GASTRO INTESTINAL SYSTEM GASTRO INTESTINAL SYSTEM PART-1PART-1..

1. SALIVARY GLAND 1. SALIVARY GLAND TUMORSTUMORS

Uncommon - <2% of tumors

Parotid – 65 – 80% (15 – 30 % malig)

Submandibular – 10% ( 40% malig)

Minor salivary glands – rare 50% malignant in minor salivary glands

70 – 90% malig in sublingual glands

PLEOMORPHIC ADENOMAPLEOMORPHIC ADENOMA(MIXED PAROTID TUMOR)(MIXED PAROTID TUMOR)Benign60% - parotid30 – 50 yrs.M:F=1:3-4Derived from epithelial &

myoepithelial cells

Show epithelial & mesenchymal differentiation

Painless, slow growing, mobile, discrete mass

Parotid, submandibular or in buccal cavity

GROSSGROSS

Round, well demarkatedEncapsulated, but capsule not

developed

Tongue like protrusions into surrounding gland

Enucleation hazardous

Recurrent tumor multifocal

MICROSCOPYMICROSCOPYEpithelial elements

Ducts, acini, tubules, strands or sheetsDucts with cuboidal to columnar cells

with underlying deeply chromatic, small myoepithelial cells

OR Strands and sheets of Myoepithelial

cells Islands of squamous differentiation

Mesenchyme like backgroundLoose myxoid tissue with chondroid /

osteoid foci

PLEOMORPHIC ADENOMA

Treatment: complete surgical excisionParotidectomy with facial nerve

preservationSubmandibular gland excisionWide local excision of minor

salivary gland

Avoid enucleation and tumor spill

Recurrence rate with parotidectomy 4%

Enucleation – 25%

Malignant mixed tumor / Ca ex pleomorphic adenoma2% for tumors < 5yrs10% for tumors > 15yrsAdenocarcinomas or undiff tumors Recognizable traces of the adenoma

MUST be found5yr mortality – 30 to 50%

WARTHIN’S TUMOR (WARTHIN’S TUMOR (AKA PAPILLARY CYSTADENOMA LYMPHOMATOSUM)

BenignParotid gland ONLYMale preponderance5th to 7th decade10% multifocal10% bilateral

GROSSGROSSRound to oval

2 – 5 cm dia

Encapsulated

Arises in the superficial parotid gland

C/S – pale gray surface with narrow cystic or cleft like spaces filled with mucinous or serous secretion

MICROSCOPYMICROSCOPYSpaces lined by double layer of neoplastic

epithelial cellsSurface palisade of columnar cells with

abundant, finely granular, eosinophilic cytoplasm – “oncocytic”

On a layer of cuboidal to polygonal cellsDispersed secretory cells in columnar

cell layerSquamous metaplasia

Dense lymphoid stroma ( GCs )

Recurrence rate 2% after resection

OTHER SALIVARY GLAND TUMORS

Adenoid cystic carcinoma

Mucoepidermoid carcinoma

Acinic cell carcinoma

Gross appearance of mucoepidermoid carcinoma. This particular tumor is entirely solid, without the cystic formations commonly seen in low-grade lesions

Mucoepidermoid carcinoma Mucous, squamous, and intermediate cells can be seen.

GASTROINTESTINAL TRACT

Oral cavity—Inflammatory diseases, precancerous lesions, Carcinoma

Salivary gland tumors

INFLAMMATORY LESIONS OF ORAL CAVITY

Stomatitis Aphthous ulcers [canker sores]—Painful oral

ulcers of unknown etiology ,Precipitated by emotional stress, Allergy, hormonal imbalence,Nutritional deficiencies and truma

Herpetic stomatitis --Herpes simplex virus

Cancrum oris or noma [Necrotising stomatitis ]—Necrosis of gingiva oral mucosa may lead to gangrene of cheek -- Feature of Kwashiorkor,measels, immunodeficiency states and stress

Mycotic infections –Actinomycosis and Candidiasis [ oral thrush]

ORAL CAVITY

Precancerous lesions LeukoplakiaErythroplakia

Carcinoma

LEUKOPLAKIA

White patch or plaque that cannot be scraped off and cannot be characterized clinically or pathologically as any other disease

Incidence – 3%, 5 – 25% of these are premalignant

Age – 40 -50 yrs.M:F = 2:1DD – Lichen planus, candidiasis

1. Homogeneous leukoplakia – lesion that was uniformly white and unscrapable.

2. Non Homogeneous leukoplakia – lesion predominantly white and speckled with red.

WHO CLASSIFICATIONS (1980)

1. Thin, smooth leukoplakia (preleukoplakia older terminology) – translucent thin gray soft flat plaques usually with sharply demarcated borders.

2. Thick, fissured leukoplakia – 2/3 of white plaques has distinctly white appearance (from thickening of keratin layer), fissured and are leathery to palpation.

3. Granular, verruciform leukoplakia – lesions have surface irregularities of nodular or granular nature with verrucous appearance.

4. Erythroleukoplakia – lesion showing intermixed red and white areas, because the epithelial cells are so immature that they no longer are able to produce keratin.

WHO CLASSIFICATIONS (1998)

In 2002 WHO reclassified the above variants depending on the probability of a malignant change and prognosis of these lesions as

1. Phase I: thin, smooth leukoplakia – better prognosis.

2. Phase II: thick, fissured leukoplakia. 3. Phase III: proliferative verrucous

leukoplakia (PVL) – higher malignant transformation rate.

