5-6 git pdf - dr nadia

GASTROINTESTINAL TRACT Lec 5-6 TUCOM-DEP. OF PATHOLOGY

Disorders of the Stomach

CONGENITAL ANOMALIES:

 1- Diaphragmatic Hernia.

 2- pyloric stenosis.

 3- Pancreatic and gastric heteretopia.

Diaphragmatic Hernia.

 Weakness or partial to total absence of a region of a diaphragm,

usually on the left may permit the abdominal content to herniate into
the thorax. (away from hiatal orifice).

 In utero, neonatal, adult presentation.

 Differ from the hiatal hernia in that the defect in the diaphragm does

not involve the hiatal orifice.

 Hernial wall composed of peritoneum and pleura.

 Usually the stomach or small bowel and even part of liver accompany

it, lethal respiratory embarrassment in the newborn.

Pyloric stenosis

 Called as congenital hypertrophic pyloric stenosis.

 Affects male three to four times more often than females.

Congenital Hypertrophic Pyloric Stenosis:

• Clinical manifestations

 Symptoms develop during third and

fourth week of life or in second week.

 Non bilious vomiting

 Vomiting increases in frequency and

becomes projectile

• Diagnosis

 History

 Palpated firm, ovoid palpable mass in the epigastrium with visible

peristalsis.

 Occur due to hypertrophy and possibly hyperplasia of the muscularis

properia of pylorus.

GASTRITIS

 DEF: inflammation of gastric mucosa.

 ACUTE G:

 .transient.

 .hemorrhage into mucosa.

 .asymptomatic, may cause nausea, vomiting and epigastric pain or

bleeding in severe cases.

 .Micro. Neutrophilic infiltration, erosion, and purulent exudate.

PATHOGENESIS:

•  .Heavy use of NSAIDs especially aspirin.
•  .Excessive alcohol consumption.
•  .heavy smoking.
•  .Chemotherapy, uremia, systemic infections.
•  .Severe stress, (trauma, burn, surgery).
•  .Ischemia, suicidal, (acid and alkali).
•  .Irradiation.
•  .intubation.
•  (increase  acid  sec,  decrease  bicarbonate,  direct  damage  to  mucus

layer, damage to epithelium).

Acute Esophagitis & Gastritis

CHRONIC GASTRITIS

 Is the presence of chronic mucosal inflammatory changes leading

eventually to mucosal atrophy and epithelial metaplasia, usually in the
absence of erosions.

Pathogenesis:

 .The major etiologic associations are:

 1- pernicious anemia. (immunologic)
 2- chronic infection (H. pylori).

 3- Toxic. (alcohol, cigarette).
 4- post surgical ( antrectcomy and gastro enterostomy)

 5- motor and mechanical.
 6- radiation.

 7- granulomatous conditions.
 8- Miscellaneous ( graft VHD , amyloidosis, uremia).

AUTOIMMUNE GASTRITIS:

 CALLED AS DIFFUSE CORPORAL ATROPHIC GASTRITIS:

 Auto antibodies = parietal cells and intrinsic factor.



result in gland destruction and atrophy and loss of acid production.

 IF Ab == PA.

 Associated with other autoimmune diseases.

CHRONIC INFECTION:

 S- shaped G- ve.

 antrum and corpus.

 increase with age, with 50% of asymptomatic adults over 50 Y.

 mechanism in gastritis unclear but may be H. pylori colonization of

mucosa may be damaged by other events leads to retarded healing
and inflammation.

 also role of metabolic cellular alterations due to infection, bacterial

toxins, and host inflammatory response.

 RESPONSE TO ANTIMICROBIALS.

 risk of ulcer and cancer.

MORPHOLOGY
GROSS:

 reddened, coarser texture than normal. May be flattening of the

mucosa. Sometimes, there is thick folds.

 differ according to type or cause or severity of the disease.

Microscopy:

 In early stages there is lymphocytes and plasma cell infiltration in

lamina properia, if limited to upper third = chronic superficial gastritis.

 In severe cases there is inflammatory cell infiltration in all mucosa

thickness with lymphoid aggregates.

 Additional features include:

 1- activity: if neutrophils, active gastritis.
 2- regenerative changes: enlarged hyperchromatic cells with mitotic

activity in mucosal cells.

 3- metaplasia: columnar absorptive cells, goblet intestinal cells.
 4- atrophy: loss in glandular structure .
 5- H pylori found on mucosal cells seen by different stains in antrum

of 95% of active cases, but absent in areas of intestinal metaplasia.

