Presentation on theme: "Pathology of Upper GIT Dr. Manal M. Sami. Learning objectives: By the end of this activity you should be able to: Give examples of common oral infections."— Presentation transcript:
Pathology of Upper GIT Dr. Manal M. Sami
Learning objectives: By the end of this activity you should be able to: Give examples of common oral infections. List the causes of esophageal mucosal inflammation. Define Barrett esophagus & reflux esophagitis. Define acute and chronic gastritis and describe the morphologic picture of each. Define peptic ulcer, explain its pathogenesis and describe the morphology. List benign and malignant gastric neoplasms.
Examples of oral lesions Aphthous ulcer. Single shallow ulceration with an erythematous halo surrounding a yellowish fibrinopurulent membrane. It is covered by a thin exudate. The underlying inflammatory infiltrate is at first largely mononuclear, but secondary bacterial infection introduces numerous neutrophils
Pyogenic granuloma. Erythematous, hemorrhagic, and exophytic mass arising from the gingival mucosa. Histologically, they demonstrate a highly vascular proliferation that is similar to granulation tissue. Because of this, pyogenic granulomas can also be considered a form of capillary hemangioma
INFECTIONS Acute herpetic gingivostomatitis is caused by herpes simplex virus type 1 (HSV-1). Primary HSV infection typically occurs in children age 2 to 4 years, is often asymptomatic, and does not cause significant morbidity. There is an abrupt onset of vesicles and ulcerations throughout the oral cavity, especially in the gingiva. These lesions are also accompanied by lymphadenopathy, fever, anorexia, and irritability.
Also known as "thrush," pseudomembranous candidiasis typically takes the form of a superficial, curdy, gray to white inflammatory membrane composed of matted organisms enmeshed in a fibrinosuppurative exudate that can be readily scraped off to reveal an underlying erythematous inflammatory base.
Oral candidiasis is common in immunocompromised hosts, such as those with HIV infection. There is a hairy coating of the tongue seen here mixed with a pale tan exudate.
Oral manifestations of systemic infections Scarlet fever:Fiery red tongue with prominent papillae (raspberry tongue); white coated tongue through which hyperemic papillae project (strawberry tongue) Measles:A spotty enanthema in the oral cavity often precedes the rash; ulcerations on the buccal mucosa about Stensen duct produce Koplik spots Infectious mononucleosis: An acute pharyngitis & tonsillitis that may cause coating with a gray-white exudative membrane; enlargement of lymph nodes in the neck Diphtheria: A characteristic dirty white, fibrinosuppurative, tough, inflammatory membrane over the tonsils and retropharynx AIDS:Predisposition to opportunistic oral infections, particularly with herpesvirus, Candida, other fungi; sometimes oral lesions of Kaposi sarcoma & hairy leukoplakia
Normal esophagus This is a normal esophagus with the usual white to tan smooth mucosa seen at the left. The gastroesophageal junction (not an anatomic sphincter) is at the center, and the stomach is at the right.
This is normal esophageal squamous mucosa at the left, with underlying submucosa containing mucus glands and a duct surrounded by lymphoid tissue. The muscularis is at the right.
Esophagitis Reflux esophagitis: Reflux of gastric contents (e.g. in cases of hiatal hernias), most common type. Morphology: hyperemia, thickened basal zone, neutrophil and eosinophil infiltration and superficial necrosis and ulceration. Infectious& chemical esophagitis: due to prolonged gastric intubation, ingestion of alcohol, corrosive acids or alkalis, hot fluids, smoking, chemo or radiotherapy, bacterial & viral (herpesvirus, cytomegalovirus) or fungal (candidiasis, mucormycosis, aspergillosis)
Clinical findings Dysphagia, heartburn, hematemesis and melena. Stricture or Barrett esophagus can result from long standing reflux.
Acute Esophagitis & Gastritis This is Candida esophagitis. Tan-yellow plaques are seen in the lower esophagus, along with mucosal hyperemia. The same lesions are also seen at the upper right in the stomach
Acute esophagitis is manifested here by increased neutrophils in the submucosa as well as neutrophils infiltrating into the squamous mucosa at the right.
Two sharply demarcated "punched out" ulcerations of the mid esophagus in an immunocompromised patient with herpes simplex infection.
A herpetic ulcer with sharp margin. The ulcer base at the left shows loss of overlying squamous epithelium with only necrotic debris remaining. These lesions reveal intranuclear inclusions in squamous epithelial cells indicative of herpes simplex virus esophagitis. This patient was immune compromised from chemotherapy.
This is the view of the lower esophagus seen on endoscopy. Note the areas of dark red friable mucosa representing Barrett esophagus. Note the polypoid mass which on biopsy proved to be a moderately differentiated adenocarcinoma. This patient had a 30 year history of poorly controlled gastroesophageal reflux disease.
Barrett's esophagus in which there is gastric-type mucosa above the gastroesophageal junction. Note the columnar epithelium to the left and the squamous epithelium at the right. This is "typical" Barrett's mucosa, because there is intestinal metaplasia as well (note the goblet cells in the columnar mucosa).
Epithelial cell dysplasia can arise in Barrett esophagus. Adenocarcinoma risk is increased fold.
This irregular reddish, ulcerated exophytic mid- esophageal mass as seen on the mucosal surface is a squamous cell carcinoma (most common type). Risk factors for esophageal squamous carcinoma include mainly smoking and alcoholism in the U.S. In other parts of the world dietary factors may play a role.
At the upper left is a remnant of squamous esophageal mucosa that has been undermined by an infiltrating squamous cell carcinoma of the mid- esophagus. Solid nests of neoplastic cells are infiltrating down through the submucosa at the right. Esophageal cancers often spread to surrounding structures, making surgical removal difficult.
