Pathology Of Esophagus, Stomach, Duedenum

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Reflux oesophagitis, The most frequent cause of oesophagitisis the reflux of gastric juice.

morphology of reflux oesophagitis;

Intraepithelial inflammatory cells: Eosinophiles: early and specific trait, Lymphocytes, Neutrophiles:

Basal hyperplasia: the thickness of basal layerexceeds 20% of epithelial layer

 Elongated papillae with dilated capillaries. Thelength of papillae exceeds 2/3 of epithelial layerthickness.

HIV infection, candida.

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The gross view of oesophageal squamouscell cancer

 Small white elevations in the mucosa inearly stage

 Later: 60% polypoid masses; 15% flat / diffuse , 25% ulcer-like.

Definition: malignant epithelial tumour withglandular differentiation.

Squamous cell cancer;

- Keratinization, intercellular brigdges

- Invasion, metastatsis

- Atypical mitosis

- Nuclear atypia

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Invasive squamous cancer with keratinzatio;

keratinization with cancer

Definition: inflammation in gastric mucosa

Classification by the course:

Acute gastritis; The essence – acute inflammation in gastricmucosa:

Infiltration of neutrophiles

Increased capillary permeability Oedema Haemorrhage Possible erosions: loss of superficial epitheliumgenerating a defect in the mucosa that is limitedto the lamina propria mucosae

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Definition – chronic inflammation in gastricmucosa:Inflammatory infiltrate; Mucosal atrophy;Epithelial metaplasia

morphology of chronic gastritis

Infiltration of lymphocytes and plasmocytes inthe gastric mucosa

Lymphoid follicles

Activity: infiltration of neutrophilic lekocytes Epithelial regeneration

Epithelial metaplasia

Glandular atrophy and / or glandular microcysticdilation

Possible epithelial dysplasia s. intraepithelialneoplasia

Presence of Neutrophils leads to Active acute gastritis!

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H. Pylori;

Peptic cancer, gastritis, lymphoma,

We can see H. pylori in the surface of epithelium

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Chronic gastritis: active secondarylymphoid follicle;

Chronic gastritis: epithelial regeneration;

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Chronic gastritis: epithelial dysplasia;

All the other cells dysplaasia, except one gland in the corner in the left.

Epithelial regeneration in chemical gastritis;

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Gross view of peptic ulcer

Round or elongated, Demarcated, (Elevated margins are more typical for ulcerated carcinoma), Convergence of gastric folds, The basis covered with detritus: necrotic substance, Sometimes thrombosed blood vessels can be seen, The adjacent mucosa is reddish and oedematous due to inflammation.

Four (4) layers in active ulcers:

Necrosis

Non-specific inflammation

Granulations

Scar(fibroblast)

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Gastric Cancer

Epithelial tumours:

Benign: adenoma

Malignant (carcinoma):

- Invasive, Irregular,

Adenocarcinoma:

Intestinal and Diffuse

Signet ring cell cancer

Non-differentiated

Other types

Carcinoid: neuroendocrine tumour (NET)

TNM (2010) of gastric cancer:

TT – the local characteristics of tumour

Tis – intraepithelial carcinoma

T1 – invasion in lamina propria

T2 – invasion in submucosa or lamina muscularis propria

T3 – invasion in the subserosa

T4 – invasion through serosa or in adjacent organs

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Gastric cancer(intestinal type)

Lauren classification of gastric cancer;

Diffuse - Patients with symptoms typically

Intestinal - can grow without symptoms

Lauren classification:

Predicts prognosis;

Different risk factors, precursors and epidemiology

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Gastric Cancer(diffuse type),

Lauren classification of gastric cancer

Diffuse - Specific pattern (signet ring cells), sepcific histochemistry used to see growing tumor cells

Intestinal -

Lauren classification:

Predicts prognosis;

Different risk factors, precursors and epidemiology

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MALT Low Grade lymphoma - highly differentiated

MALT: mucosa – associated lymphoid tissueMALT lymphoma: haematologic malignant tumour developing from mucosal lymphoid cells

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High Grade Lymphoma;

MALT lymphoma: haematologic malignant tumour developing from mucosal lymphoid cells - poorly differentied

- C20 staining

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Active Peptid duentitis

Inflammation

Epithelial damage

Foveolar metaplasia in the epitheliumOedema, small haemorrhages

Brunner gland hyperplasia

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Celiac disease

Intraepithelial lymphocytes: >40 IEL / 100 epithelial cells, CD3+, CD8+

Villous atrophy

Crypt hyperplasia

In European societies, prevalence 0.5 – 1%Chronic disease manifesting by malabsorption

Immune reaction against gluten:

Gluten: major storage protein of wheat and similar grain products

Gliadin: alcohol soluble fraction of gluten. It contains most of the antigens inducing celial disease

The symptoms disappear upon gliadin exclusion from the diet

The morphological changes have diagnostic significance.

T – cell mediated chronic inflammation / autoimmunity

Interaction:

Immune system;

Environmental factors;

Genetic predisposition:

Almost all patients: MHC II HLA-DQ2 or HLA-DQ8 haplotype.

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CD3

Celiac disease - hyperplasia

0. Normal mucosa

1. Infiltrative lesion (IEL)

2. Hyperplastic lesion (IEL + crypt hyperplasia)

3. Destructive lesion (IEL + villous atrophy and crypt hyperplasia): 3a, 3b, 3c

4. Hypoplastic lesion (IEL + atrophy of both villi and crypts

Count 100 intraepitalial cells

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Celiac disease - proliferation in crypts, hyperlasia

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Normal vs Celaic disease

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Whipple disease, caused by bacteria

Etiology –Tropheryma whippeli

Most frequent locations:

Intestines

CNS(mental retardation)

joints

Morphology - thickened epitahlial, macrophage infiltaration, mucosal production