Gastroduodenal Pathology Updated Sri

8/8/2019 Gastroduodenal Pathology Updated Sri

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Stomach


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Gastritis

Inflammation of stomach wall

Acute gastritis- polymorphs- epithelium

Chronic gastritis-

Lymphocytes & plasma cells in lamina propriaintestinal metaplasia

atrophy of mucosa

H pylori infection


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Classification of Chronic Gastritis

Distribution in stomach, associated other

morphological features1. Autoimmune chronic atrophic gastritis

2. H Pylori chronic gastritis- diffuse antral ormultifocal gastric atrophy

3. Chemical Gastritis (reactive gastritis,

reactive gastropathy)


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Autoimmune chronic atrophic gastritis

Site- gastric body with sparing of antrum,

not associated with H pyloriGastric parietal cells and intrinsic factor

(IF) auto-antibodiesFailure to absorb Vit B12 due to lack of IF-

megaloblastic anaemia

Risk of carcinoma - 10% in 20 years.


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H pylori associated gastritis Gram negative bacteria.

Rod shaped organism, resides

on surface of epithelial cells &mucus

Identified by urease testonstomach bx.

Organism produces a potenturease which splits urea intoammonia.

Diffuse antral and Multifocal

chronic atrophic gastritis


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Helicobacter pylori:

Most common infection in the world (50% of

worlds population; 80% asymptomatic)

10% of men, 4% women develop PUD * Positive in 70%-100% of PUD patients.

H.pylori related disorders (Hp is present in):

Chronic gastritis 90%

Peptic ulcer disease 95%-100%

Gastric carcinoma 70%

Gastric lymphoma

Reflux Oesophagitis.

Non ulcer dyspepsia


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H. pylori


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H. pylori H & E stain


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H. pylori silver stain


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Chemical gastritis/ reactive gastritis

Seen in association with:

- Bile reflux: surgery, direct bile injury

- NSAIDs (eg naproxen, indomethacin,

ibuprofen) (decreased prostaglandinswhich protect from acid damage)

Damage to mucosa, minimal inflammation

Elongation and tortuosity of foveolae


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Treatment of gastritis

Aim at H pylori eradication - risk ofcarcinoma and lymphoma

Intestinal metaplasia and autoimmunegastritis - increased risk of gastriccarcinoma

Triple therapy for 7 d effective in 90%cases

- Clarithromycin 500mg bd

- Amoxycillin 1g bd/ metronidazole400 mgbd

- PPI (eg omeprazole 20mg bd)


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Inflammation acute gastritis


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Acute gastritis


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Chronic atrophic gastritis


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Haemorrhage - gastritis


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Peptic Ulcer - mechanismUlceration in GI tract.

Basic principle: Gastric acid secretion bypeptic cells; Protection of mucosa bygastric mucus production

Due to increased gastric acid +/- decreasedmucosal resistance to gastric acid(produced by gastric peptic cells)

Effect occurs in non-acid secreting mucosa


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Classification, site & risk factors

Erosion (mucosa only), Acute (mucosa andsubmucosa), Chronic (till muscle coat)

Sites - Stomach (antrum), Duodenum (1st

part), Lower oesophagus, Jejenum,Meckels diverticulum, Umbilicus

Blood group O; Toxic/ injuries- burns, drugs,cigarette smoking.


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Erosion & Acute Peptic Ulcer - causes

Acute stress

Severe illness Sepsis

Burns (Curlings ulcer)

Post surgical op

CNS neurological

disturbance(Cushings Ulcer)

Trauma (stress ulcer)

Long term steroids Aspirin and NSAID

injestion,

Lye* pretzels, ricedumpling, noodles

Radiotherapy

*USP 2009


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Erosion & Acute PU - features

Wide distribution in stomach, first few cm

of duodenumMucosa (erosion) and submucosa (Acute

PU)

Small, often multiple, upto 1-2 cmdiameter

Main symptoms and signs- due tohaemorrhage

Usually heal completely without scarring


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Erosion


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Chronic PU Stomach

Chronic Gastric Ulceration (GU), age 50+

>90% are solitary, approx 5% multiple

junction between gastric antrum and body onlesser curve approx 5cm from pylorus,

Morphology- extends through muscle coat,fibrosis - stomach/ duodenal wall distorted

Round, oval or linear ulcer, convergingmucosal folds, fibrous tissue base


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Gastric ulcer


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Chronic PU Microscopic features

Similar for GU, DU other sites

Floor- covered with pus.

Base- fibrosis extending till muscle wall

Adjacent mucosa, vessels inflamed(granulation)

Fibrosis- adhesions to pancreas,omentum, liver +/- local perforation


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Chronic Duodenal Ulcer (DU)M>> F , blood group O

Usually single , rarely multiple. Associated with gastric acid hypersecretion +/-

decreased mucosal resistance

Within first 2 cm of duodenum- less commonly2nd part duodenum

Punched out ulcer, fibrosis- distortion of

duodenumComplications - Healing & scarring, Perforation,

Haemorrhage, ? carcinoma


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Duodenal ulcer


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Giant gastric ulcer


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Chronic ulcers Diagnosis & Rx- Radiology- ulcer seen on barium meal

- Endoscopy- visualise, photograph andbiopsy

Medical Rx antacids, H2 blockers, >

80% heal in 1 month medical treatmentRemove cause- chronic NSAIDs

Indications for surgery - failure of medicalTx, complications, recurrence, Giant ulcer


