Tuesday, November 28 (ellen)

Oral Cavity and GIT Pathology – November 28, 2006 Ulcerative and Inflammatory Lesions A) Aphthous Ulcers (Canker Sores) ~ filled with exudates ~ erythematous rim ~ triggered by stress, fever, ingestion of certain foods, activation of IBS B) Herpes Virus Infection (Stomatitis) ~ extremely common ~ multiple vesicles in mouth and pharynx ~ d/t HSV 1 (upstairs), HSV 2 (usually downstairs) ~ on lips or nasal orifices ~ can stay dormant in ganglia and can reactivate ~ aggravated by L-arginine; ameliorated by L-lysine ~ worst case – go into brain  encephalitis or visceral lesions on organs ~ can also lead to keratoconjunctivitis ~ can affect esophagus if nasogastric tub touches infected oral cavity C) Fungal Infection ~ candida albicans (part of normal flora) ~ oral thrush – white, curdlike, plaque in oral cavity ~ fungus usually loosely attach using pseudomembrane ~ if severe can affect all layers of the mucosa ~ can detach and spread ~ disseminated candidiasis is life threatening D) AIDS ~ AIDS/HIV often associated with candidiasis, Kaposi’s sarcoma, leukoplakia (white patches that are hairy; can also be caused by EBV) Leukoplakia ~ white plaque because of hyperkeratosis ~ see on border of lower lip, buccal mucosa, hard/soft palate ~ leather, white, discrete area ~ causes: tobacco, chronic friction, alcohol abuse CA of Oral Cavity and Tongue ~ mainly squamous cell carcinoma ~ usually later in life, rare before 40 yoa Salivary Gland Diseases A) Sialadenitis ~ mainly autoimmune

~ inflammation of salivary glands ~ m/c parotid glands – mumps (RNA paramyxovirus) ~ see local edema, with macrophages, eventually leading to necrosis ~ childhood mumps self-limited ~ adult mumps – pancreatitis/orchitis (testes) ~ bacterial sialadenitis: secondary to stone formation (sialolithiasis) ~retrograde entry from oral cavity ~ may see interstitial / focal necrosis / abscess ~ if chronic  decrease saliva production ~ m/c autoimmune – Sjogren syndrome [dry eyes = keratoconjunctivitis, dry mouth = xerostomia, with autommune disease (m/c RA)] B) Salivary Gland Tumours ~ usually in parotid glands, then submandibular ~ neoplasm in submaxillary glands present more of a problem than parotid ~ m/c benign pleomorphic adenoma (mixed tumour of salivary gland origin) ~ slow growing, well demarcated, encapsulated, painless, discrete mass ~ at angle of jaw ~ less common Warthin tumour (papillary cystadenoma lymphomatosum) ~ usually parotid gland ~ small, well encapsulated, round/ovoid mass ~ both malignancy rare Esophagus ~ all ss/sxs will involve dysphagia (hard to swallow) and heartburn ~ less common: hematemesis and melena (blood in stool)  these mean severe inflammation or lesion A) Hiatal Hernia ~ separated diaphragmatic crura leading to a bigger space between the muscular crura and esophagus wall ~ the dilated segment of ST protrudes above diaphragm ~ 2 patterns: ~ 1) sliding hernia (axial) – bell shape dilation ~ protrution of ST above diaphragm ~ 2) paraesophageal (axial) – separate portion protrudes, m/c greater curvature B) Achalasia ~ lower esophageal sphincter does not relax when swallowing ~ get obstruction then consequent dilation of proximal esophagus ~ 3 major abnormalities ~ 1) aperistalsis ~ 2) can’t relax lower esophageal sphincter ~ 3) increase resting tone of esophageal sphincter ~ primary achalasia – can’t inhibit contraction of sphincter (therefore can’t relax) ~ innervation problem

