Lect 4- gastric disord

SMS 2044

Condition CommentPyloric stenosis 1 in 300 to 900 live births

Male to female ratio 3:1

Pathology: muscular hypertrophy of pyloric smooth muscle wall

Symptoms: persistent, nonbilious projectile vomiting in young infant

Diaphragmatic hernia Rare

Pathology: herniation of stomach and other abdominal contents into thorax through a diaphragmatic defect

Symptoms: acute respiratory embarrassment in newbornGastric heterotopia Uncommon

Pathology: a nidus of gastric mucosa in the esophagus or small intestine ("ectopic rest") (The Latin word for "nest“)

Symptoms: asymptomatic, or an anomalous peptic ulcer in adult

Stomach

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Gastric heterotopia

In keeping with the limited sensory apparatus of the alimentary tract, gastric disorders give rise to symptoms similar to esophageal disorders, primarily heartburn and vague epigastric pain.

Gastric mucosa and bleeding, hematemesis or melena may ensue.

Unlike esophageal bleeding, however, blood quickly congeals and turns brown in the acid environment of the stomach lumen.

Vomited blood hence has the appearance of coffee grounds.

Gastritis: includes a myriad of disorders that involve inflammatory changes in the gastric mucosa, including:

Gastritis: is simply defined as inflammation of the gastric mucosa. By far the majority of cases are chronic gastritis, but occasionally, distinct forms of acute gastritis are encountered.

1. Erosive gastritis caused by a noxious irritant

2. Reflux gastritis from exposure to bile and pancreatic fluids

3. Hemorrhagic gastritis

4. Infectious gastritis

5. Gastric mucosal atrophy

Acute Gastritis Acute gastritis is an acute mucosal inflammatory process, usually of a

transient nature. The inflammation may be accompanied by hemorrhage into the mucosa and, in more severe circumstances, by sloughing of the superficial mucosal epithelium (erosion).

This severe erosive form of the disease is an important cause of acute gastrointestinal bleeding.

Pathogenesis: The pathogenesis is poorly understood, in part because normal mechanisms for gastric mucosal protection are not totally clear. Acute gastritis is frequently associated with the following:

Heavy use of nonsteroidal anti-inflammatory drugs (NSAIDs), particularly aspirin

Excessive alcohol consumption Heavy smoking Treatment with cancer chemotherapeutic drugs Uremia Systemic infections (e.g., salmonellosis) Severe stress (e.g., trauma, burns, surgery) Ischemia and shock

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Suicide attempts with acids and alkali Mechanical trauma (e.g., nasogastric intubation) After distal gastrectomy with reflux of bilious material One or more of the following influences are thought to be

operative in these varied settings: disruption of the adherent mucous layer, stimulation of acid secretion with hydrogen ion back-diffusion into the superficial epithelium, decreased production of bicarbonate buffer by superficial

epithelial cells, reduced mucosal blood flow, and direct damage to the

epithelium. Finally, acute infection with H. pylori induces neutrophilic

inflammation of the gastric mucosa, but this event usually escapes the notice of the patient.

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H pylori (most common cause of ulceration) NSAIDs, aspirin Gastrinoma (Zollinger-Ellison syndrome) Severe stress (eg, trauma, burns), Curling ulcers Alcohol Bile reflux Pancreatic enzyme reflux Radiation Staphylococcus aureus exotoxin Bacterial or viral infection

There is a spectrum of severity ranging from extremely localized (as occurs in NSAID-induced injury) to diffuse and from superficial inflammation to involvement of the entire mucosal thickness with hemorrhage and focal erosions.

(Non-steroidal anti-inflammatory drugs)Concurrent erosion and hemorrhage is readily visible

by endoscopy and is termed acute erosive gastritis.

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All variants are marked by mucosal edema and an inflammatory infiltrate of neutrophils and possibly by chronic inflammatory cells.

Regenerative replication of epithelial cells in the gastric pits is usually prominent.

Provided that the noxious event is short lived, acute gastritis may disappear within days with complete restitution of the normal mucosa.

