Stomach Pathology 2024 Revised STU PDF

PATHOLOGY OF STOMACH  Objectives- Pathology of Stomach Review normal anatomy and physiology of the stomach Describe common congenital anomalies of Stomach Compare the etiology and pathogenesis, pathology, clinical manifestations and complications of acute and chronic gastritis and pept...

PATHOLOGY OF STOMACH  Objectives- Pathology of Stomach Review normal anatomy and physiology of the stomach Describe common congenital anomalies of Stomach Compare the etiology and pathogenesis, pathology, clinical manifestations and complications of acute and chronic gastritis and peptic ulcer disease Describe the pathology of benign and malignant tumors of the stomach SELF STUDY: Disorders of Esophagus: Dysphagia; GERD and complications  STOMACH Mucosal Protection Mucus – Barrier Bicarbonate secretion – Neutralizes the acid Epithelial cell – Resist back diffusion of H+Ions Regeneration/repair Mucosal blood flow – O2, Bicarb, Nutrients, Remove H+ ions PG secretion – Blood flow, Bicarb synthesis, Mucus Neural / Muscular components- Vasodilatation limit injury  Congenital and Developmental Abnormalities Stomach Small Intestine (Foregut) (Mid gut) Congenital absence Non rotation, malrotation Dextroposition Reverse rotation Microgastria Cysts, duplication Cysts, duplication Diverticula Diverticula – Meckel’s Atresia, Atresia, Cong. Pyloric Stenosis Stenosis, volvulus, ileus Hamartoma, neoplasms Hamartoma, Hirchsprung’s, neoplasms CONG.PYLORIC STENOSIS 3-4x –M (first born) Genetic, 5x Siblings Turner/trisomy 18 2-3 wk of life Hypertrophic Circular Muscle Persistent projectile non-bilious vomiting “Hungry Vomiter” Peristaltic epigastric mass  Gastritis inflammation associated with mucosal injury Gastritis is usually due to infectious agents (such as Helicobacter pylori) and autoimmune and hypersensitivity reactions. Epithelial cell damage and regeneration without associated inflammation is referred to as "gastropathy Gastritis: Acute OR Chronic  Gastritis Acute refers to short term inflammation; neutrophilic infiltrate Chronic referring to longer duration + mononuclear cell infiltrate especially lymphocyte and macrophages. Acute Gastritis: usually transient. There may be hemorrhage into the mucosa or sloughing of the mucosa. Severe erosive form is an important cause of severe GI bleeding  Acute Gastritis Frequently associated with: heavy use of NSAIDS, especially aspirin, excessive alcohol consumption, heavy smoking, severe stress e.g. trauma, burns, surgery, Ischemia Systemic infection, Often, idiopathic. Stages of Acute Gastritis: Acute superficial, Acute erosive gastritis, Acute Gastric Ulceration  Acute Gastritis Morphology: ranges from edema with neutrophil infiltration, vascular congestion & an intact epithelium, to erosion (mucosal defect that does not cross the muscularis mucosa) and hemorrhage. C/F: broad range of signs and symptoms that depend on the severity of the condition; Asymptomatic, Epigastric pain, nausea & vomiting.  Hemorrhage, massive hematemesis, melena, or fatal blood loss; One of the major causes of massive hematemesis, particularly in alcoholics. ~25% patients taking aspirin for rheumatoid arthritis will develop acute gastritis, and some will bleed.  Chronic Gastritis Chronic mucosal inflammatory changes leading to atrophy and metaplasia (usually without erosions), Dysplasia and ultimate neoplasia are complications. Type A Autoimmune Gastritis pernicious anemia, Chronic atrophic gastritis is associated with Ab’s - intrinsic factor - patietal cell; Morphology: Diffuse mucosal damage of the body and fundic mucosa. Antrum less involved.  Type B (Antral Gastritis): 90% of patients with antral chronic gastritis: Helicobacter pylori infected, Motile, gram negative curvilinear rods --urease (buffers gastric acid) & toxins and have adhesins to bind to the epithelium. 