This is the normal appearance of the gastric fundal mucosa, with short pits lined by pale columnar mucus cells leading into long glands which contain bright pink parietal cells that secrete hydrochloric acid.
Acute Gastritis This is a typical acute gastritis with a diffusely hyperemic gastric mucosa. There are many causes for acute gastritis: alcoholism, drugs( NSAID like aspirin), infections, smoking, severe stress, shock, chemotherapy, uremia & truama.
Pathogenesis Increased acid production. Decreased bicarbonate production. Direct mucosal damage. Decreased mucus production with acid back-diffusion.
At high power, gastric mucosa demonstrates infiltration by neutrophils. This is acute gastritis
Chronic gastritis It is defined as the presence of chronic mucosal inflammatory changes leading to mucosal atrophy and epithelial dysplasia. Pathogenesis: 1. Chronic infection with H. pylori 2. Autoimmune destruction of the glands. 3. Toxic: alcohol& smoking. 4. Postsurgical, Radiation, mechanical obstruction. 5. Granulomatous diseases (Crohn disease)
Helicobacter pylori Gram negative, Spiral bacilli Spirochetes Do not invade cells – mucous Breakdown urea - ammonia Breaks down mucosal defenses Chronic Superficial inflammation Biopsy - Toludine blue stain, silver stain Urease test, Breath test.
Helicobacter pylori Gastritis is often accompanied by infection with Helicobacter pylori. This small curved to spiral rod-shaped bacterium is found in the surface epithelial mucus of most patients with active gastritis. The rods are seen here with a methylene blue stain.
Urease production test
Chronic atrophic gastritis Another association with gastritis is pernicious anemia. Chronic atrophic gastritis is associated with autoantibodies that block or bind intrinsic factor. Another type of autoantibody demonstrated here is anti-parietal cell antibody. The bright green immunofluorescence is seen in the paritetal cells of the gastric mucosa.
Morphology Grossly, the mucosa is reddened, boggy& coarse-textured. Microscopically, there is lymphocyte & plasma cells infiltrate the lamina propria, intraepithelial neutrophilic infiltration, regenerative change of surface columnar cells, variable gland atrophy, metaplasia of the surface epithelium to intestinal-type epithelium and dysplasia in long standing cases.
Peptic Ulcer Disease An ulcer is a breach of the mucosa extending through the muscularis mucosa into deeper layers. Peptic ulcers are chronic, typically solitary ulcers arising from exposure to acid-peptic secretion. Clinically, there is epigastric burning or aching pain, worse at night and 1 to 3 hours after meals. Nausea, vomiting and weight loss also occur.
Peptic ulcer - Endoscopy
Gastric Ulcer A 1 cm acute gastric ulcer is shown here in the upper fundus. The ulcer is shallow and sharply demarcated, with surrounding hyperemia. It is probably benign. However, all gastric ulcers should be biopsied to rule out a malignancy.
Here is a much larger 3 x 4 cm gastric ulcer that led to the resection of the stomach shown here. This ulcer is much deeper with more irregular margins. Complications of gastric ulcers (either benign or malignant) include pain, bleeding, perforation, and obstruction.
Microscopically, the ulcer is sharply demarcated, with normal gastric mucosa on the left falling away into a deep ulcer whose base contains inflamed, necrotic debris. An arterial branch at the ulcer base is eroded and bleeding.
Duodenal Peptic Ulcer The strongest association with Helicobacter pylori is with duodenal peptic ulceration--over 85% of duodenal ulcers. Seen here is a penetrating acute ulceration in the duodenum just beyond the pylorus.
Complications of peptic ulcers Ulcers might penetrate over time if they do not heal. Penetration leads to pain. If the ulcer penetrates through the muscularis and through adventitia, then it is said to "perforate" and leads to an acute abdomen. An abdominal radiograph may demonstrate free air with a perforation. Erosion of the ulcer into the artery will lead to another major complication of ulcers-- hemorrhage. This hemorrhage can be life threatening. Chronic blood loss may lead to an iron deficiency anemia. Obstruction from edema or scarring may occur
Tumors Benign tumors include: Non-neoplastic polyps (e.g. hyperplastic polyps, 90% of cases, inflammatory polyps and hamartomatous polyps) Neoplastic polyps: adenomas which have proliferative dysplastic epithelium. They are usually single, either sessile or pedunculated.
Gastric carcinoma occurs as either 1. Intestinal (gland-forming columnar epithelium, mucin secreting, polypod expansile growth pattern) 2. Diffuse (poorly differentiated, single, signet-ring cells, mucin producing, infiltrative growth pattern).
Morphologic types of Carcinoma Stomach Fungating Ulcerating Diffuse
Fungating Carcinoma Stomach
Linitis Plastica This is an example of linitis plastica, a diffuse infiltrative gastric adenocarcinoma which gives the stomach a shrunken "leather bottle" appearance with extensive mucosal erosion and a markedly thickened gastric wall. This type of carcinoma has a very poor prognosis.
At high magnification, the neoplastic glands of gastric adenocarcinoma demonstrate mitoses, increased nuclear/cytoplasmic ratios, and hyperchromatism. There is a desmoplastic stromal reaction to the infiltrating glands.
At high power, this gastric adenocarcinoma is so poorly differentiated that glands are not visible. Instead, rows of infiltrating neoplastic cells with marked pleomorphism are seen. Many of the neoplastic cells have clear vacuoles of mucin.
This is a signet ring cell pattern of adenocarcinoma in which the cells are filled with mucin vacuoles that push the nucleus to one side, as shown at the arrow.