 6- dysplasia cytologic changes with atypia in severe cases.

Clinical features

 Nausea, vomiting and upper abdominal discomfort.

 With severe parietal loss in autoimmune gastritis hypochlorhydria and

achlorhydria.

 Circulating gastric autoantibodies.

 Pernicious anemia in 10%.

 Relation with peptic ulcer.

 Long term risk of carcinoma in gastric atrophy in

about 2-4%.

Gastric ulceration

Definition:

 Ulceration (breach in mucosa) due to acid & pepsin attack – peptic

ulcer.

Esophagus & Stomach Normal Normal Stomach

1-Peptic ulcer

 Is a chronic, most often

solitary, lesions that
occur in any portion of
the

gastrointestinal

tract exposed to the
aggressive action of
acid-

Etiology of PUD

Normal

Increased Attack

Hyperacidity

Weak defense

Helicobacter

pylori*

Stress, drugs,
smoking

Imbalance between gastroduodenal mucosal defense mechanisms and

the damaging forces.

Etiology:

 Helicobacter pylori infection.
 Hyperacidity - eg. Zollinger Ellison. (increased gastrin and acid

secretion).

 Drugs - anti-inflammatory (NSAIDs) & impaired defense cause

suppression of prostaglandin synthesis, and direct irritative.

Corticosteroids promote ulcer.

 Cigarette smoking impairs healing and favors recurrence.
 Rapid gastric emptying

 Personality and stress
 Alcohol in cirrhotic patients.

Pathogenesis:

1-Helicobacter pylori infection

 Colonization of gastric mucous

 Urease ammonia neutralization of acid  Rebound acid

production.

 Protease – Mucous and glycoprotein break down.

 Weak mucosal resistance

 Acid & Pepsin digestion of mucosa

 Deeper than just mucosa

 Single, punched out, clean base.

 Chronic Ulceration

 Most common infection in the world (20%)

 10% of men, 4% women develop PUD *

 Positive in 70-100% of PUD patients.

 H.pylori related disorders:

 Chronic gastritis – 90%

 Peptic ulcer disease – 95-100%

 Gastric carcinoma – 70%

 Gastric lymphoma

 Reflux Oesophagitis.

 Non ulcer dyspepsia

 Gram negative, Spiral bacilli

 Spirochetes

 Do not invade cells – only mucous

 Breakdown urea - ammonia

 Break down mucosal defense

 Chronic Superficial inflammation

2- Gastric acid and pepsin

Peptic Ulcer Morphology:

 90% ulcers in first portion of duodenum or lesser curvature of

stomach(4:1).

 80 to 90% cases single ulcer. Round Small ulcers with sharply

punched out edges* It has a smooth clean base with puckering of
surrounding mucosa and the mucosal folds are radiating from the
crater in a spoke like fashion.

 Small <2cm, clean base*.

 Microscopy: 4 zones.

 Superficial necrotic layer.

 Inflammatory cells zone.

 Granulation tissue zone

 Collagenous scar layer.

Complications:

 Bleeding – Chronic-IDA, Acute, Massive

 Fibrosis, Stricture obstruction – pyloric stenosis.

 Perforation – Peritonitis- emergency.

 Gastric carcinoma. (not duodenal ca)

Base of Ulcer Eroded artery

Active granulation tissue
proliferating small blood Base of Ulcer – Rt.Side of image
vessels fibroblasts,
Inflammatory cells

Normal
gastric
mucosa

Gastric mucosa
demonstrating S-
shaped bacilli
Helicobacter pylori

In addition to
lymphocytes
And plasma cells in the
lamina properia,
neutrophils
are visible within the
epithelium above the
basement membrane

Gastric peptic ulcer

Peptic ulcer – Endoscopy Duodenal Peptic Ulcer

Gastric Ulcer Gastric Ulcer

Gastric Ulcer



Punched out ulcer



Clean base



Small single



Radiating mucosal
folds.



Benign ulcer.



No tumor.

Peptic Ulcer Microscopy Perforation

Peptic Ulcer

PUD - Diagnosis

 Endoscopy

 Barium meal – contrast x-ray

 Biopsy – bacteria & malignancy

 H.Pylori:

  Endoscopy cytology
  Biopsy – Special stains
  Culture - difficult
  Urease Breath test.

