Upper GI Pathology PDF

M. Vincent Mesa, DO Upper GI Topics Congenital Defects Achalasia Non-inflammatory esophageal conditions Esophageal Inflammatory conditions Barrett’s Esophagus Gastric Inflammatory conditions Neoplastic conditions Congenital Abnormalities of UGI Tracheoesophageal Fistulae Defect resulting in connection between the esophagus and trachea Congenital Pyloric stenosis Hypertrophy of the pyloric smooth muscle Diaphragmatic hernia Development defect of the diaphram allowing abdominal contents into thoracic cavity Ectopia Normal tissue found in abnormal locations ○ Gastric mucosa most common, upper third esoph Tracheoesophageal Fistulae Non-inflammatory Disorders of Esophagus Achalasia Esophageal Webs/Rings (Ledges) Zenker’s Diverticulum (Outpouching) Lacerations (Mallory-Weiss, Boerhaave Syndrome) Esophageal Varices (Portal HTN) ACHALASIA Lack of progressive peristalsis and partial/incomplete relaxation of lower esophageal sphincter (LES) Usually young adults. Primary: Idiopathic, but may be due to T cell mediated destruction or complete absence of myenteric ganglion cells; Secondary causes (egs: Chagas dz, amyloidosis, sarcoidosis, diabetic neuropathy) Symptoms: dysphagia, difficulty belching, CP Increased risk for: aspiration, Barrett’s, candida infection, squamous cell carcinoma Achalasia (Bird-beak sign) Esophageal Webs/Rings Webs are semi-circumferential protrusions of mucosa Episodic dysphagia Mostly in upper esophagus in women over 40 Associated with, bolting, GERD, rad. Tx., chronic GVHD, blistering skin diseases, and may be part of Plummer-Vinson syndrome (Iron def. anemia, dysphasia [classic triad]) Esophageal Rings (Schatzki rings) Similar to webs, but fully circumferential and thicker (long-term damage due to reflux?) Schatzki Ring Zenker’s Diverticulum Acquired outpouching of muscular wall superior to the UES (false diverticulum) Due to impaired relaxation of the cricopharyngeal sphincter (jct. of the esophagus and pharynx). Uncommon, >50yrs old Smaller lesions may be asymptomatic Larger lesions may cause food accumulation, regurgitation, cough, and halitosis Lacerations Mallory-Weiss Syndrome Longitudinal tears (intramural) at the GE junction Usually due to severe retching associated with alcoholism (50-70%) 5-10% of upper GI bleeds Presents with painful hematemesis No surgery necessary Boerhaave Syndrome Transmural tear and rupture of esophagus Severe mediastinitis, subcutaneous emphysema Surgical emergency ESOPHAGITIS Chemical Accidental ingestion/attempted suicide ETOH, hot fluids, tobacco, pills Iatrogenic Radiation tx., chemotherapy, GVHD Desqaumative skin disease Bullous pemphigoid, Crohn’s disease Infections Herpes simplex, CMV, Fungal ESOPHAGITIS Gastroesphageal Reflux Disease (GERD) Eosinophilic Esophagitis Lymphocytic Esophagitis Gastroesophageal Reflux Disease (aka: GERD, reflux esophagitis) Most common cause of esophagitis Most common OP GI diagnosis in U.S. Reflux of gastric/duodenal contents into LE Decreased tone of LES, most common Risk factors: ETOH, tobacco, preg., caffeine, obesity, hiatal hernia, CNS depressants, high gastric volume, sclerosing diseases GERD: Clinical Features Most common >40yrs age Infants and children less frequent Symptoms Most common: heartburn, dysphasia, regurgitation Less common: enamel damage, cough, chest pain Commonly improve with PPI’s Tx. Complications erosions/ulcers, stricture, melena, hematemesis, and Barrett’s esophagus GERD: Histologic Features No consensus on minimum criteria Commonly identified histologic changes Intraepithelial eosinophils Basal cell hyperplasia Papillomatosis Vascular ectasia May show erosion/ulceration GERD: Histologic Features EOSINOPHILIC ESOPHAGITIS An allergic inflammatory condition Incidence of EoE is increasing- like atopic dz. More common in children/young adults Symptoms: dysphagia,odynophagia feeding intolerance, failure to thrive, GERD-like, food