MORPHOLOGY


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Histopathology usually demonstrates increased numbers of eosinophils

Depending on the severity of the anatomic changes, acute gastritis may be entirely asymptomatic,

may cause variable epigastric pain with nausea and vomiting, or may present as overt hematemesis, melena, and potentially fatal blood loss.

Overall, it is one of the major causes of hematemesis, particularly in alcoholics.

Even in certain other settings, the condition is quite common; as many as 25% of persons who take daily aspirin for rheumatoid arthritis develop acute gastritis at some time in their course, many with occult or overt bleeding.

The risk of gastric bleeding from NSAID-induced gastritis is dose related, thus increasing the likelihood of this complication in patients requiring long-term use of such drugs.

Epigastric to left upper quadrant

Frequently described as burning

May radiate to the back

Usually occurs 1-5 hours after meals

May be relieved by food, antacids (duodenal), or vomiting (gastric)

Typically follows a daily pattern specific to patient

Often, a diagnosis can be made based on the patient's description of his or her symptoms, but other methods may be used to verify:

Blood tests: Blood cell count Presence of H. pylori Pregnancy Liver, kidney, gallbladder, or pancreas functions

Urinalysis Stool sample, to look for blood in the stool X-rays ECGs Endoscopy, to check for stomach lining inflammation and

mucous erosion Stomach biopsy, to test for gastritis and other conditions

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Malignancy

Hemorrhage

Perforation Obstruction

Chronic Gastritis is defined as the presence of chronic mucosal

inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia.

It is notable for distinct causal subgroups and for patterns of histologic alterations that vary in different parts of the world.

In the western world, the prevalence of histologic changes indicative of chronic gastritis exceeds 50% in the later decades of adult life.

Schematic presentation of the presumed action of H. pylori in the development of chronic gastritis and peptic ulceration. The histologic features of the two disease conditions are depicted

The most important etiologic association is chronic infection by the bacillus Helicobacter pylori .

This organism is a worldwide pathogen.

Prevalence of infection among adults maybe reached to 80%

it seems to be acquired in childhood and persists for decades. Most individuals with the infection also have the associated gastritis but are asymptomatic.

A – autoimmune B – bacterial (helicobacter) C - chemical

Autoantibodies to gastric parietal cellsHypochlorhydria/achlorhydriaLoss of gastric intrinsic factor leads to malabsorption

of vitamin B12 with macrocytic,megaloblastic anaemia

H. pylori is a noninvasive, non-spore-forming,S-shaped gram-negative rod measuring approximately 3.5 × 0.5 μm.

Adapted to live in association with surface epithelium beneath mucus barrier

Causes cell damage and inflammatory cell infiltration

In most countries the majority of adults are infected

Acute inflammation mediated by complement and cytokines

Polymorphisms infiltrate epithelium and may be partly responsible for its destruction

An immune response is also initiated (antibodies may be detected in serum)

2 patterns of infectionDiffuse involvement of body and antrum (“pan gastritis”

associated with diminishing acid output) Infection confined to antrum (antral gastritis, associate

with increased acid output)

Commonly seen with bile reflux (toxic to cells)

Prominent hyperplastic response (inflammatory cells scanty)

With time – intestinal metaplasia

Gastritis develops owing to the combined influence of bacterial enzymes and toxins and release of noxious chemicals by the recruited neutrophils.

Improvement in the underlying chronic gastritis may take much longer.

Peptic ulcer disease (Helicobacter)Adenocarcinoma (all types)The “African enigma” – are complications of H.pylori

infection less frequent in Africans?Case not yet resolved

Regardless of the cause or histological distribution of chronic gastritis,

the inflammatory changes consist of a lymphocytic and plasma cell infiltrate in the lamina propria, occasionally accompanied by neutrophilic inflammation of the neck region of the mucosal pits.

The inflammation may be accompanied by variable gland loss and mucosal atrophy.

When present, H. pylori organisms are found nestled within the mucus layer overlying the superficial mucosal epithelium.

MORPHOLOGY

A Steiner silver stain demonstrates the numerous darkly stained H. pylori organisms along the luminal surface of the gastric epithelial cells. Note that there is no tissue invasion by bacteria.