~ secondary achalasia – pathological ~ ex: Chagas disease – destroy myenteric plexus of esophagus, duodenum, colon, ureter ~ progressive dysphagia and can’t get food to ST ~ can progress to esophageal squamous cell carcinoma C) Lacerations (Mallory-Weiss Syndrome) ~ b/w esophagus and ST = esophagogastric junction ~ chronic alcoholics – from retching and vomiting ~ don’t relax lower esophageal sphincter when vomiting  tears esophagus-ST junction ~ can get infection  ulcer mediastinitis D) Varices ~ dilated esophageal plexus veins ~ intra-abdominal splanchnic circulation and systemic venous circulation communication through esophagus ~ if portal venous blood flow blocked, leads to portal HTN, which forces the use of collateral bypass ~ portal blood flow now through coronary veins of ST to plexus of esophageal subepithelial and submucosal veins to azygos vein then SVC ~ when it passes through esophageal subepithelial veins, it causes abnormal dilation of these veins  varices ~ if rupture can produce massive hemorrhage E) Esophagitis ~ usually reflux of gastric contents ~ contributory factors: ~ 1) can’t clear reflux material ~ 2) poor esophageal clearance of reflux ~ 3) sliding hiatal hernia ~ 4) increase gastric volume ~ 5) can’t repair damaged esophageal mucosa F) Barrett Esophagus ~ long-term gastroesophageal reflux ~ replacement of distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells (b/c columnar epithelial more resistant to acid which is from the decreased pH in reflux) G) Esophageal Carcinoma ~ 2 main types ~ 1) squamous cell carcinoma – more in black people) ~ 2) adenocarcinomas – more white if from Barrett esophagus ~ increased risk if increase exposure of food through esophagus and increase mucosal exposure to carcinogens ~ strong association with HPV

~ Barrett esophagus is only recognized precursor of esophageal adenocarcinoma Stomach ~ ss/sxs mainly heartburn and vague epigastric pain ~ hematemesis or melena ~ if hematemesis blood turns brown because of acid A) Congenital Gastric Anomalie ~ 1) pyloric stenosis – hypertrophy of smooth muscle wall ~ 2) diaphragmatic hernia – hernia of ST and abdominal contents into thorax ~ 3) gastric hetertopia – gastric mucosa in esophagus and SI B) Chronic Gastritis ~ inflammation of gastric mucosa ~ majority of cases, it’s chronic gastritis, but can be acute ~ chronic mucosal inflammation – changes leading to atrophy and epithelial metoplasia (changes to different cell type) ~ usually asymptomatic ~ m/c Helicobacter pylori ~ bacterial enzymes and toxins cause inflammation ~ can have autoimmune gastritis (m/c in Scandinavia) ~ autoAb to parietal cells leading to gland destruction and mucosal atrophy C) Acute Gastritis ~ acute mucosal inflammatory process, usually transient ~ erosion of epithelium ~ disrupts mucous layer, increases acid, decrease HCO3, decrease mucosal blood glow ~ leads to H, pylori induced infection D) Peptic Ulceration ~ ulcers extend through muscularis mucosae and submucosa ~ erosion – epithelial only ~ peptic – usually duodenum and ST ~ affects Chief cells which secrete pepsinogen ~ expose GI tract to acid-peptic juices ~ causes relapsing lesions ~ duodenal ulcers are m/c with alcoholic cirrhosis, COPD, renal failure, hyperparathyroidism ~ increased Ca in blood stimulates gastrin, and therefore acid secretion ~ 2 key factors in pathogenesis ~ 1) expose mucosal layers to gastric acid and pepsin ~ 2) H, pylori infection ~ H. pylori causes immune response (pro-inflammatory cytokines, especially IL-8 which activates neutrophils) ~ also increase gastric acid = gastric metaplasia ~ also decrease HCO3

~ bacterial protease and phospholipase breaks glycoprotein lipid complexes and therefore breaks down first line mucosal defense ~ NSAIDs major cause without H. pylori ~ inhibit prostaglandin I and II synthesis  increase H and decrease HCO3 and decrease mucin  allows acid to reach epithelium ~ also decreased glutathione synthesis ~ Zollinger-Ellison syndrome – associated multiple peptic ulcerations d/t excess gastrin secondary to tumour E) Acute Gastric Ulceration ~ stress ulcers! ~ m/c seen: ~ 1) trauma ~ 2) excess burns ~ 3) surgery / injury to CNS ~ 4) chronic exposure to gastric irritant drugs (corticosteroids and NSAIDs) Gastric Tumours A) Gastric Polyps ~ project above level of surrounding mucosa ~ mainly in colon ~ if in ST, m/c ~ 1) hyperplastic ~ 2) fundic gland ~ 3) adenamatous – dangerous, can lead adnenocarcinoma B) Gastric Carcinoma ~ 2 morphological types: ~ 1) intestinal – intestinal cells going into gastric mucosa ~ 2) diffuse – new gastric cells, poorly differentiated (increase risk of CA) ~ metastasis – penetrate wall to involve serosa, spread to regional and distant lymph nodes ~ earliest metastasis often to Virchow’s nodes – supraclavicular node ~ Krukenberg tumour – both ovaries thorough intraperitoneal spread