Points to Remember:

 A peptic ulcer is a sore in the lining of the stomach or duodenum due

to attack by acid & Pepsin.

 The major cause - H. pylori bacterium. Others are NSAIDs. spicy food,

stress are risk factors.

 H. pylori can be transmitted from person to person through close

contact

 A combination of antibiotics and H pump inhibitors is the most

effective treatment.

Helicobacter pylori

Urease production test H. Pylori organisms- silver st.

Toludine Blue stain – H pylori

ACUTE GASTRIC ULCERATYION

 Focal, acutely developing gastric mucosal defects may appear

following severe stress so called as: stress ulcer.

 Usually multiple, mainly in the stomach.

 From erosion to deep ulcer.
 Seen in : shock, extensive burns (Curling’s ulcer in proximal

duodenum), sever trauma, head injury (Cushing’s ulcer), drugs (
NSAIDs).

 Intracranial lesions associated with vagal stimulation and increased

gastric secretions.

Morphology

Gross:

 usually less than 1 cm, circular and small. Rarely deep.
 anywhere in the stomach.
 rugae normal, margins and base not indurated.

Micro:

 Abrupt lesions.
 suffusion of blood into mucosa and sub mucosa, no scar.
 heal by complete re epitheialization.

Clinical course

 In 5-10% of patients admitted to intensive care unit.
 May be asymptomatic or may create an emergency due to bleeding.
 1- ability to correct underlying condition.

2- antacid.
3- blood transfusion.

HYPERTROPHIC GASTROPATHY

 a group of uncommon conditions with enlarged and giant rugae,

caused not by inflammation, but by hyperplasia of the mucosal
epithelial cells.

 1- Menetrier’s disease : hyperplasia of surface mucous cells with

glandular atrophy.

 2- hypertrophic hypersecretory gastropathy: hyperplasia of parietal

cells and chief cells within the glands.

 3- Zollinger-Ellison syndrome: gastric gland hyperplasia secondary to

excessive gastrin secretions in gastrinoma.

CLINICAL IMPROTANCE:

 1- mimic infiltrative carcinoma or lymphoma on radiology.

 2- peptic ulcer risk.

 old age , male 3:1 , present with epigastric discomfort, diarrhea,

weight loss, and sometimes bleeding.

 protein loss, hypoalbuminemia.

 Prone to metaplasia and carcinoma.

Tumours of the stomach and duodenum



Polyp

: is any nodule or mass that projects above the level of the

surrounding mucosa.

 Any lesion in the wall may project to lumen but the term is restricted

to mucosal lesions.

 Most (90%), are non neoplastic, small, sessile and multiple in 25%.

Usually in setting of chronic gastritis and has no malignant potential.

 Tumors of mucosal origin benign or malignant may present as

polypoid lesions.

Adenoma

 Benign called as adenoma, that has malignant potential and has

proliferative dysplastic cells.

 5-10% of polyps of stomach.

 Gastric adenomas called also as adenomatous polyps present as

sessile or pedunculated (with stalk) mostly in distal portion of the
stomach.

 Up to 40% of gastric adenomas contain a focus of carcinoma at the

time of diagnosis, and the risk of cancer is 30% in near mucosa.

 Usually arise in chronic gastritis with prominent intestinal

metaplasia.

INTRODUCTION

Benign



Polyps



Non neoplastic



Hyperplastic



Fundic gland



Neoplastic



Adenomas



Tumors



Adenomas



Leiomyomas



Lipomas

Malignant



Tumors



Carcinoma 90-
95%



Lymphoma 4%



Carcinoid 3%



Sarcoma 2%

Gastric carcinoma

Epidemiology:

 World wide, incidence vary, high in Japan, Chile, Costa Rica,

Colombia, China, Portugal, Iceland, Finland, Scotland.

 Lower in UK, US, Canada, Australia, New Zealand, Greece, Honduras

and Sweden.

 3

most common GI malignancy (after colorectal and pancreatic)

 14

cause of cancer related death in U.S.