2 patterns of infection: Diffuse involvement of body and antrum (pan gastritis‖ associated with diminishing acid output)& Infection confined to antrum (antral gastritis, associated with increased acid output)  Chronic Gastritis H. pylori affect antral mucosa Histology: Lymphocytic & plasma cell infiltrate of the lamina propria, atrophy, regeneration, metaplasia (to intestinal type mucosa) & dysplasia. H. pylori detected on the mucosal surface. Dysplasia– precursor lesion to gastric cancer in atrophic gastritis. Others: psychologic stress, caffeine, alcohol, tobacco, radiation, bile reflux, Crohn’s, GVH  Case study Mr.Big, a 48 year-old man presented with h/o of episodes of severe epigastric pain and on and off indigestion. His bowel habits were normal. He drinks 2-3 beers daily and is a smoker. He loves to eat smoked meat and pickles. O/E: mild pallor, Vital signs-normal, anicteric. CVS & RS are normal. Abd. Examination revealed epigastric tenderness. He also complained of passing tarry stools (Black).  Peptic Ulcers Occurs where mucosa is exposed to acid – pepsin Chronic, usually single, < 4 CMS in diameter Common sites: Duodenum I part – Stomach –Antrum – Barrett’s Mucosa – Gastro-jejunostomy – Jejunum Meckel’s Diverticulum  Epidemiology Prevalence: Remitting and Relapsing Nature- Morbidity, Loss of work Hrs, Costly DU: 22- 55 Y, M GU: 40 – 70, F/M  Aetio- Pathogenesis Imbalance: Acid pepsin & Mucosal Integrity 1. ↑ Acid- pepsin activity – DU 2. Impaired Mucosal defense – GU 3. H.Pylori infection – Duodenitis/ Gastritis 4. Other influences  Morphology: Gross: A) DU – I part, Anterior wall, Kissing ulcers B) GU - Lesser curvature, body & antral Size: < 2cms in dia, round – oval, punched out, straight walls & variable depth. Base of Ulcer: Smooth, clean, adherence to liver/ pancreas +/-. Scarring & puckering – Spoke like folds  Micro: Active ulcers – 4 Zones I – Necrosis and fibrin II – Non- specific Inflmmn III – Granulation tissue IV – Fibrous/Scar tissue Adjacent mucosa shows Gastritis, H.pylori+/_  Investigations: Barium meal, Blood counts, HP testing, GFT, Endoscopy Complications: 1. Perforation,2. Bleeding 3. Stenosis- pyloric, Tea-pot deformity, Hour glass stomach 4. Penetration 5. Carcinoma? 6. Intractable pain  Case study-Contd A few weeks later Mr.Big underwent endoscopy, which revealed a bleeding ulcerative lesion. Upon re-evaluation, he had an enlarged L.Supraclavicular node.  Carcinoma of the Stomach Most common type of malignant tumor- Adenocarcinoma Incidence: 5-7 decade, 2M: 1F, Low SE groups, Asian/S. American Countries Etiology: 1. Genetic: Familial, BG ‘A’, Mutations CDH1 2. ENV. Factors: Dietary factors 3. Premalignant conditions Like Chr. Gastritis (Correa’s cascade),GU, Polyps, etc Morphology: Site: I. A) Pylorus and antrum B) Cardia C) Body and Fundus Can affect: A) Lesser curvature B) Greater curvature  Early gastric cancer Involves Mucosa and Submucosa, LN +/- Type I – Protruding TypeII – Superficial Type III – Excavated  Advanced gastric cancer I. Cauliflower like growth II. Ulcerative III. Scirrhous- Localized, Diffuse (LINITIS PLASTICA) Micro: Lauren Classification: - Intestinal Adenocarcinoma (ENV), - Signet ring cell Adeno Ca (Genetic)  Clinical Features: Anorexia, Fullness, Wt.Loss, Anemia, dysphagia, vomiting, epigastric distress, pain and mass Virchow’s node, Sis Mary Jo nodule Investigations: Barium meal, Blood counts, HP testing, Endoscopy/bx, CT/PET; CEA, CA 19-9 Spread of Ca. Stomach: Direct, Lymphatic, Haematogenous & Transcoelomic – E.g.: Krukenberg’s Tumor  Prognosis- Staging EGC: 85 – 95% cure AGC: < 15% - 5 yr. survival Others: Polyps; Lymphoma, Carcinoid, GIST-fleshy, protruding mesenchymal tumor, c-KIT marker, spindle/epithelioid type