salivary gland and esophagus

1. SALIVARY GLAND

2. Learning Outcomes
Classify salivary gland neoplasm.
Enlist the common benign neoplasms
Differential diagnosis of salivary glands swellings
Describe morphology of pleomorphic adenoma
Understand esophagitis and its types
Describe reflux esophagitis, contributory factors, morphological changes,
clinical features and its relation to Barrett’s Esophagus
Define Barrett’s Esophagus its etiology, gross appearance and its related
risk to esophageal carcinoma.
Know oesophageal carcinoma, etiology, pathogenesis, risk factors, gross
and microscopic appearance

3. Normal Histology of Salivary Glands

4. Non-neoplastic Lesions
Sialadenitis
Bacteria; e.g, Styph. aureus or strep. viridans
Virus; mumps, may be accompanied by pancreatitis or orchitis or ophoritis
Autoimmune; e.g, Sjögren syndrome, salivary and lacrimal glands
involvement leads to, dry mouth and dry eyes
Mucocele
Nodular lip swelling, due to blockage or rupture of salivary gland duct
Sialolithiasis
Duct obstruction - stone formation, common in submandibular gland

5. Salivary gland Neoplasms
Represent >2% of human neoplasms
Total tumor Malignant %
Parotid 65-85% 15-30%
Submandibular 10% 40%
Sublingual rest 70-90%
Minor salivary 50%
Malignancy; inversely proportional to size of the gland

6. Histologic Classification-Salivary Gland Neoplasm
Benign Tumors
Pleomorphic adenoma 50%
Warthin tumor 5-10%
Oncocytoma 1%
Adenomas 5-10%
- Basal cell adenoma
- Myoepthelioma
Ductal papillomas
Note: Remember the common
Malignant Tumors
Mucoepidermoid carcinoma15%
Adenocarcinoma (NOS) 10%
Acinic cell carcinoma 5%
Adenoid cystic carcinoma 5%
Malignant mixed 3-5%
Squamous cell carcinoma1%
Metastatic carcinoma
Lymphoma

7. Pleomorphic Adenoma (Benign mixed tumor)
Composed of cells exhibiting ability to
differentiate into; epithelial cells and
mesenchymal components
Gross:
Round to ovoid, encapsulated or partly
encapsulated mass
Cut surface; homogeneous tan to white

8. Pleomorphic Adenoma
Microscopy:
Epithelial cells
- Trabeculae/ ducts
- Cysts lined by squamous
epithelium
Mesenchymal components
- Fibrous
- Myxochondroid
- Osseous

9. Pleomorphic Adenoma
Clinical Course
Most common, any age , common in females
Slow growing, asymptomatic, presents as single nodular, firm, mobile mass
rarely exceed 6cm in diameter
Malignant transformation increases with duration (2% less than 5 yrs
and10% less than 15 yrs duration)
Carcinoma ex pleomorphic adenoma; adenocarcinoma or undifferentiated
carcinoma-a very aggressive tumor
S/S of malignancy; sudden increase in size in short period, fixity to
surrounding tissue or facial nerve palsy
Diagnosis; clinical assessment, FNA, excision biopsy

10. Warthin’s Tumor
May be unilateral or bilateral, common in
males (26:1) and in smokers
Gross
Round, encapsulated mass, 2-4cm in size
Cut surface multiple cysts exude a clear fluid
Microscopy
Cystic spaces, papillary projections lined by
tall columnar cells
Lymphoid tissue with/without germinal center

11. Esophagus
Normal gross Normal histology

12. Esophagitis
Inflammation of the esophageal mucosa
Etiological factors
Physical; e.g intubation, radiations
Chemical; e.g uremia, ingestions of corrosive
Biologic agents; e.g tuberculosis, candidiasis, herpes simplex, CMV
Others; Crohn disease, Graft verses host disease (GVHD)

13. Reflux Esophagitis (GERD)
Reflux of gastroduodenal contents into esophagus due to dysfunction of LES
Contributory factors
Presence of sliding hiatal hernia
Vagal dysfunction
Increased gastric volume and slowed esophageal clearance of refluxed
material
Impaired reparative capacity of mucosa by prolong exposure to gastric juices
Others ; CNS depressants, tobacco and alcoholism
Pathogenesis
Reflux of gastric juices, mucosal injury, in severe cases duodenal bile reflux
increases the mucosal damage

14. Reflux Esophagitis (GERD)
Gross
Mucosa, hyperemic and red
Microscopy
Epithelial hyperplasia due to basal
cell proliferation
Intraepithelial eosinophils
Lamina propria; neutrophils,
eosinophils and lymphocytes
Tips of elongated lamina propria
papillae shows congested venules

15. Reflux Esophagitis
Clinical manifestations
Heartburn, chest pain ,dysphagia
Outcome: reflux esophagitis may progress to:
Superficial ulceration
Bleeding, hematemesis and melena
Spread of inflammation to the wall
Circumferential fibrosis with stricture formation
Tendency to develop Barrett esophagus

