New GIT 1Dr Basu

Part I: Oral Cavity diseases, Vocal cord, salivary gland

Part II: EsophagusStomach

Dr Amitabha Basu MBBS, MD

Part I

Oral Cavity diseases, Vocal cord, salivary gland

Oral Cavity diseases

Tumors and tumor like condition

Tumors and tumor like condition: Oral cavity

Papilloma Epithelial tumor, Benign lesion (a Squamous papilloma)

Leukoplakia Irregular white mucosal plaque

Squamous papilloma has fibro vascular stalk

Also seen in vocal cord : singers nodules: where

talking/ singing is a profession !

Leukoplakia

Description → Leathery, white, discrete areas of mucosal thickening.

Microscopy→ Hyperkeratosis + dysplasia or carcinoma in situ of squamous epithelium.

Risk factors → Chronic friction, Alcohol abuse.

Types → Hairy leukoplakia ,

Verrucous leukoplakia,

Erythroplasia.

Hairy leukoplakia: factsEtiology:Almost exclusive to HIV infection, Often EBV infection alsoMorphology:“Hairy” white plaques on oral mucosa caused by epithelial thickeningLab: CD 4 cell count (low below 200 cells/cumm).

Carcinoma of oral cavity

Risk factors → Leukoplakia, Alcohol abuse, Tobacco use, HPV (types 16, 18, and 33), Protracted irritation.

Molecular pathology

Activation of cyclin-dependent kinase.

Type of neoplasm→

Squamous cell carcinoma

HPV infection: koilocytosis

Squamous cells with white cytoplasmic vacuole and curved nuclei

Study other similar picture

Prognosis

• Lips and early detection – Lower lip - commonest

• 90% survive for 5 years without recurrence.

– Floor of mouth, Base of tongue, pharynx : Poor prognosis

Favored site for metastasis : cervical Lymph node

Neoplasms of vocal cords

• Benign: Squamous papilloma: – in vocal cord and larynges: singers

nodule.– HPV infection: koilocytic change.

Singers nodule

Malignant tumor of vocal cord: large white necrotic mass : Squamous cell carcinoma.

Salivary gland lesions

• Sialadenitis: inflammation

• Neoplasms

Sialadenitis : Etiology• Viral

– Mumps (esp. parotids)– Other organ

involvement in mumps• Acute Pancreatitis (

↑ serum amylase) • Mumps Orchitis

( infertility)

• Bacterial: due to– Ductal obstruction– Dehydration

• Immunological : Sjogren's syndrome

Sialadenitis

Acute Bacterial infection

Neutrophils infiltrating the parotid gland.

Chronic autoimmune

(Sjogren's / Sicca syndrome).

Dry mouth and eye

Fibrosis, lymphoid infiltrates & Acinar atrophy.

Type of ANA present = SS-A and SS-B autoantibody

Tumors of salivary glands

Pleomorphic adenoma

Parotid gland, and other glands

MOST common

Benign.

Can recur,

Malignant transformation rare

Papillary Cystadenoma

Lymphomatosum

Or,

Warthin tumor

Benign, may be bilateral

Pleomorphic adenoma

• A mixed tumor• Gross: Capsulated• Micro:

– Chondroid region + myoepithelial cells in myxoid stroma

Gross and micro

C

myxoid stroma

myoepithelial cells

WARTHINS TUMOR

SECOND MOST COMMON SALIVARY GLAND TUMOR

Gross: capsulated

Micro:

1. Double layer epithelial (oncocyte) CELLS.

2. LYMPHATIC STROMA WITH GERMINAL CENTERS.

2 layers of oncocyte or oxyphilic cells, lymphoid stroma

Let us relax : Part II

Esophagus

1. Tracheoesophageal fistula

2. Esophageal web

3. Esophageal Achalasia

4. Mallory Weiss Syndrome

5. Esophageal varices

6. Gastroesophageal reflux

1. Esophagitis

2. BARRETT ESOPHAGUS

Esophagus

Tracheoesophageal fistula

Associated with Artesia of esophagus.

Complication: aspiration of gastric content after birth and LUNG abscess.

