GIT

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.

Chapter 1

* 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.

Pyloric stenosis

Menu
B
F

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.
AUTOIMMUNE GASTRITIS:



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.

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 infectionColonization of gastric mucousUrease ammonia neutralization of acid  Rebound acid production.Protease – Mucous and glycoprotein break down.Weak mucosal resistanceAcid & Pepsin digestion of mucosaDeeper than just mucosaSingle, 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 lymphomaReflux Oesophagitis.Non ulcer dyspepsia

Helicobacter pylori

Gram negative, Spiral bacilli SpirochetesDo not invade cells – only mucousBreakdown urea - ammoniaBreak down mucosal defenseChronic Superficial inflammation2- 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

Base ofUlcer
Active granulation tissueproliferating small blood vessels fibroblasts, Inflammatory cells
Eroded artery
Base of Ulcer – Rt. Side of image

Peptic ulcer

Normalgastricmucosa
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

Complications:

Bleeding – Chronic-IDA, Acute, MassiveFibrosis, Stricture obstruction – pyloric stenosis.Perforation – Peritonitis- emergency.Gastric carcinoma. (not duodenal ca)

Gastric peptic ulcer:

Gastric peptic ulcer:

Gastric Ulcer

Duodenal Peptic Ulcer

Gastric Ulcer

Peptic ulcer - Endoscopy

Gastric Ulcer

Gastric 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
EndoscopyBarium meal – contrast x-rayBiopsy – bacteria & malignancyH.Pylori:Endoscopy cytologyBiopsy – Special stainsCulture - difficultUrease 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 (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.3rd most common GI malignancy (after colorectal and pancreatic)14th cause of cancer related death in U.S.85-95% are caused by adenocarcinoma15% are caused by Non-Hodgkin’s 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 causePernicious anemiaChronic atrophic gastritisGastric polypAchlorhydria Barrett’s esophagusHaving had a Billroth 2 procedureGenetic factors include:First degree relativesType 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 jaundiceEnlarged 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:

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

GastricLymphoma
Gastriccarcinoma
BenignUlcer
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

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