In the autoimmune variant, loss of parietal cells is particularly prominent.

Two additional features are note. Intestinal metaplasia refers to the replacement of gastric

epithelium with columnar and goblet cells of intestinal variety.

This is significant, because gastrointestinal-type carcinomas appear to arise from dysplasia of this metaplastic epithelium.

Second, H. pylori-induced proliferation of lymphoid tissue within the gastric mucosa has been implicated as a precursor of gastric lymphoma


Chronic inflammatory cell infiltration

Mucosal atrophyIntestinal (goblet cell)

metaplasia

Seen in Helicobacter and autoimmune gastritis (not chemical)

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Chronic gastritis with lymphoid follicle formation in the gastric mucosa (arrow)Some gastric glands are still found (arrowhead).

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Chronic gastritis with chronic inflammatory cell infiltration and lymphoidfollicle formation (arrowhead) in the gastric mucosa. Atrophy of the gastric glands is seen.(arrow). (M: mucosa, and SM: submucosa)

Clinical Features

Chronic gastritis usually causes few or no symptoms; upper abdominal discomfort, nausea and vomiting.When severe parietal cell loss occurs in the setting of autoimmune gastritis, hypochlorhydria or achlorhydria (referring to levels of gastric luminal hydrochloric acid) and hypergastrinemia are characteristically present.

Individuals with chronic gastritis from other causes may be hypochlorhydric, but because parietal cells are never completely destroyed, these patients do not develop achlorhydria or pernicious anemia.

Serum gastrin levels are usually within the normal range or only modestly elevated.

Most important is the relationship of chronic gastritis to the development of peptic ulcer and gastric carcinoma.

The long-term risk of gastric carcinoma for persons with H. pylori-associated chronic gastritis is increased about five-fold relative to the normal population.

For autoimmune gastritis, the risk for cancer is in the range of 2% to 4% of affected individuals, which is well above that of the normal population.

Ulcers are defined as a breach in the mucosa of the alimentary tract that extends through the muscularis mucosa into the submucosa or deeper.

This is to be contrasted to erosions, in which there is a breach in the epithelium of the mucosa only.

Erosions may heal within days, whereas healing of ulcers takes much longer.

Although ulcers may occur anywhere in the alimentary tract, none are as prevalent as the peptic ulcers that occur in the duodenum and stomach.

Peptic Ulcers Peptic ulcers are chronic, most often solitary (single), lesions that

occur in any portion of the gastrointestinal tract exposed to the aggressive action of acid-peptic juices.

At least 98% of peptic ulcers are either in the first portion of the duodenum or in the stomach, in a ratio of about 4:1.

GASTRIC ULCERATION

Focal, acutely developing gastric mucosal defects may appear after severe stress and are designated stress ulcers.

Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. Stress ulcers are most commonly encountered in the following conditions: Severe trauma, including major surgical procedures,

sepsis, or grave illness of any type Extensive burns (the ulcers are then referred to as

Curling ulcers) Traumatic or surgical injury to the central nervous system

or an intracerebral hemorrhage (the ulcers are then called Cushing ulcers)

Chronic exposure to gastric irritant drugs, particularly NSAIDs and corticosteroids

The pathogenesis of these lesions is uncertain and may vary with the setting.

The systemic acidosis that can accompany severe trauma and burns, for example, may contribute to mucosal compromise presumably by lowering the intracellular pH of mucosal cells alreadyrendered hypoxic by impaired mucosal blood flow.

With cranial lesions, direct stimulation of vagal nuclei by increased intracranial pressure is proposed, because gastric acid hypersecretion has been documented in these patients.

Neurogenic or catecholamine-induced vasoconstriction

Mucosal ischemia

Damage the mucosal barrier

Directly injure mucosal cells by oxygen or metabolic deprivation


Acute stress ulcers are usually circular and small (less than 1 cm in diameter).

The ulcer base is frequently stained a dark brown by the acid digestion of extruded blood.

Unlike chronic peptic ulcers, acute stress ulcers are found anywhere in the stomach.

They may occur singly, but more often they are multiple, located throughout the stomach and duodenum

Microscopically, acute stress ulcers are abrupt lesions, with essentially unremarkable adjacent mucosa.