impaction Tx: Dietary restriction, corticosteroids, dilatation PPIs do not relieve symptoms! Eosinophilic Esophagitis EOSINOPHILIC ESOPHAGITIS LYMPHOCYTIC ESOPHAGITIS A subset of chronic esophagitis Etiology unknown No definitive association with other conditions (Crohn’s?) Often young age, but also older adults (women) Symptoms and endo findings similar to EoE Treatment: +/- PPIs, topical steroids, dilation Long term outcomes uncertain Intraepithelial lymphocytes, peripapillary distribution, spongiosis, no granulocytes LYMPHOCYTIC ESOPHAGITIS Barrett’s Esophagus (Disease) Intestinal metaplasia of the distal esophageal mucosa Usually due to chronic GERD (1-3% bx’d). Most common in males, 40-60yrs old Risk of epithelial dysplasia up to 2%/yr Low grade dysplasia High grade dysplasia Risk of progressing to adenocarcinoma, rare Barrett’s Esophagus (Disease) Endoscopically Barrett’s Esophagus (Disease) Histopathologically Barrett’s metaplasia with dysplasia TUMORS BENIGN MALIGNANT –Squamous cell carcinoma –Adenocarcinoma BENIGN TUMORS Squamous Papillomas FIBROMAS HEMANGIOMAS LIPOMAS NEUROFIBROMAS LYMPHANGIOMAS Leiomyomas SQUAMOUS CARCINOMA ALCOHOL TOBACCO POVERTY - DIET CAUSTIC ESOPHAGEAL INJURY ACHALASIA HOT BEVERAGES HPV INFECTION SQUAMOUS CARCINOMA DYSPLASIAàIN-SITUàINFILTRATION ADENOCARCINOMA Most common esoph. CA in the West BARRETT’s ***** (heterotopic gastric or submucosal glands) Lower third/distal esoph. ADENOCARCINOMA STOMACH NORMAL: Histo, Physio. PATHOLOGY CONGENITAL GASTRITIS PEPTIC ULCER TUMORS BENIGN ADENOCARCINOMA OTHERS Anatomy, Upper GI Histology, Upper GI CELLS MUCOUS: MUCOUS, PEPSINOGEN II CHIEF: PEPSINOGEN I, II PARIETAL: ACID, INTRINSIC FACTOR ENTEROENDOCRINE: HISTAMINE, SOMATOSTATIN, ENDOTHELIN ACID PROTECTION MUCOUS HCO3- EPITHELIAL BARRIERS BLOOD FLOW PROSTAGLANDIN E, I CONGENITAL ECTOPIC Gastric/Pancreas ( panc. tissue à stomach; gast. Tissue àesoph), very common Diaphragmatic HERNIAà Failure of diaphragm to close, not rare OMPHALOCELE GASTROSCHISIS PYLORIC STENOSIS PYLORIC STENOSIS CONGENITAL: (1/500), Neonatal obstruction symptoms, pyloric splitting curative ACQUIRED: Secondary to extensive scarring such as advanced peptic ulcer disease Congenital Pyloric stenosis Acute Gastritis/Gastropathy Acute inflammation in gastric mucosa “Reactive Gastropathy” (cell poor rxn) Mucosal damage from acid back diffusion Symptoms: May be asymptomatic, nausea/vomiting NSAID-related epigastric pain relieved with AAs or PPI 20% develop overt bleeding, fatal in up to 5% Reactive (chemical) Gastropathy Acute Gastritis/Gastropathy Risk Factors NSAIDs Ingestion of harsh chemical Uremia Portal HTN Radiation/Chemotherapy Age High altitudes Bile reflux Acute Gastritis/Gastropathy Stress-Related Risk Factors Stress Ulcers critically ill patients Shock Sepsis Severe trauma Curling Ulcers Severe burn patients; hypovolemia Tend to be multifocal ulcerations Cushing Ulcers Increased ICP; vagal nerve stimulation Chronic Gastritis Two major causes Chronic Autoimmune Gastritis Chronic H. pylori-associated gastritis Less common causes Radiation injury Bile reflux Mechanical injury Systemic diseases (Crohn’s, amyloidosis, GVHD) Autoimmune Gastritis Destructive mucosal lymphocytic inflammation Common cause for diffuse atrophic gastritis Represents 90%) Gross and Histologic subclassification Intestinal-Type ○ Bulky tumors composed of glandular structures ○ Mean age 55yrs, 2/3 males ○ Risk Factors: H. pylori, autoimmune gastritis, nitrosamines, cigarette smoking Diffuse-Type ○ Signet ring cells diffusely infiltrate gastric wall, desmoplasia results in thickened wall (linitis plastica) ○ Mean age 48yrs, M=F ○ Not associated with H. pylori, intestinal metaplasia or nitrosamines Intestinal-Type Adenocarcinoma Diffuse-Type Adenocarcinoma Diffuse-Type Adenocarcinoma aka: SIGNET RING CELL CARCINOMA

Upper GI Pathology PDF

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