Upper gastrointestinal tract

Published on 19/03/2015 by admin

Filed under Pathology

Last modified 19/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1232 times


16.1 Inflammation and infection154
16.2 Oral and salivary gland neoplasia154
Part 2: Oesophagus, stomach and proximal duodenum156

16.3 Inflammation, infection and benign conditions156
16.4 Oesophageal and gastric neoplasia157
Self-assessment: questions160
Self-assessment: answers162

Chapter overview
This chapter covers the common pathology of the mouth, salivary glands, oesophagus, stomach and proximal duodenum. Inflammatory conditions of this region are frequent, and include oral ulcers, oesophagitis, gastritis and gastroduodenal (peptic) ulceration. Carcinoma of the oesophagus and stomach has a particularly poor prognosis. While the incidence of gastric cancer is decreasing in the UK, oesophageal carcinoma is rising in frequency. The role of Helicobacter pylori infection in gastric pathology, and the significance of lower oesophageal epithelial metaplasia (Barrett’s oesophagus) will be discussed. Oral squamous cell cancer is relatively uncommon in the Western world but is a major health problem in India and other parts of Asia.

Part 1: Mouth and salivary glands

16.1. Inflammation and infection

Learning objectives
You should:

• know the common benign pathologies affecting the oral cavity
• understand the terms leucoplakia and erythroplakia and their clinical significance.
The following conditions are common in the mouth:

• non-specific ulceration (‘aphthous ulcers’)
• herpes simplex type 1 infection (‘cold sore’)
• candidiasis, especially in diabetic and immunosuppressed patients
• benign fibroepithelial polyp (reactive fibrous proliferation secondary to chronic irritation)
• cysts associated with teeth (developmental or inflammatory).
The oral mucosa can manifest several inflammatory conditions seen in the skin, such as lichen planus, bullous pemphigoid and erythema multiforme. Xerostomia (dry mouth) can be a feature of autoimmune disease in Sjögren’s syndrome (see below).
Salivary gland inflammation can be due to:

• viral infection, e.g. mumps
• bacterial infection – staphylococcal and streptococcal, associated with salivary duct calculi (stones) and dehydration
• autoimmune disease.
Sjögren’s syndrome results from autoimmune inflammatory damage to the salivary glands, lacrimal glands and small mucous glands of the nasal mucosa. Clinically this can present with dry mouth and dry eyes. There is a close association between Sjögren’s syndrome and rheumatoid arthritis.
Leucoplakia is a clinical term describing a ‘white patch’ of oral mucosa. Leucoplakia does not reflect a specific pathological diagnosis and is often caused by inflammation or reactive hyperkeratosis (thickened keratin layer), but on occasion it can represent epithelial dysplasia or malignancy (Box 22). A more sinister lesion is erythroplakia, a velvety red patch of oral mucosa, which typically shows high-grade epithelial dysplasia on biopsy.
Box 22

• Candida infection
• Smoking-related keratosis
• Traumatic keratosis from rubbing denture plate
• Lichen planus
• Squamous epithelial dysplasia

16.2. Oral and salivary gland neoplasia

Learning objectives
You should:

• know the pathology of oral squamous cell carcinoma
• know the common benign and malignant tumours of the salivary glands.
Benign tumours of the oral cavity include squamous cell papilloma (analogous to skin lesions) and haemangiomas. Squamous cell carcinoma accounts for over 95% of oral malignancies (Table 24).
Table 24 Cancer checklist: oral squamous cell carcinoma
Incidence Age 50–70years. Less than 5% of non-skin cancers in Western world; up to 40% of all cancers in India
Risk factors Smoking, alcohol, betel nut chewing (India/Asia), chronic infl ammation
UV light and pipe smoking in lip carcinoma
Protective factors Fruit and vegetable consumption
Associated lesions Epithelial dysplasia, may be erythroplakia (over 50% progress to invasive cancer) or less frequently leucoplakia
Clinical presentation Mass noted by patient or dentist
Location Floor of mouth, tongue and hard palate most frequent
Macroscopic appearance Raised fi rm mass ± ulceration
Histological features Vary from well-differentiated tumours with orderly keratinisation to anaplastic (undifferentiated) tumours
Pattern of spread Local infi ltration of oral structures, regional lymph nodes, lung, liver, bone
Prognosis (per cent 5-year survival) Dependent on site: lip 90%; anterior tongue 60%; other sites 20–30%
Salivary gland tumour pathology is complex, as both epithelial cells and associated myoepithelial cells may give rise to neoplasms. Most tumours arise in the parotid gland, and over 80% of these are benign. Neoplasms arising in the submandibular and sublingual glands and the minor salivary glands scattered throughout the oral mucosa have a much higher likelihood of being malignant (approximately 50%).

