Gastrointestinal Pathology Slides by Dr. Doaa Alqaidy PDF

Gastrointestinal Pathology Dr. Doaa Alqaidy Assistant professor, ABPath AP/CP Consultant oncologic surgical pathologist and Hematopathologist  Esophagus ’ Esophagitis ’ Barrett Esophagus ’ Esophageal Carcinoma Normal Esoph...

Gastrointestinal Pathology Dr. Doaa Alqaidy Assistant professor, ABPath AP/CP Consultant oncologic surgical pathologist and Hematopathologist  Esophagus ’ Esophagitis ’ Barrett Esophagus ’ Esophageal Carcinoma Normal Esophagus - Gross Normal Esophagus - Histology b must must  Reflux Esophagitis Is the most common cause of esophagitis: Due to reflux of gastric acid through a relaxed lower esophageal sphincter into the lower esophagus It commonly accompanies hiatus hernia  1 Reflux Esophagitis ’ Reflux of acid  inflammation & reactive changes in epithelium:  Expansion of basal layer  Elongation of papillae  Eosinophils Acute esophagitis is manifested here by increased neutrophils in the submucosa as well as neutrophils Expansion of Basal Layer infiltrating into the squamous mucosa at the right. Elongation of Papillae Eosinophils  Reflux Esophagitis Clinical Features:  Dysphagia (difficulty in swallowing) & heartburn Complications: 1. Bleeding 4318,85 2. Ulceration  healing by scarring  stricture 3. Barrett’s esophagus  2 Barrett’s Esophagus Definition: aN  The squamous mucosa of the distal esophagus is replaced by metaplastic columnar epithelium  It is a complication of long-standing reflux esophagitis = response to prolonged injury Barrett’s esophagus appears as a red, velvety mucosa above GEJ  Barrett’s Esophagus Complications:  Bleeding  Ulceration  stricture  Is a premalignant lesion  ↑ risk of esophageal ol adenocarcinoma (30 to 40-fold increased risk over the general population) Metaplasia  Dysplasia  Adenocarcinoma Endoscopy & biopsy  Esophageal Carcinoma  Two major types: Squamous cell carcinoma (SCC) & adenocarcinoma ATS  In USA incidence of adenocarcinoma 2ry to Barrett esophagus is > SCC 0am  But Worldwide, SCC constitutes 90% of esophageal cancers  Squamous Cell Carcinoma Adults > 50 years M:F = 2-20:1 male female  Squamous Cell Carcinoma Risk Factors  Esophageal disorders: e.g. Long standing esophagitis  Dietary factors:  Fungal contamination of foodstuffs  High content of nitrosamine/nitrites “China”  Vitamin deficiencies “A & C, pyridoxine, riboflavin”  Deficiency of trace metals “Zinc”  Squamous Cell Carcinoma Risk Factors Life-style:  Smoking “tobacco”  Alcohol consumption Genetic predisposition  Squamous Cell Carcinoma Site: 20% in the upper third 50% in the middle third 30% in the lower third of the esophagus  Patients present clinically with progressive dysphagia & later in the course by obstruction  Patients usually present late with advanced disease  Prognosis is poor  Stomach ’ Gastritis ’ Gastric Ulceration ’ Gastric Carcinoma Stomach - Anatomy I Stomach - Anatomy Gastritis – Definition & Types Is inflammation of the gastric mucosa Types: Acute gastritis Chronic gastritis “most common”  Acute Gastritis Itis an acute inflammation with neutrophil infiltration of gastric mucosa Is Usually of a transient nature Clinical Features: a May be asymptomatic vomitblood May cause epigastric pain, nausea, vomiting, hematemesis, melena “black stool” & potentially fatal blood loss F  Acute Gastritis – Causes  Heavy use of NSAIDs, especially aspirin  Excessive alcohol consumption  Heavy smoking  Treatment with cancer chemotherapeutic drugs  Uremia Aurea in blood  Infections (e.g., salmonellosis) III  Severe stress (e.g., trauma, burns, surgery)  Suicidal attempts with acids and alkali  Mechanical trauma (e.g., nasogastric intubation) Acute Gastritis – Morphology Diffuse hyperemia & edema of gastric mucosa. These changes can be localized. Acute Gastritis – Morphology Gastric mucosa demonstrates edema & infiltration by neutrophils  Chronic Gastritis Two main types: 1. Auto-immune associated chronic pangastritis (5%) 2. H. Pylori associated chronic gastritis of the antrum (80%) WIP  H. pylori Associated Chronic Gastritis  Prevalence: Worldwide  Etiology: Helicobacter pylori is non-sporing, spiral, gram-negative bacterium that adhere to mucous & colonize the gastric mucosa indefinitely mostcommonsiteaffect Antrum  Site affected: second Pylorus Antrum & pylorus  Complications: 1. Peptic ulcer 2. Intestinal metaplasia  carcinoma 3. Lymphoma Helicobacter pylori  Gastric Ulceration  Ulcers are defined as a loss of the mucosa, which extends through a the muscularis mucosa into the submucosa or deeper, secondary to acidic gastric juices  Types: Chronic peptic ulcers  Acute gastric ulceration “may accompany acute gastritis”  Anothername of gastriculcer Peptic Ulcer (PU) Sites of Involvement: Duodenal Ulcer (DU) “98%”:mostcommonlocation  Occur in the first part of the duodenum firstpart Gastric Ulcer (GU):  Usually in the antrum along the lesser curvature oONS I im 3 310261 4371.6 Peptic Ulcer – Pathogenesis Produced by an imbalance between E mucosal defenses & damaging forces Mucosal defenses: Mucous secreted by surface epithelial cells Bicarbonate secretion to buffer acidity Epithelial regenerative capacity Mucosal damaging forces: Gastric acid & pepsin H. pylori infection NSAIDs “pain killers” Peptic Ulcer – Morphology a Usually solitary, punched out & oval Surrounding mucosa shows stellate folds Peptic Ulcer – Morphology  Peptic Ulcer – Complications Minority may present with complications: oo1. Bleeding in 1/3 of patients: Minor & chronic  anemia vomitblood Major, can be life-threatening  hematemesis 2. Perforation (5%)  peritonitis WI. O 3. Healing by scarring  stricture  pyloric obstruction “rare” 4. Malignant transformation: Rare in GU (2%) None in DU Bleeding Perforation o  Gastric Carcinoma It is a worldwide disease Isthe 2nd leading cause of cancer related deaths in the world High incidence Japan, China, Italy & Chile fp I Gastric Carcinoma  Gastric Carcinoma – Risk Factors Diet 2401 Is  Lack of refrigeration  food preservation by: nitrites  carcinogenic nitrosamines “used as preservatives in prepared meats”  Smoked foods & pickled vegetables  Decreased intake of fresh fruit and vegetables “antioxidants” Chronic gastritis with intestinal metaplasia  Infection with H. pylori  Pernicious anemia Altered Anatomy  After partial gastrectomy  Appendix ’ Acute appendicitis  Acute Appendicitis  Is acommon cause of abdominal pain requiring surgery  Etiology: im  Appendiceal inflammation usually follows obstruction of the lumen in 50 to 80% of cases so  Obstruction is caused by: drystoolfaeces): the most common  Faecolith (inspissated  Gallstone  Tumor  Ball of worms (oxyuriasis vermicularis) way  reactive hyperplasia of lymphoid follicles  Viral infection  Obstruction of lumen  bacterial proliferation  inflammation & mucosal ulceration  Acute Appendicitis  Peak incidence: 2nd & 3rd decades with a second smaller peak in elderly  Males are slightly more often affected than females  Classically patients present with: Pain, at first is periumbilical & colicky  RLQ constant pain Nausea & vomiting Mild fever RLQ abdominal tenderness Elevation of the peripheral WBC “leukocytosis”  Acute Appendicitis – Gross Morphology see Appendix is swollen, congested & covered with fibrinous exudate  Acute Appendicitis – Microscopic Morphology a Neutrophils must be seen within muscularis propria  mm Acute Appendicitis - Complications 1. Generalized peritonitis:  toxaemia  death 2. Appendicular abscess 3. Adhesions  intestinal obstruction 4. Liver abscesses: rare  Colon 8 MMans ’ Polyps ’ Colonic Tumors  Polyps Pedunculated Polyp a 88 Sessile Polyp  Adenomatous Polyps 1. Tubular adenoma:  Most common subtype  Majority occur in rectum & sigmoid colon me  In older individuals  Start as sessile polyp  pedunculated polyp  Frequently multiple 2. Villous adenoma:  Majority occur in the rectum  Usually sessile & large 3. Tubulovillous adenoma mixture  Tubular Adenoma To Dysplastic glands arranged in tubular Normal glands lining pattern stalk “pedicle”  Villous Adenoma finger like Delicate finger-like Broad base with no structures lined by pedicle “Sessile” dysplastic epithelium  Adenomatous Polyps  ClinicalFeatures: Majority are asymptomatic Occult bleeding  anemia Bleeding per rectum Intestinal obstruction or intussusception Rarely, large sessile villous adenoma  excessive production of mucus & fluid  hypokalemia (low potassium)  muscle weakness Malignant transformation  colorectal carcinoma  L Familial Adenomatous Polyposis Syndrome (FAP)  Autosomal dominant disease  Mutation of APC gene o  500 to 2500 colonic adenomas that carpet the mucosal surface en ar  Adenomatous polyps may also arise in stomach & small intestine un  Start to appear in late childhood  Have 100% frequency of progression to colon cancer by 3rd or 4th decade  Prophylactic colectomy should be performed as soon as possible PP.is  Colonic Tumors: OH Colorectal Carcinoma wow  98% of all  Is the 3rd if Lemage cancers in large intestine are adenocarcinoma commonest cancer in the world  Peak incidence is 60 to 70 years of age  M:F= 1- 2:1  Highest incidence rates are in USA & western countries  gray Colorectal Adenocarcinoma Thank you