GIT word

Disorders of the Stomach

Lecture 3
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

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).

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%.


Definition:
Ulceration (breach in mucosa) due to acid & pepsin attack peptic ulcer.

Normal Stomach



Esophagus & Stomach Normal
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-peptic juices.
Etiology of PUDNormalIncreased Attack HyperacidityWeak 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
Helicobacter pylori:
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
Helicobacter pylori
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.
Peptic Ulcer




Peptic ulcer

Complications:
Bleeding Chronic-IDA, Acute, Massive
Fibrosis, Stricture obstruction pyloric stenosis.
Perforation Peritonitis- emergency.
Gastric carcinoma. (not duodenal ca)

Gastric peptic ulcer:




Gastric Ulcer
Punched out ulcer
Clean base
Small single
Radiating mucosal folds.
Benign ulcer.
No tumor.
Peptic Ulcer
Peptic Ulcer Microscopy:
Perforation:





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.
H. Pylori organisms- silver st.
Helicobacter pylori
Toludine Blue stain H pylori
Urease production test
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 (Curlings ulcer in proximal duodenum), sever trauma, head injury (Cushings 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- Menetriers 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.


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.
3rd most common GI malignancy (after colorectal and pancreatic)
14th cause of cancer related death in U.S.
85-95% are caused by adenocarcinoma
15% are caused by Non-Hodgkins lymphoma & leiomyosarcomas


Etiology

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
Etiology cont.
Epstein-Barr virus is now implicated as a cause
Pernicious anemia
Chronic atrophic gastritis
Gastric polyp
Achlorhydria
Barretts 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
Physical Assessment cont.
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 Virchows node ( supraclavicular n.)
Sister Mary Josephs node (infiltration of the umbilicus)
Blumers shelf( a mass in pelvic cul-de-sac)
Krukenbergs 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:
polypoid/ fungating carcinoma
Ulcerating/ penetrating carcinoma( 70% )
Infiltrating / scirrhous carcinoma = linitis plastica( 5~15% )
Superficial spreading carcinoma = confined to mucosa / submucosa; 5-year survival of 90%
Advanced carcinoma
Endoscopic View - Differential
GASTRIC CARCINOMA
Gastric Carcinoma
Linitis Plastica  Schirrhous Carcinoma.
Fungating Carcinoma
linitis plastica
histo: frequently signet ring cell type+ increase fibrous tissue
Firmness, rigidity, reduced capacity of stomach, a peristalsis in involved area
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









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