 85-95% are caused by adenocarcinoma

 15% are caused by Non-Hodgkin’s lymphoma & leiomyosarcomas
 H. pylori: 80 percent of gastric carcinomas result from H. pylori due

to the result of free radicals

 Dietary nitrates (bacteria in stomach breaks down nitrites to

compounds that are carcinogenic in animals)

 Hypochlorhydria: occurs in gastric atrophy and promotes bacterial

growth in stomach

 Foods such as starch, pickled vegetables, salted fish and meat,

smoked foods and salt

 People who smoke cigarettes or use alcohol are 3-5 times more likely
 Epstein-Barr virus is now implicated as a cause

 Pernicious anemia

 Chronic atrophic gastritis
 Gastric polyp

 Achlorhydria
 Barrett’s esophagus

 Having had a Billroth 2 procedure

 Genetic factors include:

 First degree relatives

 Type A blood

Anatomy of the stomach

location

 37% in the proximal third of the stomach

 30% in the distal stomach

 20% in the midsection

 Remaining 13% in the entire stomach

 Pylorus and antrum= 50-60%.

 Cardia= 25%.

 Body and fundus= 40%.

 Greater curvature=12%.

Clinical features: Onset

 Insidious (slowly developing)

 Usually discovered in advanced stages

 Men>Women

 Occurs between the ages of 50-70

 Increased mortality in

 Japanese

 Costa Ricans
 Chileans

  Native Americans
  African Americans
  Scandinavians

Assessment

 History:

 High risk foods
 Alcohol/tobacco use

  Treated for H. Pylori infection
  Gastritis, pernicious anemia, gastric surgery, polyps
  Immediate family dx gastric cancer

 Blood type

Physical Assessment

 Early gastric cancer

 Indigestion

 Abdominal discomfort initially relieved with antacids

 Feeling of fullness

 Epigastric, back, or retrosternal pain

 NOTE: most people will show no clinical manifestations

 Advanced stage:

 Nausea/vomiting

 Obstructive symptoms

 Iron deficiency/anemia

 Palpable epigastric mass

 Enlarged lymph nodes

 Weakness/fatigue

 Progressive weight loss

Evidence of metastatic cancer

 Abdominal mass, ascites or jaundice

 Enlarged Virchow’s node ( supraclavicular n.)

 Sister Mary Joseph’s node (infiltration of the umbilicus)

 Blumer’s shelf( a mass in pelvic cul-de-sac)

 Krukenberg’s tumor( enlarged ovaries on PE)

Diagnosis: Labs

 Decreased hematocrit and hemoglobin

 Macrocytic or microcytic anemia (decreased vit.B12 and iron

absorption)

 Stool positive for occult blood

In Advanced stages:

 Hypoalbuminemia

 Bilirubin and alkaline phosphate will be abnormal

 Increased level of carcinoembryonic antigen

Radiographic assessment

 Double contrast upper GI series

 C.T.

 Esophago -gastroduodenoscopy (EGD)

 Endoscopic ultrasound (EUS)

 Other findings include

 Polypoid mass

 Ulcer crater

 Thickened fibrotic gastric wall

Morphology: Gross:

1. polypoid/ fungating carcinoma

2. Ulcerating/ penetrating carcinoma( 70% )

3. Infiltrating / scirrhous carcinoma = linitis plastica( 5~15% )

4. Superficial spreading carcinoma = confined to mucosa / submucosa;

5-year survival of 90%

5. Advanced carcinoma

GASTRIC CARCINOMA



Gastric tumors - 2 to 4 per cent of

upper GI bleeds



Gastric lymphoma usually located in

the corpus. Prognosis better.



Helicobacter pylori

has

been

associated to the development of

mucosa-associated lymphoid tissue

(MALT). Major role of H. pylori in the

development of MALT lymphoma

Benign
Ulcer

Gastric
carcinoma

Gastric
Lymphoma

Linitis Plastica – Schirrhous Carcinoma

Fungating Carcinoma

Gastric Carcinoma

linitis plastica

1. histo: frequently signet ring cell type+ increase fibrous tissue

2. Firmness, rigidity, reduced capacity of stomach, a peristalsis in

involved area

3. Granular/ polypoid fold with encircling growth

Microscopy:

 It has two histologic subtypes, intestinal and diffuse, according to

Laurens classification.

 Intestinal composed of neoplastic intestinal glands as colonic

adenocarcinoma, with expanding growth pattern.

 Diffuse composed of gastric type mucous cells not forming glands

but permeate in mucosa and arrange as scattered cells or small
clusters in infiltrative growth pattern. The mucin expand the cells
and push nucleus to periphery creating signet-ring cells. Associated
fibrosis and rigidity occur due to mucin causing desmoplastic
reaction.

Gastric adenocarcinoma