Pearls Morphology (arrow) amidst dysplastic mucosal epithelium o Similar development to other SCC, with characteristic benign transformation through carcinoma in situ, and presence of keratin pearls Lung Esophagus Tumor o Appear as gray‐white plaques or elevations (unnoticed except on endoscopy) o Location of tumor may help identify Sqaumous Cell Carcinoma can grow anywhere in the esophagus Adenocarcinoma can grow only in lower third If it is in proximal esophagus, then it must be SCC Clinical o Insidious onset with without early symptoms (early detection only with endoscopy) o Dysphagia is late, ominous sign, usually indicated by a change from solid to liquid foods o Early detection = positive prognosis with resection o Late detection = poor prognosis from tumor invasion Tumor growing on top of o Hemorrhage and Weight Loss (tumor steals nutrients and causes malnutrition from lungs, from the mid stenosis) are also possible. esophagus, means it must be SCC 3 | Owl Club Review Sheets Path GI – Liver – Biliary – Exocrine Pancreas Malignant Tumors – Adenocarcinoma ‐ Definition o True metaplasia of the esophagus to gastric mucosa with subsequent dysplasia; when Barrett’s turns to cancer ‐ Etiology and Prevention o Most common esophageal tumor in the US o Essentially this is caused by Barrett’s Esophagus High grade Dysplasia o Helicobacter may contribute, but the only way to get glandular tissue in the esophagus is metaplasia or local spread of gastric carcinoma ‐ Morphology o Located in the distal esophagus o They are flat, mucin producing glandular tissue resembling the duodenum/stomach o Degree of anaplasia varies even in locations adjacent to obvious lesions ‐ Clinical o Presents with dysphagia, hemorrhage, and ulceration, just like SCC o Prognosis is very poor once they reach this stage o They have an obvious clinical course Gross image of esophageal 10 years of “heartburn” without treatment for GERD adenocarcinoma. Normal 2‐5 years of Barrett’s without treatment for GERD mucosa (blue), gastgric mucosa (red), 1‐5 years of adenocarcinoma leading to their death adenocarcinoma (yellow) o Proton Pump Inhibitor Therapy prior to adenocarcinoma formation is curative and reversed metaplasia/dysplasia back to esophageal mucosa Initial symptoms of GERD where The burn begins to spontaneously Metaplasia has given way to dysplasia. You’ve got cancer. heartburn is controlled by PRN antiacids, disappear over the course of years. You Cancerous growth shows no signs or symptoms until you cant followed by OTC drugs. The burn means “feel better” but your esophageal eat (dysphagia) or a fistula is made to your lungs (aspiration your esophagus is normal pneumonia). You die within 5 years (20% 5 year survival) 5‐10 epithelium has undergone metaplasia years 2‐5 years 1‐5 years Heartburn, Acid Reflux, GERD Barrett’s Esophagus Adenocarcinoma Death Proton Pump Inhibitors are Proton Pump Inhibitors are curative. You are screwed. At this point its too preventative of disease. Get an They reverse the metaplasia and late, as these are nasty invaders and endoscopy to track changes hold off dysplasia. Get endoscopy for have a very poor prognosis, even diagnosis and to track changes with resection Progression of GERD to Carcinoma 4 | Owl Club Review
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