Esophageal web

Plummer Vinson syndrome

Weblike protrusion of esophageal mucosa.

Morphology: Dysphagia.

Tracheoesophageal fistula

Esophageal web

Microcytic hypo chromic anemia,

chance of Cancer.

Esophageal Achalasia

Definition: Failure of relaxation of LES

Etio-pathogenesis: Loss of ganglion cells in myenteric plexus(often by Trypanosoma Cruzi- south America)

Gross: proximal dilatation of esophagus.

Clinical: Progressive dysplasia and regurgitation.

X- ray and gross:

rat tail (bird beak) appearance of lower esopgahous

Study other similar picture

MALLORY WEISS SYNDROME

• Def: Longitudinal Tears of the mucosa of esophagus at GE Junction

• Occur after violent retching or vomiting.

• Cause: – Retching IN ALCOHOLIC stupor – Also in non alcoholic without

any history [Hiatal hernia].Study other similar picture

Clinical:

• Sudden Hematemesis: fresh blood ( usually not profuse )

• Blood mixed with gastric contents or mucus

• Light-headedness, dizziness, or syncope

• Complication: Boerhaave syndrome (is rupture of the esophagus- massive hematemesis may

occur )

?

Esophageal varices

• Def: Dilated submucosal esophageal veins in lower third of esopgahous .

• Cause: Portal hypertension following alcoholic cirrhosis.

• Effect: Result in massive upper GI hemorrhage when ruptured.

Gross and micro

Dilated and thrombosed vessels on

the sub mucosa

Gastroesophageal reflux disease

• Etiology: Sliding Hiatal hernia and incompetent lower esophageal sphinter, alcohol, Scleroderma.

• Complications: Reflux Esophagitis, Barrett esophagus

• Clinical: heart burn , relieved by antacids.

BARRETT ESOPHAGUS

• Morphology: columnar epithelial metaplasia of esophageal squamous epithelium.

• Complications: esophageal adenocarcinoma (lower 1/3rd of esophagus).

Columnar epithelial metaplasia with goblet cellsor, Intestinal metaplasia → adenocarcinoma

Esophageal Squamous cell Carcinoma

Etiopathogenesis Alcohol, tobacco, HPV ( High risk groups), smoking.

Type of tumor Squamous cell carcinoma

Morphology Upper 2/3rd of esophagus.

Gross: tumor with central necrosis and microscopy of SCCA

Clinical Progressive weight loss, dysphagia.

central necrosisStudy other similar picture

End of esopgahous

Disease of Stomach

Stomach

• Pyloric stenosis

• Menetrier disease

• Gastritis

• Peptic ulcer

• Malignant tumors

Pyloric stenosis

• Congenital.• More in male• Cause: hypertrophy of the circular muscle• Clinical:

– Outlet obstruction, Projectile vomiting.– First 2 weeks of life.– Oval mass upper abdomen.– Association with Turner syndrome (45, X0)

/ Edward syndrome (Trisomy 18).

Multifactorial inheritance

• If present in female – more chance (than male) that she will pass this disease to her offspring.

• So, If a child with PS is female:– the likelihood of having a future son with PS is

one in five. – the likelihood of having a future daughter with

PS is one in 14.

Gastritis

• Acute hemorrhagic gastritis

• Chronic gastritis

Acute hemorrhagic gastritis

Def: acute inflammation, erosion and hemorrhage in present in gastric mucosa.

Cause : aspirin, NSAIDs, smoking, burns, brain injury, stress, uremia, post surgery.

Gastric erosion: acute gastritis

Time for chronic gastritis

Chronic inflammation → atrophy of gastric mucosa = atrophic gastritis

Autoimmune gastritis Helicobacter pylori associated gastritis

Pernicious anemia:

site: fundus

Site: antrum

Reduced acid secretion Curved, gram negative and silver

stain (GMS) positive rod

In duodenum

• Auto-antibodies to parietal cell or intrinsic factors are present in the serum.• Megaloblastic amenia.•Peripheral (nerve) myelin loss.

