1. 556
امراض / ثالث اسنان كركوك
د.زانا
2017/4/26
GIT pathology

2. Oral cavity and Oropharynx
Proliferative lesions: most common includes:
Irritation fibroma.
Ossifying fibroma.
Pyogenic granuloma.
Peripheral giant cell granuloma.
B. Inflammatory ulcerations: most common.
traumatic.
Aphthos.
Herpetic.

3. Inflammatory conditions- infections includes;
1. Viral infections- Herpes simplex infection, Herpes zoster, measels.
2. Oral candidiasis.
3. Deep fungal infection.
4. Diphtheria: dirty white , fibrino-suppurative, tough inflammatory pseudomembrane over tonsils and posterior pharynx.

4. Leukoplakia
Definition: a whitish patch or plaque that cannot be characterized clinically or pathologically as any other disease, and is not associated with any physical or chemical causative agent, except the use of tobacco.
between 5% and 25% of these lesions are premalignant

5. Leukoplakia: Etiology
No etiologic factor can be identified for most persistent oral leukoplakias (idiopathic leukoplakia). Known causes of leukoplakia include the following:
Trauma (eg, chronic trauma from a sharp or broken tooth or from mastication may cause keratosis)
Tobacco use: Chewing tobacco is probably worse than smoking.
Alcohol
Infections (eg, candidosis, syphilis, Epstein-Barr virus infection): Epstein-Barr virus infection causes a separate and distinct non–premalignant lesion termed hairy leukoplakia.
Chemicals (eg, sanguinaria)
Immune defects: Leukoplakias appear to be more common in transplant patients.

6. Homogeneous Leukoplakia
Caption: Picture 1. Homogeneous leukoplakia.

7. Leukoplakia- Histopathology
Features highly variable
Ranging from hyperkaratosis and hyperplasia to atrophy and severe dysplasia
Significant intrapathologist and interpathologist variation in diagnosing dysplasia
Molecular studies indicated

9. Squamous cell carcinoma
Vast majority 95 % of head and neck cancers, arise most commonly in oral cavity.
Early there is full thickness dysplasia (carcinoma-insitu) follow by invasion of underlying connective tissue stroma.
Grade vary from well differentiated keratinized to poorly differentiated.

10. Esophagus Main function of esophagus :
Conduct food and fluids from pharynx to stomach.
Prevent reflux of gastric contents.
Congenital anomalies
Ectopic gastric mucosa and pancreatic tissue within esophageal wall.
Congenital herniation of esophageal wall into thorax.

11. 3. Atresia : segment of esophagus represented by only a noncanalized cord, with the upper pouch connected to the bronchus or trachea and lower pouch leading to stomach. 4. Stenosis : fibrous thickening of esophageal wall, result from GERD, radiation, esophageal injury with inflammatory scarring.

12. Lesions associated with motor dysfunction:
Achalasia: means “failure to relax” , idiopathic disorder characterized by three major abnormalities
Aperistalsis ( failure to peristalsis)
Increase resting tone of lower esophageal segment (LES).
Incomplete relaxation of the LES in response to swallowing.
Wall of esophagus may be of normal thickness, thicker ( muscle hypertrophy) or thinned by dilatation, mucosa shows inflammation and ulceration.

13. Esophagitis
Inflammation of esophageal mucosa, might be caused by variety of physical, chemical or biological agents.
Reflux esophagitis is most important cause due to reflux of gastric content into esophagus.
Gross: mild esophagitis appear as simple hyperemia, while in severe shows erosion or total ulceration into submucosa.

14. Microscopic features :
Inflammatory cells including eosinophils within squamous mucosa.
Basal cell hyperplasia.
Extension of lamina propria papillae into upper third of mucosa.
Clinical manifestation consist of dysphagia, heartburn, regurgitation, hematamesis and rarely chest pain.

15. Esophageal tumors
A. leiomyoma: most common benign smooth muscle esophageal tumor. Carcinoma of esophagus represent 5 % if all GIT tumors, squamous cell carcinoma constitutes 90 % of all esophageal cancers, follow by adenocarcinoma, has poor prognosis as often discover too late.

17. Stomach
Gastritis :
Inflammation of gastric mucosa, inflammation might be acute, with neutrophilic infiltration, or chronic with lymphocytes and/ or plasma cells.

18. Acute gastritis Usually transient in nature.
Inflammation may be accompanied by hemorrhage into mucosa ( acute hemorrhagic gastritis) and some times by sloughing (erosion) of superficial mucosa (acute erosive gastritis)
Although large number of cases have no obvious cause ( idiopathic), acute gastritis can be associated with.

19. 1. Heavy use of NSAIDs, particularly aspirin, cancer chemotherapeutic drugs. 2. Excessive alcohol consumption. 3. Uremia. 4. Sever stress ( trauma, burn, surgery). 5. Mechanical trauma ( nasogastric intubation). 6. Distal gastrectomy ( reflux of duodenal content).

20. Chronic gastritis
Chronic inflammation of gastric mucosa that eventuates in mucosal atrophy and intestinal metaplasia, epithelial changes might progress to dysplasia, which constitutes a soli for carcinoma development.
Major etiological association; H.Pylori chronic infection, autoimmune, alcohol and heavy cigarette smoking, outlet obstruction, uremia and duodenal reflux after partial gastrectomy.