16. Barrett Esophagus
A segment of distal esophagus above the level of LES shows metaplastic
columnar epithelial lining with goblet cells
Pathogenesis
Ulceration and subsequent re-epithelization by columnar cells to cope with
existing conditions
Ulceration, induced by reflux and occurs in 10% of these patients
Columnar cells could arise from migration of gastric mucosa or from stem
cells of mucosa

17. Barrett Esophagus
Endoscopy
Mucosa red and velvety, involvement
might be circumferential or in the form
of finger like projections or islands
Microscopy
Intestinal metaplasia with a villiform
surface and crypts lined by columnar
and goblet cells most significant for
diagnosis
Diagnosis
Endoscopic examination and biopsy

18. Barrett Esophagus
Main complications
1. Peptic ulcer
2. Stricture
3. Bleeding
4. Dysplasia and adenocarcinoma
(Persons with Barrett esophagus have 30 to 100 fold greater risk of developing
adenocarcinoma)

19. Tumors of Esophagus
Non-neoplastic
Mucosal polyp
Squamous papilloma
Benign neoplasms
Leiomyoma
Fibroma
Neurofibroma
Malignant neoplasms
Squamous cell carcinoma
Adenocarcinoma
Carcinoid

20. Squamous Cell Carcinoma
Epidemiology
Most frequent in men over 50yrs of age
Male to female ratio; 4:1
Blacks are at higher risk than whites
Relatively common in China, Iran, Southern Brazil and other oriental
countries, most common tumor of alimentary tract in African Bantus
Smoking and alcoholism; two well known risk factors
In western countries, there has been a recent epidemiologic switch from
tobacco and alcohol-related SCC to Barrett’s-related adenocarcinoma

21. Risk Factors for SCC of the Esophagus
Esophageal Disorders
Long-standing esophagitis
Genetic Predisposition
Long-standing celiac disease
Others
HPV found in SCC
P53 and p16INK4 mutations
Ampilfication of CyclinD1, C-MYC,
and EGFR
Dietary
Betel chewing
Deficiency of vitamins (A, C, riboflavin,
thiamine, pyridoxine)
Deficiency of trace elements (zinc,
molybdenum)
Fungal contamination of foodstuffs
High content of nitrites or nitrosamines
Lifestyle
Burning-hot beverages or food
Alcohol consumption
Tobacco use

22. SCC Esophagus
Location
Any part of esophagus; middle thirds
50%, lower thirds 30%, upper thirds 20%
Gross
Three morphologic pattern; Exophytic 60%, Ulcerated
25%, Flat 15%
Early lesion small grey white plaque like thickenings
Late circumferential tumor mass, thickened wall, often
ulcerated with sharply demarcated margins

23. SCC Esophagus
Microscopy
Intraepithelial neoplasia/dysplasia/ carcinoma-in-situ
Intramucosal carcinomas; that do not invade beyond
lamina propria
Superficial carcinomas; do not invade beyond
submucosa
Superficially spreading carcinomas; shows a lateral
intramucosal spread of at least 2cm beyond the
invasive tumor
Grade; Well to Poorly-differentiated

24. SCC Esophagus
Clinical features
S/S: Slow on set of dysphagia, Weight loss, hemorrhage
and anemia
Diagnosis: Exfoliative cytology and Endoscopic biopsy
Prognosis: Overall prognosis is poor; the median survival after
diagnosis being one year
Metastasis: To distant organs particularly liver, lung and adrenal
gland common
Stage: In situ and intramucosal carcinomas are almost
always curable

25. Adenocarcinoma of Esophagus
Typically arises in a background of Barrett's esophagus
Accounts for 5-10% of all esophageal cancers
Most patients, white males, average age 57 years
Tumor may be multicentric and is usually advanced at the time of diagnosis
with extension through the wall and nodal metastasis
Molecular alterations identified in Barrett's esophagus containing lesions
within dysplasia-adenocarcinoma sequence includes
- Mutation and overexpression of p53 gene
- Mutation of beta-catenin and HER-2 /NEU

26. Adenocarcinoma Esophagus
Morphology:
Initial flat or raised patches intact
mucosa
Late; nodular polypoid mass up to
5cm
Diffusely infiltrative or deeply
ulcerated
Mucin producing glandular tumor of
intestinal type
Diagnosis: Multisite biopsy
Prognosis: Poor, stage by
stage same as to SCC

27. Self Assessment
A 20-year-old female presented in the OPD with swelling in the pre-auricular
region. Swelling is from childhood and is slow growing.
On clinical examination the swelling is firm, mobile, painless and measures
4.5cm in diameter.
Give short answer to these questions
1. What is the origin of this swelling?
2. Give two differential diagnosis.
3. What is your definite diagnosis?
4. How will you confirm your diagnosis?

28. References
Basic Pathology, 10th edition Kumar, Abbas & Aster
www.studentconsult.com
www.webPathology.com.