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Diseases of the gastrointestinal tract Diseases of the gastrointestinal tract

Diseases of the gastrointestinal tract - PowerPoint Presentation

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Diseases of the gastrointestinal tract - PPT Presentation

Dr Nesreen Bataineh MD FRCPath STOMACH Congenital disorders Gastric heterotopia Diaphragmatic hernia Pyloric stenosis Gastritis Gastric ulceration Tumors Gastric disorders ID: 909507

gastric gastritis chronic pylori gastritis gastric pylori chronic amp mucosal bacterial acute cells autoimmune inflammatory intestinal production inflammation metaplasia

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Slide1

Diseases of the gastrointestinal tract

Dr.

Nesreen

Bataineh

MD,

FRCPath

Slide2

STOMACH

Slide3

Congenital disorders

Gastric

heterotopia

Diaphragmatic hernia

Pyloric stenosisGastritisGastric ulceration Tumors

Gastric disorders

Slide4

Definition:

“Inflammation of the gastric mucosa”.

Acute gastritis

Chronic gastritis

(majority of cases).Gastritis

Slide5

Definition:

“An acute inflammation of gastric mucosa”.

Usually of a

transient

nature. May be accompanied by hemorrhage and erosion  UGIT hemorrhage.Acute Gastritis

Slide6

Pathogenesis

Acute gastritis is frequently associated with:

Heavy use of

NSAIDs

, particularly aspirin

Excessive

a

lcohol

consumption and heavy

smoking

Severe

stress

(e.g., trauma, burns, surgery)

Anticancer

chemotherapeutic drugs

Systemic bacterial or viral infections

(e.g.,

salmonellosis

or CMV

)

Uremia

Ischemia and shock

Suicidal attempts (e.g., acids and alkali)

Gastric radiation

Mechanical trauma (e.g.,

nasogastric

intubation)

Following

antrectomy

with re

flux of bilious material

Slide7

Slide8

Gross appearance:

Localized (as in NSAID)

OR

diffuse.

Superficial inflammation OR Acute erosive gastritis: Inflammation involves the entire mucosal thickness with hemorrhage & focal erosions. Morphology

Slide9

Acute

errosive

gastritis

Slide10

Microscopic appearance:

Mucosal edema

Inflammatory infiltrate rich in

neutrophils

+ Erosions, hemorrhage & regeneration of epithelial cellsRemoval of the cause may lead to complete restitution of the normal mucosa.Morphology

Slide11

Acute gastritis

Slide12

Depends on the

severity

.

May be asymptomatic

Epigastric pain, nausea and vomitingHematemesis, melena or potentially fatal blood loss. It is one of the major causes of hematemesis.Clinical Features

Slide13

Definition:

“The presence of

chronic inflammatory

changes in the gastric mucosa leading to

mucosal atrophy + epithelial metaplasia”.Chronic Gastritis

Slide14

The major etiologic associations

Chronic infection by H. pylori,

most important

Autoimmune

:

Pernicious anemia (10%)

Toxic:

A

lcohol and cigarette smoking

Postsurgical:

F

ollowing

antrectomy

with

gastroenterostomy

and reflux of bile

Motor and mechanical:

Obstruction, bezoars* ,

and gastric

atony

Granulomatous

conditions

(e.g.,

Crohn

disease)

Miscellaneous:

U

remia, Radiation.

Slide15

The most common GI infection.

A worldwide pathogen with the highest infection rates in

developing countries

(

Low socioeconomic status).In developed countries, the infection rate is 50% in adults > age 50.

Most individuals have

asymptomatic gastritis

~10%

develop peptic ulcer*.

Helicobacter pylori

Slide16

Slide17

H. pylori

is a

noninvasive

curvilinear gram-negative rod.

Mechanism of tissue injuryDirect (Bacterial virulence):Flagella: allow the bacteria to be motile in viscous mucus.

Urease

: generates ammonia from urea

elevating gastric pH around the organisms and protecting it from the acidic secretions.

Adhesins

: enhance bacterial adherence to surface

foveolar

cells.

Toxins

, such as that encoded by

cytotoxin

-associated gene A (

CagA

), proteases and

phospholipase

.

Indirect:

Bacterial products lead to:

production of cytokines as IL-1, IL-6 … that recruits inflammatory cells with subsequent inflammation and tissue damage.