Autoimmune gastritis• Atrophic gastric mucosa + intestinal metaplasia

(goblet cells) + few lymphocytes

Increased chance of gastric carcinoma

Helicobacter pylori associated gastritis

• Mucosa shows acute and chronic inflammatory cells+ atrophy + silver stain positive curved organism.↑ chance of both gastric carcinoma / lymphoma

Peptic ulcer

• Location

• Etiology

• Pathogenesis

• Morphology

• Complication

Peptic ulcer

• Location: 1. Duodenum : first portion

[ common]

2. Stomach, usually antrum

3. In Zollinger-Ellison syndrome [multiple non healing ulcers]

4. Meckel diverticulum that contains ectopic gastric mucosa.

Peptic ulcer of the duodenum

Etiology and pathogenesis

1. Etiology: 1. H. pylori ( more with duodenal ulcer than gastric

ulcer), chronic use of NSAIDs, Aspirin, Cigarette smoking, Corticosteroids.

2. Pathogenesis:• Increased secretion of hydrochloric acid and pepsin

and reduced mucosal defence.

Duodenal peptic ulcer- DU

• More common than gastric • Etiology :

– H.pylori (100%), Blood group O– Zollinger-Ellison syndrome ( gastrinoma):

multiple non healing ulcer.– Increased gastric emptying

• Location: Anterior wall: first portion of duodenum• C/F: Pain which is relieved by food.

Gastric ulcer

Small, oval ( 1-3 cm), single

Punched out margins

Clean ulcer base

Benign or Malignant?

C/F: Pain aggravated by food.

Benign vs malignant gastric ulcer

Small, oval ( 1-3 cm), single

Large

Punched out margins Rolled up ( heaved up) margins

Clean ulcer base Necrotic base

Complications: Peptic ulcer

• Bleeding: more with DU

• Perforation: more with DU

• Obstruction : due to edema and scarring: more with DU

• Cancer: more with gastric ulcer.

Time for gastric tumors

Menetrier disease

Adenocarcinoma

Menetrier disease• Enlarged gastric rugal fold-

like brain.• Massive foveolar

hyperplasia• Reduced gastric acid• Reduced serum protein

( protein loosing enteropathy- edema, low plasma protein).

Gastric tumors: facts

• Age: >50 years• Sex: Men, Blood Group A: frequent• Geographic Location: More in Japan,

Finland, Iceland, less in USA.

• Anatomical location: The lesser curvature of the antropyloric region.

Etiology: Gastric CA

1. H.Pylori (Chronic atrophic gastritis)

2. Nitrosamine: smokes fish and vegetable, pickle ( preservative > Japan).

3. Increased salt and low fresh food intake.

Morphology

Adenocarcinoma ( always)

• Early– Early gastric carcinoma-is defined as a

lesion confined to the mucosa and submucosa.

• Advanced– neoplasm that has extended below the

submucosa into the muscular wall.

Morphology of advanced Gastric carcinoma

• Gross Micro Etiology

Exophytic

( polypoid)

Intestinal type of malignant glands

Associated with H.Pylori

Infiltrating or diffuse

Signet ring cells in all layers of stomach

Not associated with H.Pylori

Intestinal type of malignant glands

Infiltrating or diffuse

• Also known as: linitis plastica

• Diffuse infiltration of malignant cells in the stomach.

• Produce ‘leather bottle’ stomach: small shrunken stomach.

linitis plastica

Diffuse type: signet ring cells(contain mucin in the cytoplasm): poorly differentiated

Other facts

• Metastasis– To the left supraclavicular sentinel

(Virchow) node: hypothetical first lymph node.

• Metastasize to both ovaries : Krukenburg tumor.

• Prognosis: poor• Hematemesis and melena- black stool +.

Prognosis depends on Grading

• Well differentiated tumor : well formed glands, small in size, less mitosis : good prognosis.

• Moderate differentiated (more irregular glands but still identifiable) : intermediate prognosis.

• Poorly differentiated (predominant unrecognizable glands and cells): bad prognosis

• Undifferentiated : barely recognizable primary tissue: very bad prognosis

• Anaplastic: bizarre and large cells, more mitosis: worse prognosis

Thank you