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Stomach tumoursBenign Tumours

Adenomas

Leiomyoma

Malignant Tumours

Adenocarcinoma

Lymphoma

Endocrine Tumours -carcinoids

GI Stromal Tumours

Leiomyosarcoma Kaposis Sarcoma


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Gastric Cancer 2nd most common

tumour

1,100,000 affected in2008-09 (850,000deaths)

Diet, Bile reflux, HPylori, DNA damage(point mutations in E-

cadherin gene), Bloodgroup A

SE AsiaE Asia (Korea,China, Taiwan, Japan)

Africa

rest ofEurope

E Europe

N AmericaS America (Chile,Venezuela)

LowHigh


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Gastric adenocarcinoma and diet

High risk:

Preserved food (nitrites derived from

nitrates)High intake of nitrate Smoked/cured

meat/fish

High intake of complexcarbohydrates chiefly derived from

grains and tuberous roots

High intake of salt/ Pickled

vegetables/ Chilli peppersLow intake of protein, green, leafy

vegetables and fruits


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Gastric Adenocarcinoma and diet

Benefits of fruit and

vegetablesanti-oxidant effect

Key protective agents-

Ascorbic acid, alphatocopherol,

carotenoids, folate,

Role unclear- alcohol,tobacco


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Helicobacter pyloriCauses :

Chronicgastritis

Decreased acid

secretion.

Decreased intra gastric

ascorbic acid

Increased oxidants

Results of these:

Intestinal metaplasiaIncreased pH-

nitrosated products

(carcinogens)Loss of anti-oxidant

DNA point mutations


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Definitions for Gastric cancers

Intraepithelial neoplasia= confined to

surface epithelium (dysplasia)Intramucosal carcinoma= invasion of lamina

propria

Early Gastric Cancer= carcinoma confinedto mucosa or into submucosa

Advanced Gastric cancer = invasion deeperthan submucosa

G t i Ad i


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Gastric Adenocarcinoma

Symptoms and Signs

Often very late in presentation

Persistent abdominal pain, unrelieved byeating, bleeding (ulceration),haematemesis, gastric outlet obstruction,anorexia & weight loss (disseminateddisease)

Diagnosis- endoscopy, multiple punch biopsy,barium meal, MRI for staging.


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Morphology

Localization of tumour

Pylorus and antrum

Cardia

Other areasLesser curvature

Greater curvature

Body : Ant/ post walls

Prevalence

50 to 60%

25%

15 to 25% 40%

12%

48%

G t i Ad i


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Gastric Adenocarcinoma

macroscopic appearance

Commonest site- distal stomach (antro-

pyloric region, followed by body ofstomach- greater or lesser curve

Advanced Gastric Cancer- polypoid,fungating, ulcerative, infiltrative

Linitis plastica-diffusely infiltrative leather

bottle stomach contracted

Gastric adenocarcinoma


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Gastric adenocarcinoma

Microscopic classification

WHO classification

Tubular adenoca

Papillary adenoca

Mucinous ca

Signet ring cell adenoca

Undifferentiated

Adenosquamous

Lauren classification

Intestinal ca

Diffuse infiltrative ca


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Diffuse type Intestinal type

More frequent in youngerage groups, little difference

between sexes.

Arise from gastric mucosalcells, not associated with

chronic gastritis.

No glandular pattern seen.Signet ring cells or smallclusters in infiltrativepattern.

More frequent in malesand at older age

groups. Arise from gastric

mucosal cells that haveundergone intestinalmetaplasia (due to chrgastritis).

Better differentiated,

resemble colonicadenocarcinoma.


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EGC


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Ad f i i l


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Adenco ca of intestinal type


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Li iti l ti


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Linitis plastica


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Spread


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Spread

Direct spread

Transcoelomic dissemination into peritoneal cavity.

Spread into oesophagus/ pancreas/ liver/ common bile

duct/ diaphragm/ spleen and transverse colon.Krukenberg tumour : Secondary deposits in both ovaries-

from stomach (& breast, pancreas, GB)

Lymphatic spread

Regional lymph nodes (lesser/ greater curvature)

Involvement of the supraclavicular lymph node(Virchows sign ) in some cases.

Haematogenous spreadTo liver ,lungs, brain, bones, kidneys /adrenals.

Complications


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Complications

Haemorrhage : haematemesis +/- melaena.

Obstruction: especially in the pyloric antrum.

Perforation: due to necrosis and penetrationthrough all the layers.

Jaundice: when there is extension into thecommon bile duct / porta hepatis

Ascitis : Fluid accumulation in the peritoneum

Staging and prognosis


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Staging and prognosis

TNM staging. Required for both treatment, follow up andpredicting prognosis.

TX = primary tumour (T) cannot be assessed

T0 = no evidence of primary tumour

Tis = carcinoma in situ, no lamina propria invasion

T1 = tumour invades lamina propria or submucosa

T2 = tumour invades muscularis propria/subserosa

T3 = tumour penetrates serosa without invasion of

adjacent structures T4 = tumour invades adjacent structures .

Gastric Carcinoma Prognosis


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Gastric Carcinoma Prognosis

Early Gastric Cancer- small mucosal lesions

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Gastroduodenal Pathology Updated Sri