Pathophysiology

Slide18

Antral

-type gastritis (commoner):

High HCL production (

hyperchlohydria

)*.Higher risk for the development of DU.Pangastritis:Multifocal mucosal atrophylow HCL production (hypochlorhydria

)

Increased risk for intestinal

metaplasia

&

adenocarcinoma

.

H. Pylori associated gastritis

Slide19

H. pylori

gastric acid secretion

and impairs duodenal bicarbonate production.

↓ luminal pH in the duodenum.This favor gastric metaplasia in the first part of the duodenum D1. Such metaplastic

foci provide areas for H. pylori colonization.

Peptic

duodenitis

Slide20

Gastric

metaplasia

Slide21

Chronic inflammatory infiltrate in the lamina

propria

.

Predominance of lymphocytes & plasma cell

Neutrophilic infiltration indicates activity.Gland loss and mucosal atrophy. Morphology of chronic gastritis

Slide22

Chronic gastritis

Slide23

H.

pylori

related gastritis

Organisms seen within the mucus layer overlying the superficial mucosal epithelium

Giemsa

Silver

Slide24

Complications

Peptic ulcer

Duodenal

ulcer or gastric ulcer

Intestinal

metaplasia

:

The replacement of gastric epithelium with

intestinal epithelium including goblet cells

.

Dysplasia

Intestinal type

adenocarcinoma

Gastric lymphoma

Marginal zone lymphoma of MALT-type.

H. pylori related gastritis

Slide25

Intestinal

metaplasia

Slide26

High grade dysplasia

Slide27

Clinical Features

Asymptomatic

Upper abdominal discomfort, N & V

May be

hypochlorhydric* (pangastritis), but these persons do not develop achlorhydria or pernicious anemia.Serum gastrin levels are either normal or only modestly elevated. H.pylori associated gastritis

Slide28

Diagnosis:

Noninvasive tests:

Serologic test for anti–

H. pylori antibodies

Fecal bacterial detectionThe urea breath test based on the generation of ammonia by bacterial urease. Invasive tests: (

Antral

biopsy specimen*):

The rapid

urease

test, bacterial culture, or PCR

Histologic

identification of the organism

Treatment:

Triple therapy (two antibiotics and PPIs)

H. Pylori associated gastritis

Slide29

10%

of cases of chronic gastritis

Common in

Scandinavians

. F>M.In association with pernicious anemia*.May be seen with other autoimmune diseases as Hashimoto thyroiditis and Addison diseaseProduction of autoantibodies to parietal cells and intrinsic factor that can be detected in serum and gastric secretions.

Autoimmune gastritis

Slide30

Spares the

antrum

and

cardia.The autoimmune injury leads to gland destruction and diffuse mucosal atrophyLoss of parietal cells & intrinsic factorLoss of gastric acid (hypochlorhydria or achlorhydria)

Reduced serum pepsinogen I levels.

Hypergastrinemia

,

antral

endocrine cell hyperplasia

&

risk of gastric

carcinoid

Increased risk of gastric carcinoma.

Autoimmune gastritis

Slide31

Slide32

H. pylori–Associated

Autoimmune

Loaction

Antrum

Fundus

& body

Inflammatory

infiltrate

Lymphocytes, plasma cells and

neutrophils

Lymphocytes, macrophages

Acid production

Increased to slightly decreased

Decreased

Gastrin

Normal (usually*)

Increased

Other lesions

Hyperplastic

/inflammatory polyps

Neuroendocrine

hyperplasia

Serology

Antibodies to

H. pylori

Antibodies to parietal cells or

intrinsic factor)

Sequelae

Peptic ulcer, adenocarcinoma

Diffuse Atrophy, pernicious anemia, adenocarcinoma,

carcinoid

tumor

Associations

Low socioeconomic status, poverty,

residence in rural areas

Autoimmune disease;

thyroiditis

, diabetes

mellitus, Graves disease

Characteristics of Chronic Gastritis

Slide33

Periumbilical

pain that ultimately localizes to the right lower quadrant.

Nausea, vomiting & low-grade fever.

McBurney’s

sign.Mildly elevated peripheral white cell count.Complications:Appendiceal perforation.Peritonitis.Portal venous thrombosis.Liver abscess.Bacteremia.

Clinical Features

Slide34

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