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ORAL CAVITY, OESOPHAGUS &

STOMACH
Amr Mahmoud

Outlines
Learn basics of 3 tumours
A.
B.

Oral cancer is associated with people who smoke and drink alcohol.
Dentists are campaigning for early detection
2 cancer with dismal prognosis: oesophageal cancer and gastric cancer

Oesophageal cancer is associated with Barretts oesphagus. Patients with


Barretts 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

Miscellaneous: Apthous Ulcers

Developmental disorder

Ulcer mostly on lower lip

Inherited form with other disorders

Can be associated with Crohn


disease

Interfere with feeding


Surgical intervention

Oral Cavity: Inflammatory Conditions


Oral Candidiasis/Thrush

Angular Cheilitis

Candida Albicans
White plaques

Inflammation at the angles of


mouth (crack).

Neonates and immunocompromised

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 Factors


TOBACCO
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

Erythroplakia

Leuko = White patch

Erythro = red patch

Hyperkeratosis +/- dysplasia

High risk

Chronic irritation
<5% malignant potential
Particularly on atrophic epithelium
on floor of mouth, under-surface
and lateral margins of tongue

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

Mucocele

Usually CaCo3/CaPo4

Most common lesion of salivary glands

Submandibular & parotid

Clinical picture:

Clinical presentation: unilateral pain &


swelling on eating

Swelling commonly on lower lips

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

Extravasation: due to trauma

Types:
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

Epithelial

Histology:

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


Capsule

Encapsulated
Epithelial elements: epithelial/myoepithelial
Stromal element: myxoid/ cartilaginous
Complications
Recurrence due to

Seeding of tumour
Incomplete excision

Cartilage

Warthins Tumour
Incidence:
5% of all salivary tumours; 2nd
commonest
Clinical appearance:
Painless mass
Benign

Less Common Tumours

Adenoid Cystic Carcinoma

10-15% minor salivary glands tumour


Clinical features:
Middle age/elderly
Slowly enlarging painful tumour
Slowly progressive - facial palsy

Histology:
Papillary cystic structure
Epithelial element double layer
epithelium/oesinophilic cytoplasm
Lymphoid stroma/germinal centres

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

Diverticula

Failure or embryological canalisation

Out-pouching of the oesophageal wall

Several types:

Complications:

Fistula between oesophagus and


trachea (commonest)

Dysphagia (difficult swallowing)

Clinically:

Aspiration
Treatment:
Urgent surgical intervention

Regurgitation

Aspiration pneumonia

Miscellaneous Conditions
Oesophageal Haemorrhage
Causes:
Reflux Oesophgitis
Varices: distended veins of portosystemic anastomosis most
commonly due to cirrhosis
Ulcerating cancer
Foreign body
Mallory Weiss Syndrome / Boerhaave
syndrome 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

Barretts Oesophagus
Diagnosis:

Endoscopy: flesh/pink salmon patch


Histology: intestinal metaplasia of
lower oesophageal mucosa
Prognosis:
Premalignant: dysplasia
adenocarcinoma sequence
Regular endoscopic surveillance

Normal

Barretts
Oesophagus

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

Adenocarcinoma

Middle Age M>F

Increasing incidence esp. West

Marked geographic variation

Lower oesphagus

Higher incidence Central China & Iran.

Barretts oesophagus

Middle oesophagus

Aetiology:
Alcohol/Tobacco synergy

Nitrosamine preservatives in diet


Rarely: achalasia &Plummer Vinson
Syndrome

Stomach: Functions, Anatomy & Histology


Reservoir of food
Fundus/body
Secrete HCL, pepsin & intrinsic factor

Pylorus & Cardia


Secrete mucin for protection

against acid

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:
Ramstedts 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

Helicobacter Pylori Gastritis


Very common infection
Any part of stomach, esp. pylorus
Characteristics:

Characteristics:

Patchy chronic & acute inflammation with


plasma cells and lymphoid aggregates;
neutrophils with activity.

Full thickness inflammation

Diagnosis:

loss of parietal cells- atrophy

Biopsy: 80% sensitive = curved organism


on mucosal surface

Intestinal metaplasia

Complications:
Pernicious anaemia

Urea breath test: secrete urease enzyme


breakdown urea -> ammonia

Peptic Ulcer (PU)


Acute Peptic Ulcer

Chronic Peptic Ulcer

Aetiology:

Aetiology:

Acute gastritis

H. pylori present in 70% of gastric


ulcers & 90% of duodenal ulcers

Severe stress as Cushing: trauma;


Curling: burn
Histology
Mucosal ulceration -> acute inflammation
& haemorrhage

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

N.B: peptic ulcer can occur in duodenum


and lower oesophagus

Haemorrhage

Tumours: Benign Neoplasms


Epithelial Polyps
Hyperplastic, fundic gland polyps
Hamartomatous polyp PeutzJeghers 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

Diffuse infiltrative type

70%

30%

H pylori

Usually hereditary type; poor


prognosis

Gross: ulcerative carcinoma raised,


rolled edges or polypoid/fungating
Prominent gland formation lined by
mucus cells
Variable differentiation

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 (Virchows) 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

GIST GI Stromal Tumour

5% of all gastric tumours

New entity

Commonly marginal zone


lymphoma

Unpredictable: usually low


malignant potential

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

(Depends on presence or absence


of necrosis ad mitosis)
Arise from interstitial cell of Cajal
Respond to Tyrosin kinase
inhibtors

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