Pleomorphic adenoma

Pleomorphic adenoma is the commonest salivary tumour, arising most frequently in the parotid gland. The histological appearance is very variable, with epithelial glands or cell sheets, embedded in a connective tissue stroma showing myxoid changes, fibrosis, cartilaginous areas or even bone formation. Pleomorphic adenomas are benign tumours that appear well circumscribed macroscopically and do not infiltrate local structures (the facial nerve is, therefore, usually spared by pleomorphic adenomas arising in the parotid). However, there are often microscopic projections of tumour into the adjacent tissues, and attempted removal by enucleation carries a significant risk of multifocal recurrence, which can be difficult to treat. Up to 5% of pleomorphic adenomas may undergo malignant transformation to a high-grade carcinoma. The risk of malignant change is increased in longstanding adenomas.

Warthin’s tumour

This tumour accounts for approximately 10% of salivary neoplasms, and arises almost exclusively in the parotid. There is a strong male preponderance. Ten per cent of tumours are bilateral, and a similar number are multifocal. The microscopic appearance is distinctive, with a double layer of eosinophilic epithelial cells covering reactive lymphoid tissue. The eosinophilic cells (oncocytes) are the neoplastic population. Warthin’s tumour is benign and malignant change does not occur.

Salivary gland carcinoma

Many different histological variants of salivary gland carcinoma (Table 25) are now recognised. The two commonest are:

Adenoid cystic carcinoma – this malignancy appears low grade on histological grounds, but is locally invasive and 50% will metastasise. The long-term survival is poor. Adenoid cystic carcinoma is composed of regular small epithelioid cells in a cribriform (‘sieve-like’) architectural pattern, associated with basement-membrane-like material. Perineural invasion by the tumour is a characteristic feature.
Table 25 Cancer checklist: salivary gland carcinoma
Incidence Uncommon; adults; slight female predominance
Risk factors Irradiation (muco-epidermoid carcinoma)
Associated lesions Small percentage of pleomorphic adenomas undergo malignant transformation
Common clinical presentation Mass, pain, facial nerve involvement (parotid tumours)
Location Parotid, 15% of tumours are malignant
Submandibular, 40% malignant
Minor salivary glands, majority malignant
Macroscopic appearance Variable, usually infi ltrative margin
Histological features Variable
Pattern of spread Adenoid cystic, local perineural invasion, late dissemination to lung, liver, bone, brain (50%)
Muco-epidermoid, low-grade lesions recur locally, high-grade lesions may disseminate widely
Prognosis (per cent 5-year survival) Adenoid cystic, 60% at 5years, but 15% at 15years
Muco-epidermoid, 50–90%, depending on grade

Part 2: Oesophagus, stomach and proximal duodenum

16.3. Inflammation, infection and benign conditions

Learning objectives
You should:

• understand gastro-oesophageal reflux disease and Barrett’s oesophagus
• know the causes and complications of acute and chronic gastritis, and of peptic ulcer disease.


This disease may be due to infection, particularly by Candida in debilitated and immunosuppressed patients. Gastro-oesophageal reflux disease (GORD) is the commonest cause of oesophagitis in the UK, and its prevalence appears to be increasing. It is associated with sliding hiatus hernia, smoking, obesity, pregnancy and ingestion of certain foods. GORD classically presents with burning epigastric pain, which may be accentuated by bending or lying down, but is often asymptomatic. Histology shows hyperplasia of squamous oesophageal epithelium with inflammation (eosinophils, neutrophils and lymphocytes) and ulceration in more severe cases. Complications include:

• haematemesis
• anaemia
• inflammatory stricture
• Barrett’s oesophagus (see below).
Other causes of oesophagitis include alcohol, corrosive chemical ingestion, chemotherapy, radiotherapy and graft-versus-host disease.

Barrett’s oesophagus

This syndrome describes a metaplastic change of the squamous epithelium of the lower oesophagus into glandular epithelium. The metaplastic glandular epithelium may resemble gastric or small intestinal mucosa. Barrett’s usually occurs in patients with more severe longstanding GORD. Endoscopically the metaplastic focus has a red, velvety appearance. Barrett’s may progress to glandular dysplasia and eventually to invasive adenocarcinoma. Both Barrett’s oesophagus and oesophageal adenocarcinoma have increased in incidence in recent years. For this reason, regular surveillance endoscopies are usually performed in patients with known Barrett’s change, to identify high-grade dysplasia and early stage malignancy. However, the degree of increased cancer risk associated with Barrett’s remains unclear, and less than half of all patients with oesophageal adenocarcinoma will describe any clinical history of reflux disease.


This is a motility disorder in which reduced oesophageal peristalsis and failure of relaxation of the lower oesophageal sphincter cause lower oesophagus dilatation. Resulting symptoms include dysphagia and food regurgitation. In most cases the pathogenesis is unknown. Achalasia can be secondary to Chagas’ disease, caused by the protozoon Trypanosoma cruzi

Buy Membership for Pathology Category to continue reading. Learn more here