Multiple stress ulcers of the stomach, highlighted by the dark digested blood in their bases.

MORPHOLOGY


They range in depth from very superficial lesions (erosion) to deeper lesions that involve the entire mucosal thickness (true ulceration).

The shallow erosions are, in essence, an extension of acute erosive gastritis.

The deeper lesions comprise well-defined ulcerations but are not precursors of chronic peptic ulcers.

Even the deeper lesions do not penetrate the muscularis propria.

A high percentage of patients admitted to hospital intensive care units with sepsis, severe burns, or trauma acutely develop superficial gastric erosions or ulcers.

These may be of limited clinical consequence or life-threatening.

Although prophylactic antacid regimens and blood transfusions may blunt the impact of stress ulceration,

the single most important determinant of clinical outcome is the ability to correct the underlying condition.

The gastric mucosa can recover completely if the patient does not die from the primary disease.

Clinical Features

Normal Acute gastritis

Chronic gastritis Atrophic gastritis

Intestinal metaplasia

Dysplasia Cancer

(FIgure 2). Four zones of active peptic ulcer. The necrotic fibrinoid debris and nonspecific

inflammatory infiltrate are labeled by arrowhead.

Beneath the necrotic and inflammatory zones, there is granulation tissue (arrow).

Below the granulation tissue, fibrotic tissue is seen (F).

Figure 3). Necrotic fibrinoid debris and inflammatory infiltrate in the ulcer base.

Figure 4). Granulation tissue in the ulcer base. New blood vessels lined by plump endothelial cells (arrow). Edema and inflammatory infiltrate are also seen.

(Figure 5). Fibrotic tissue beneath the ulcer base

(Figure 8) Intestinal metaplasia in chronic gastritis. The gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow). The intestinal epithelium has goblet cells. Chronic inflammatory cell infiltration is also seen.

(Figure 7) Chronic gastritis with intestinal metaplasia (arrow) seen in the mucosa around the peptic ulcer. The mucinous gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow).

An ulcer is distinguished from an erosion by its penetration through the muscularis mucosa or the muscular coating of the gastric or duodenal wall occurring as a result of acid and pepsin attack

The lesion of peptic ulcer disease (PUD) is a disruption in the mucosal layer of Sites:Duodenum (DU)Stomach (GU)OesophagusGastro-enterostomy stomaRelated to ectopic gastric mucosa (e.g. in Meckel’s

diverticulum)

Etiology of PUD

Normal

Increased AttackHyperacidity, Zollinger Ellison syndrome.

Weak defenseStress, drugs, smokingHelicobacter pylori*

Peptic ulcer disease results from the imbalance between defensive factors that protect the mucosa and offensive factors that disrupt this important barrier.

Mucosal protective factors include the water-insoluble mucous gel layer, local production of bicarbonate, regulation of gastric acid secretion, and adequate mucosal blood flow.

Aggressive factors include the acid-pepsin environment, infection with Helicobacter pylori, and mucosal ischemia


Peptic ulcers are remitting, relapsing lesions that are most often diagnosed in middle-aged to older adults, but they may first become evident in young adult life.

They often appear without obvious precipitating influences and may then heal after a period of weeks to months of active disease.

Even with healing, however, the propensity to develop peptic ulcers remains.

Genetic or racial influences appear to play little or no role in the causation of peptic ulcers.

Duodenal ulcers are more frequent in patients with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism.

With respect to the last two conditions, hypercalcemia, whatever its cause, stimulates gastrin production and, therefore, acid secretion.


There are two key facts. First, the fundamental requisite for peptic ulceration is

mucosal exposure to gastric acid and pepsin. Second, there is a very strong causal association with H.

pylori infection.

Despite the clarity of these two statements, the actual pathogenesis of mucosal ulceration remains murky.

It is best perhaps to consider that peptic ulcers are induced by an imbalance between the gastroduodenal mucosal defenses and the countervailing aggressive forces that overcome such defenses.