21. Gross features :
Mucosa hyperemic and has coarse gastric rugae than normal.
With long standing disease, mucosa become thinned and flattened because of atrophy.
Microscopical features :
Mucosa infiltrated by lymphocytes and plasma cells.
Lymphocytic cells aggregates ( lymphoid follicles).
Neutrophils may or may not be present.

22. Several other histological features in chronic gastritis includes:
Intestinal metaplasia: mucosa partially replaced by metaplastic columnar cells and goblet cells of intestinal morphology.
Atrophy: marked loss of mucosal glands.
Dysplasia.
Individual infected by H.pylori, organism lies in superficial mucosa within gastric pits demonstrated by silver of Giemsa stain.

23. H.Pylori infection

24. Peptic ulcer
Ulcer defined as a breach in mucosa of alimentary tract that extend to submucosa or deeper, most commonly occur in stomach and duodenum, while erosion limited to mucosa and does not extend to submucosa.
Peptic ulcer: chronic most often solitary lesions and usually small, can occur in any portion exposed to aggressive action of acid-peptic juice.

25. Pathogenesis of peptic ulcers
Produced by imbalance between gastro-duodenal mucosal defenses and the damaging forces, particularly of gastric acid and pepsin.
Hyperacidity is not necessary.
H.Pylori infection is a major factor in peptic ulcer, it present in virtually all patients with duodenal ulcers and in about 70% of gastric ulcers, and this occur due to intense inflammatory and immune response to organism, bacterial products cause epithelial injury, bacteria enhance gastric acid secretion and impaired duodenal bicarbonate production in addition to thrombotic occlusion of surface capillaries ( bacterial PAF)

26. Chronic use of NSAID.
Smoking and alcoholic cirrhosis.
Chronic renal failure.
Corticosteroid.
Gastric hyperacidity –Zollinger Ellison syndrome.

27. Gross features : round to oval ulcer with sharply demarcated crater, the margins are usually level with the surrounding mucosa or only slightly elevated, 2-4 cm in diameter.
Microscopical features:
Base and wall have a superficial thin layer of necrotic fibrinoid necrosis.
Beneath this layer a zone of predominately neutrophilic inflammatory infiltrate.
Deep still, there is granulation tissue infiltrated with inflammatory cells, this rest on.
Fibrous or collagenous scar.

29. Complication of peptic ulcer disease.
Bleeding : 20% of cases.
Perforation: much less frequent (5%), but more serious (fatal).
Obstruction ( from edema or scarring).
Malignant transformation., does not occur with duodenal ulcer and extremely rare in gastric ulcers

30. Tumors of stomach. Benign tumors.
Gastric polyps: any nodule or mass that project above the level of surrounding mucosa.
Hyperplastic polyp: small, sessile and multiple in about 25% of cases.
Adenomatous polyp: proliferation of dysplastic epithelium and hence have malignant potential.

31. Cancer of stomach:
Adenocarcinoma most common account for 90% of stomach malignant tumor, next in order lymphoma (5%), other carcinoid and gastrointestinal stromal tumor (GIST).

32. Small and large intestine
Malabsorption syndrome:
Defective absorption of fats, fat soluble vitamins, protein, carbohydrate, electrolytes and minerals
Most common presentation diarrhea and steatorrhea ( excessive fecal fat content).

33. Celiac disease
Gluten sensitive enteropathy, characteristic mucosal lesion of small intestine and impaired nutrient absorption, which improves on withdrawal of wheat gluten from diet.
Pathogenesis: sensitivity to gluten component called gliadin, which is protein present in wheat and closely related grains ( oat), T-cell mediated chronic inflammatory reaction, which develop in consequence of loss of tolerance to gluten

34. Pathological features :
Partial or total loss of duodenal villi.
Degeneration of surface epithelium, loss of microvillus brush borders and increase in intraepithelial lymphocytes.
Increase mitotic activity in crypts and hyperplasia.
Lamina propria shows increase in plasma cell and lymphocytes.

36. Idiopathic inflammatory bowel disease (IBD)
Include Crohn’s disease and ulcerative colitis.
Etiology and pathogenesis:
In normal GIT, mucosal immune system is always ready to respond against ingested pathogens but is unresponsive to normal intestinal flora, thus pathogenesis includes:
Failure of immune regulation.
Genetic susceptibility.
Environmental trigger specifically normal flora.

37. Microscopical examination:
Ulceration, inflammation and chronic mucosal damage.
Diffuse inflammatory cells infiltrate of lamina propria mainly chronic inflammatory cells.
Cryptitis and crypt abscess.
Granuloma in case of Crohn's disease.
Transmural inflammation in crohn’s and limitation to mucosa and submucosa in ulcerative colitis

39. Tumor of colon
Hyperplastic poly: most common polyp of colon and rectum, usually small less than 5 mm and appear as smooth protrusions of the mucosa, often multiple and consist of well formed glands and crypts lined by non neoplastic epithelial cells.
Adenomatous polyp: intraepithelial neoplasm range from small pedinculated lesion to large sessile neoplasm, result from dysplastic epithelial proliferation.

40. Colorectal carcinoma Most arise from preexisting adenoma.
Peak incidence y of age.
Genetic and environmental factors play role in pathogenesis.
Tumor in proximal portion tend to be polypoid exophytic mass, obstruction uncommon.
Distal portion tend to be annular encircling lesion causing obstruction.
Adenocarcinoma most common tumor ranging from well to poorly differentiated, tumor of anal canal tend to squamous cell carcinoma.