ORAL CAVITY, OESOPHAGUS & STOMACH

Amr Mahmoud

Outlines

Learn basics of 3 tumours

A. Oral cancer is associated with people who smoke and drink alcohol. Dentists are campaigning for early detection

B. 2 cancer with dismal prognosis: oesophageal cancer and gastric cancer

Oesophageal cancer is associated with Barrett’s oesphagus. Patients with Barrett’s oesphagus are under endoscopic surveillance

Gastric cancer presents late and is common in Japan

Learn a very common inflammatory disease, peptic ulcer, associated with infection with helicobacter pylori

Oral Cavity

Congenital Disorders: Cleft Lip/Palate

◦ Developmental disorder

◦ Inherited form with other disorders

◦ Interfere with feeding

◦ Surgical intervention

Miscellaneous: Apthous Ulcers

◦ Ulcer mostly on lower lip

◦ Can be associated with Crohndisease

Oral Cavity: Inflammatory Conditions

Oral Candidiasis/Thrush

◦ Candida Albicans

◦ White plaques

◦ Neonates and immunocompromised

Angular Cheilitis

◦ Inflammation at the angles of mouth (crack).

◦ Vitamin B & Fe Deficiency

Oral Cancer

Epidemiology:

◦ 3% malignancies

◦ 50 – 80 males

◦ 50% cases attributed smoking, drinking

Types:

◦ 90% Squamous carcinoma

OTHERS:

◦ Nasopharyngeal carcinoma: China, associated with EBV

◦ Malignant lymphoma of tonsils

◦ Malignant Melanoma

Oral Cancer: Predisposing FactorsTOBACCO

◦ Initiator of carcinogenesis – alter cell (DNA damage) permanently, but not sufficient to cause tumour

◦ Promoter of carcinogenesis – induce tumours in initiated cells, but non-carcinogenic themselves (reversible).

◦ Risk increases with duration, quantity

ALCOHOL:

◦ Increase the risk and decrease lag time to develop tumour.

◦ Synergistic effect of cigarettes and C2H5

HPV: Types 16&18 (high risks)- Tonsils

Rare: betel Nut Chewing; Plummer Vinson syndrome

Premalignant conditions: Leukoplakia & Erythroplakia

Leukoplakia

◦ Leuko = “White patch”

◦ Hyperkeratosis +/- dysplasia

◦ Chronic irritation

◦ <5% malignant potential

◦ Particularly on atrophic epithelium on floor of mouth, under-surface and lateral margins of tongue

Erythroplakia

◦ Erythro = “red patch”

◦ High risk

Squamous Cell Carcinoma (SCC)

Commonest site

◦ Lower Lip & lateral border of tongue

Presentation:

◦ Painless hard mass or ulcer with raised edges

Spread:

◦ Submaxillary and cervical lymph nodes

Staging: TNM

Prognosis:

◦ Good: mouth and anterior 2/3 of tongue

◦ Worse: posterior 2/3 of tongue and pharynx

(late presentation)

Salivary Glands: Inflammatory conditions

Salivary Calculi

◦ Usually CaCo3/CaPo4

◦ Submandibular & parotid

◦ Clinical presentation: unilateral pain & swelling on eating

◦ Duct obstruction---dilatation of ducts------sialadenitis----- atrophy and fibrosis

Mucocele

◦ Most common lesion of salivary glands

◦ Clinical picture:

Swelling commonly on lower lips

◦ Types:

Extravasation: due to trauma

Retention: (due to obstruction)

◦ Histology:

Cystic space lined by granulation tissue

Sjogren Syndrome

◦ Middle age F

◦ Keratoconjuctivitis Sicca (dry eyes) or Xerostomia (dry mouth)

◦ Autoimmune disease with lymphocytes and plasma cells infiltrate affecting secretory glands (HLD-DR3 tissue type)

◦ Associated with connective tissue disease (50% of rheumatoid arthritis)

◦ Complications: B-cell Lymphoma

Tumours: Pleomorphic Adenoma

Incidence:

80% parotid tumours

2nd most common tumour in mouth

Clinical appearance:

Slow-growing, painless tumour

Benign; rare malignant transformation

Histology:

◦ Known as mixed tumour (Polymorphous = Greek: Many forms…)

◦ Encapsulated

◦ Epithelial elements: epithelial/myoepithelial

◦ Stromal element: myxoid/ cartilaginous

Complications

Recurrence due to

◦ Seeding of tumour

◦ Incomplete excision

Epithelial

Cartilage

Capsule

Less Common TumoursWarthin’s Tumour

Incidence:

◦ 5% of all salivary tumours; 2nd

commonest

Clinical appearance:

◦ Painless mass

◦ Benign

Histology:

◦ Papillary cystic structure

◦ Epithelial element – double layer epithelium/oesinophilic cytoplasm

◦ Lymphoid stroma/germinal centres

Adenoid Cystic Carcinoma

◦ 10-15% minor salivary glands tumour

Clinical features:

◦ Middle age/elderly

◦ Slowly enlarging painful tumour

◦ Slowly progressive - facial palsy

Histology:

Cyst like spaces /cribriform pattern

Rich in glucosamine

Oesophagus: Normal function, Anatomy and Histology

25cm muscular cylindrical structure

Upper sphincter: controls swallowing

Lower sphincter (LES): control entry to stomach and protect against regurgitation of gastric content

Histology:

◦ Stratified squamous epithelium

◦ Transition to columnar epithelium at the oesophago-gastric junction (OGJ)

Congenital Disorders

Atresia

◦ Failure or embryological canalisation

◦ Several types:

Fistula between oesophagus and trachea (commonest)

Clinically:

Aspiration

Treatment:

Urgent surgical intervention

Diverticula

◦ Out-pouching of the oesophageal wall

Complications:

Dysphagia (difficult swallowing)

Regurgitation

Aspiration pneumonia

Miscellaneous Conditions

Oesophageal Haemorrhage

Causes:

◦ Reflux Oesophgitis

◦ Varices: distended veins of porto-systemic anastomosis most commonly due to cirrhosis

◦ Ulcerating cancer

◦ Foreign body

◦ Mallory Weiss Syndrome / Boerhaavesyndrome due to rupture of oesophageal mucosa due to repeated vomiting or trauma

Achalasia

◦ Failure of relaxation of lower oesophageal sphincter - dilatation of oesophagus

◦ Also caused by Chagas disease

Histology:

◦ Reduction of ganglion cells

Clinically:

◦ Dysphagia

Reflux oesophagitis“Heart Burn”

Prevalence:

Very common: up to 36% of western population! but not all present with symptoms!

Definition:

Chronic inflammation due to regurgitation of gastric contents (chronic oesophagitis)

Causes:

◦ Life style: smoking, alcohol, caffeine

◦ Increased intra-abdominal pressure: pregnancy

◦ Defect in lower oesophageal sphincter

◦ Hiatus hernia

Protrusion of stomach into thorax

Very common

a) Sliding 90%

b) Para-oesophageal 10%

Complications

◦ Mucosal ulceration

◦ Pain

◦ Fe def. anaemia

◦ Fibrosis- stricture

Barrett’s Oesophagus

◦ Diagnosis:

◦ Endoscopy: flesh/pink salmon patch

◦ Histology: intestinal metaplasia of lower oesophageal mucosa

Prognosis:

◦ Premalignant: dysplasia –adenocarcinoma sequence

◦ Regular endoscopic surveillance

Barrett’s

Oesophagus

Normal

Oesophageal Cancer

Morphology:

Fungating/polypoid

Ulcerating

Diffusely infiltrating/circumferential

Clinical Presentation:

Dysphagia

Odynophagia (painful swallowing)

Weight loss

Prognosis:

Poor = 5% 5 year survival due to early metastasis.

If no metastases, excellent prognosis. Early detection?

Oesophageal Cancer: Types, sites & Incidence

Squamous cell Carcinoma

◦ Middle Age M>F

◦ Marked geographic variation

Higher incidence Central China & Iran.

◦ Middle oesophagus

Aetiology:

◦ Alcohol/Tobacco– synergy

◦ Nitrosamine preservatives in diet

◦ Rarely: achalasia &Plummer Vinson Syndrome

Adenocarcinoma

◦ Increasing incidence esp. West

◦ Lower oesphagus

◦ Barrett’s oesophagus

Stomach: Functions, Anatomy & Histology

Fundus/body Pylorus & Cardia

◦ Secrete HCL, pepsin & intrinsic factor ◦ Secrete mucin for protection

against acid

Reservoir of food

Congenital disorders: Congenital Pyloric Stenosis

Epidemiology:

◦ Male : Female = 4:1

Causes:

◦ Abnormal hypertrophy of pyloric muscle

Clinical picture:

◦ Onset 3-6 weeks old – differential biliary atresia

◦ Projective vomiting (non-billous)

◦ Palpable lump in right upper quadrant during feeding

◦ Always hungry and malnourished

Treatment:

Ramstedt’s pyloromyotomy (incision of all pyloric muscle down to mucosa)

Inflammatory Disorders

‘Indigestion’

◦ Epigastric pain: suggestive of ulcer

◦ Referral for endoscopy

Pathology:

◦ Gastritis: Acute vs. Chronic

◦ Peptic ulcer: Acute vs. Chronic

Acute gastritis

◦ Acute inflammation

Causes:

◦ Damage by Chemicals: binge drinking, NSAIDS

Histology:

◦ Depend on severity: acute inflammation, ulcerations and erosions

◦ Heals by resolution and re-epithelialization

◦ Can cause massive haemorrhage

Chronic Gastritis

Autoimmune Gastritis

◦ Auto antibodies against parietal cells and intrinsic factor

◦ Associated with other autoimmune diseases such as Hashimoto of thyroid

◦ Usually body

Characteristics:

◦ Full thickness inflammation

◦ loss of parietal cells- atrophy

◦ Intestinal metaplasia

Complications:

◦ Pernicious anaemia

Helicobacter Pylori Gastritis

◦ Very common infection

◦ Any part of stomach, esp. pylorus

Characteristics:

◦ Patchy chronic & acute inflammation with plasma cells and lymphoid aggregates; neutrophils with activity.

Diagnosis:

◦ Biopsy: 80% sensitive = curved organism on mucosal surface

◦ Urea breath test: secrete urease enzyme breakdown urea -> ammonia

Peptic Ulcer (PU)

Acute Peptic Ulcer

Aetiology:

◦ Acute gastritis

◦ Severe stress as Cushing: trauma; Curling: burn

Histology

◦ Mucosal ulceration -> acute inflammation & haemorrhage

Chronic Peptic Ulcer

Aetiology:

◦ H. pylori – present in 70% of gastric ulcers & 90% of duodenal ulcers

◦ Cigarettes & stress

◦ Hyperacidity – failure of mucosal defence

Morphology:

◦ Usually less 20mm

◦ Clear edge vs. malignant ulcer

Histology:

◦ Necrotic base/granulation tissue – heals by fibrosis

Complications:

Perforation, stenosis

HaemorrhageN.B: peptic ulcer can occur in duodenumand lower oesophagus

Tumours: Benign Neoplasms

Epithelial Polyps

◦ Hyperplastic, fundic gland polyps

◦ Hamartomatous polyp – Peutz-Jeghers polyp

◦ Adenomas:

Mostly in east (Japan)

Pre-malignant

Non-epithelial/mesenchymal

Leiomyoma – smooth muscle

Malignant Tumours

Majority Adenocarcinoma

Lymphoma: less common

Incidence:

◦ Age 50-70, M: F = 3: 2

◦ Geographical variation – high incidence Japan, China & Columbia

◦ Incidence declining elsewhere

Clinical presentation:

◦ Present when clinically advance (silent killer)

◦ Few non-specific symptoms/silent (anaemia)

Gastric Adenocarcinoma

Aetiology:

Familial

Diet:

Nitrates and nitrosamines in salty and smoked food and smoking

Fruits, vegetable & antioxidants: protective

Chronic inflammation:

Intestinal metaplasia associated with chronic gastritis

Helicobacter: linked to cancer, but no definite mechanism understood yet

EBV infection

Gastric adenoma (associated with dysplasia)

Morphology & Histology (Lauren Classification)

Intestinal type

◦ 70%

◦ H pylori

◦ Gross: ulcerative carcinoma – raised, rolled edges or polypoid/fungating

◦ Prominent gland formation lined by mucus cells

◦ Variable differentiation

Diffuse infiltrative type

◦ 30%

◦ Usually hereditary type; poor prognosis

◦ Gross: “leather bottle” linitis plastica stomach

◦ Minimal/no gland formation

◦ Signet-ring cells infiltrating along stomach wall in clusters or single file

Spread:

◦ Direct – through stomach wall

◦ Transcoelomic – tumour cells may seed peritoneum or cross peritoneal cavity, e.g. ovary (Kruckenburg tumour)

◦ Lymphatic – local nodes, supraclavicular (Virchow’s) node

◦ Invade nearby organs

Prognosis:

1. Early: (intra mucosal or submucosa)

◦ Excellent prognosis up to 90%

◦ ? Early detection in Japan

2. Late:

◦ Poor – 5%

Other Tumours

Lymphomas

◦ 5% of all gastric tumours

◦ Commonly marginal zone lymphoma

Atypical lymphocytes destroying the epithelium (lymphoepithelial lesions)

◦ H-pylori related

◦ Usually good prognosis; treatable with eradication of H pylori

◦ Transition to high grade lymphoma is rare

GIST “GI Stromal Tumour”

◦ New entity

◦ Unpredictable: usually low malignant potential

(Depends on presence or absence of necrosis ad mitosis)

◦ Arise from interstitial cell of Cajal

◦ Respond to Tyrosin kinase inhibtors