Pathogenesis

Both sides of the imbalance are considered. The array of host mechanisms that prevent the gastric mucosa from being digested like a piece of meat include the following: Secretion of mucus by surface epithelial cells Secretion of bicarbonate into the surface mucus, to create a

buffered surface microenvironment Secretion of acid- and pepsin-containing fluid from the gastric pits

as "jets" through the surface mucus layer, entering the lumen directly without contacting surface epithelial cells

Rapid gastric epithelial regeneration Robust mucosal blood flow, to sweep away hydrogen ions that

have back-diffused into the mucosa from the lumen and to sustain the high cellular metabolic and regenerative activity

Mucosal elaboration of prostaglandins, which help maintain mucosal blood flow.

Among the "aggressive forces," H. pylori is very important, because this infection is present in 70% to 90% of patients with duodenal ulcers and in about 70% of those with gastric ulcers.

Furthermore, antibiotic treatment of H. pylori infection promotes healing of ulcers and tends to prevent their recurrence.

Hence, much interest is focused on the possible mechanisms by which this tiny noninvasive spiral organism tips the balance of mucosal defenses.

The possible mechanisms are as follows: Although H. pylori don’t invade the tissues, it induces an

intense inflammatory and immune response.

Common infection10% of men, 4% women develop PUD *Positive in 70-100% of PUD patients.1st Part of duodenum > antrum > G-E junction.H.pylori related disorders:

Chronic gastritis – 90%Peptic ulcer disease – 95-100%Gastric carcinoma – 70%Gastric lymphomaReflux Oesophagitis.Non ulcer dyspepsia

Bacteria over epithelial cells

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H. pylori secretes a urease that breaks down urea to form toxic compounds such as ammonium chloride and monochloramine.

The organisms also elaborate phospholipases that damage surface epithelial cells.

Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in the gastric mucus, thus weakening the first line of mucosal defense.

Epithelial injury is also caused by a vacuolating toxin (VacA). Another toxin encoded by the cytotoxin-associated gene A (CagA) is a powerful stimulus for the production of IL-8 by the epithelial cells.

H. pylori enhances gastric acid secretion and impairs duodenal bicarbonate production, thus reducing luminal pH in the duodenum.

Several H. pylori proteins are immunogenic, and they evoke a robust immune response in the mucosa.

Both activated T cells and B cells can be seen in chronic gastritis caused by H. pylori.

The B lymphocytes aggregate to form follicles. The role of T and B cells in causing epithelial injury is not established, but T-cell-driven activation of B cells may be involved in the pathogenesis of gastric lymphomas.

Gram negative, Spirochete. Does not invade cells Colonize Gastric mucosa only * Common cause of Duodenal ulcer * ? Urease Breakdown urea ammonia high

pH reflex acid prod… Protease Break down mucosa expose

epithelium for digestion. Chronic infl. Gastric Metaplasia Ulceration. Complications: Bleeding, perforation, stenosis,

Carcinoma.

NSAIDs are the major cause of peptic ulcer disease in patients who do

not have H. pylori infection.

The gastroduodenal effects of NSAIDs range from acute erosive gastritis and acute gastric ulceration to peptic ulceration in 1% to 3% of users.

Risk factors for NSAID-induced gastroduodenal toxicity are increasing age, higher dose, and prolonged usage.

Thus, those who take these drugs for chronic rheumatic conditions are at particularly high risk.

Suppression of mucosal prostaglandin synthesis is the key to NSAID-induced peptic ulceration.

Inhibition of prostaglandin synthesis increases secretion of hydrochloric acid and reduces bicarbonate and mucin production.

Loss of mucin degrades the mucosal barrier that normally prevents acid from reaching the epithelium.