4. Phase IV: erythroleukoplakia – poor prognosis.

WHO CLASSIFICATIONS (2002)

Leukoplakia is purely a clinical terminology and histopathologically it is reported as epithelial dysplasia.

WHO in 2005 proposed five grades of epithelial dysplasia based on architectural disturbances and cytological atypia.

HISTOPATHOLOGY

1. Squamous Hyperplasia – benign lesion.

2. Mild Dysplasia – better prognosis.

3. Moderate Dysplasia.

4. Severe Dysplasia.

5. Carcinoma In-situ – poor prognosis.

It has been recently proposed to modify the above 5-tier system into a binary system of ‘high risk’ and ‘low risk’ lesions to improve clinical management of these lesions.

Locations

Buccal mucosa Floor of the mouth Ventral surface of tongue Palate Gingiva

SMOOTH, THIN, WELL DEMARCATED

DIFFUSE & THICK

IRREGULAR WITH A GRANULAR SURFACE

DIFFUSE & CORRUGATED

MICROSCOPY

Hyperkeratosis

Thickened acanthotic but orderly epithelium

Markedly dysplastic changes

Carcinoma in situInflammation – lymphocytes and macrophages

Keratosis without dysplasia

Moderate dysplasia Mild dysplasia Severe dysplasia

EPITHELIAL DYSPLASIA

ERYTHROPLAKIA Red, velvety, possibly eroded

Usually flat, may be depressed

Intense subepithelial inflammatory reaction with vascular dilatation Redness

Epithelium shows marked atypia

90% show superficial erosions with dysplasia, Ca in situ or Ca at the margins

SQUAMOUS CELL CARCINOMA Most(95%) of the malignant tumours of

the oral cavity are SCC

Remainder includes salivary gland tumours and melanomas

Aggressive

PATHOGENESIS

Multifactorial

Middle aged men Smoking tobacco, alcohol HPV infection in 50% of oropharyngeal Ca

Other countries – chewing betel quid, paan

Protracted irritation from ill fitting dentures, jagged teeth, chr. infections

GROSS Raised, firm, pearly plaque

Irregular, roughened or verrucous

Background – leukoplakia or erythroplakia

Ulcerate and protrude as mass with irregular, firm and indurated (rolled) borders

MICROSCOPY

Well differentiated keratinizing tumor to anaplastic, sometimes sarcomatoid tumor

But degree of differentiation does

not correlate with clinical behavior

Local metastasis – cervical LNs

Distant metastasis:# Mediastinal LNs# Lungs# Liver# Bones

PROGNOSIS

5yr survival Early oral cancer – 80%Late stage – 19%

TUMOURS OF THE OESOPHAGUS.

BARRETT ESOPHAGITIS Complication of long standing GERD Distal squamous mucosa is replaced by

metaplastic columnar epithelium as a result of prolonged injury

Short segment(<3 cm) / long segment 2 criteria – Endoscopic evidence of columnar

lining above GE junction, Histological evidence of intestinal metaplasia

MORPHOLOGY

Red velvety

mucosa

Between pale pink

esophageal

mucosa

Tongues/ patches/

circumferential

bands

MICROSCOPYEsophageal squamous epithelium is replaced by metaplastic columnar epithelium.

Definitive diagnosis when columnar mucosa contains intestinal goblet cells

Dysplasia may be low/ high gradeEnlarged crowded hyperchromatic nuclei & loss of intervening stroma

Barrett’s esophagitis

CLINICAL FEATURES White males – 40 to 60 yrs Reflux heart burn , strictures, bleeding 30 – 40% increase in risk of adeno carcinomaProgression to adeno carcinoma – multi step

process

TUMOURS OF THE OESOPHAGUS

Benign Malignant Squamous cell carcinoma Adenocarcinoma

RISK FACTORS

Human papilloma virus HPV serotype 16 was identified in 9 percent of resection specimens from 70 Chinese patients with esophageal SCC.

Tylosis rare disease associated with hyperkeratosis of the palms of the hands and soles of the feet and a high rate of esophageal SCC

GIT neoplasms

ESOPHAGUS: Squamous cell Carcinoma

Commoner in elderly, males, blacks

Incidence higher in Iran, Central China, S Africa, S Brazil

Dietary factors: Deficiency of vitamins, trace elements;

Fungal contamination of foodstuffs, Nitrites and

nitrosamines

Lifestyle: Alcohol, Tobacco, Betel, Burning hot food,

Urban life

Esophageal disorders: Esophagitis, Achalasia, P-V

syndrome

Genetic: Racial, Celiac disease, Ectodermal dysplasia

ESOPHAGUS: SQUAMOUS CELL CARCINOMA

Insidious onset and late presentation

Dysphagia and obstruction

Extreme weight loss

Ulceration, Tracheo-esophageal fistula,

Prognosis depends on early diagnosis and

treatment.

Prognosis also depends on presence /

absence of lymph node metastases

20% are in upper 1/3

50% are in mid 1/3

30% are in lower 1/3 Three morphological patterns

Polypoid (60%)

Flat (15)

Ulcerated (25%) Early local extension Metastases to

Cervical nodes

Mediastinal nodes

Gastric and celiac nodes

Squamous Cell Carcinoma

ESOPHAGUS: ADENOCARCINOMA

Higher incidence being reported from west

Seen in lower 1/3 of esophagus

Majority arise from Barrett Esophagus (10% risk)

More common above 40 years, in men, in whites

Present with long term dyspepsia, heart burn,

dysphagia, vomiting

Prognosis is poor with < 20% 5 year survival

Adenocarcinoma

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