Some NSAIDs can penetrate the gut mucosal cells as well. By mechanisms not clear, some NSAIDs also impair angiogenesis, thus impeding the healing of ulcers.

o Alcohol has not been proved to directly cause peptic ulceration, but alcoholic cirrhosis is associated with an increased incidence of peptic ulcers.

o Corticosteroids in high dose and with repeated use promote ulcer formation.

o Even in the era of H. pylori, there are compelling arguments that personality and psychological stress are important contributing factors, although data on cause and effect are lacking.

o Finally, mention should be made of the Zollinger-Ellison syndrome. This is associated with multiple peptic ulcerations in the stomach, duodenum, and even jejunum, owing to excess gastrin secretion by a tumor and, hence, excess gastric acid production.

o Chronic gastritis is extremely common among patients with peptic ulcer disease, and H. pylori infection is almost always demonstrable in those patients with gastritis.

o Similarly, patients with NSAID-associated peptic ulcers do not have gastritis unless there is coexistent H. pylori infection.

o This feature is helpful in distinguishing peptic ulcers from acute gastric ulceration, because gastritis in adjacent mucosa is generally absent in the latter condition.


Peptic ulcer of the duodenum. Note that the ulcer is small (2 cm) with a sharply punched-out appearance. Unlike cancerous ulcers, the margins are not elevated. The ulcer base shows a small amount of blood but is otherwise clean. Compare with the ulcerated carcinoma .

Medium-power detail of the base of a nonperforated peptic ulcer, demonstrating the layers of necrosis (N), inflammation (I), granulation tissue (G), and scar (S) moving from the luminal surface at the top to the muscle wall at the bottom.

All peptic ulcers, whether gastric or duodenal, have an identical gross and microscopic appearance.

By definition, they are defects in the mucosa that penetrate at least into the submucosa, and often into the muscularis propria or deeper.

Most are round, sharply punched-out craters 2 to 4 cm in diameter.

Those in the duodenum tend to be smaller, and occasional gastric lesions are significantly larger.

Favored sites are the anterior and posterior walls of the first portion of the duodenum and the lesser curvature of the stomach.

The location within the stomach is dictated by the extent of the associated gastritis:

antral (antrum) gastritis is most common, and the ulcer is often along the lesser curvature at the margin of the inflamed area and the upstream acid-secreting mucosa of the corpus.

Occasional gastric ulcers occur on the greater curvature or anterior or posterior walls of the stomach, the very same locations of most ulcerative cancers.

Classically, the margins of the crater are perpendicular and there is some mild edema of the immediately adjacent mucosa, but unlike ulcerated cancers there is no significant elevation or beading of the edges.

The base of the crater appears remarkably clean, owing to peptic digestion of the inflammatory exudate and necrotic tissue.

Infrequently, an eroded artery is visible in the ulcer (usually associated with a history of significant bleeding).

If the ulcer crater penetrates through the duodenal or gastric wall, a localized or generalized peritonitis may develop.

Alternatively, the perforation is sealed by an adjacent structure such as adherent omentum, liver, or pancreas.

o The histologic appearance varies with the activity, chronicity, and degree of healing.

o In a chronic, open ulcer, four zones can be distinguished:o (1) the base and margins have a thin layer of necrotic fibrinoid debris

underlain by----------------------- o (2) a zone of active nonspecific inflammatory infiltration with neutrophils

predominating, underlain by --------------------------

o (3) granulation tissue, deep to which is-------------------------- o (4) fibrous, collagenous scar that fans out widely from the margins of the

ulcer. o Vessels trapped within the scarred area are characteristically thickened

and occasionally thrombosed, but in some instances they are widely patent.

o With healing, the crater fills with granulation tissue, followed by re-epithelialization from the margins and more or less restoration of the normal architecture (hence the prolonged healing times).

o Extensive fibrous scarring remains.

Histologic Appearance

Most peptic ulcers cause epigastric gnawing, burning, or boring pain, but a significant minority first come to light with complications such as hemorrhage or perforation.

The pain tends to be worse at night and occurs usually 1 to 3 hours after meals during the day.

Classically, the pain is relieved by alkalis or food, but there are many exceptions.

Nausea, vomiting, bloating, belching, and significant weight loss (raising the specter of some hidden malignancy) are additional manifestations.

Bleeding is the chief complication, occurring in up to one third of patients, and may be life-threatening.

Pain or discomfortBloatingA feeling of fullness -- people with severe dyspepsia

are unable to drink as much fluid as people with mild or no dyspepsia

Hunger and an empty feeling in the stomach, often 1 - 3 hours after a meal

Mild nausea (vomiting may relieve symptoms)Regurgitation (sensation of acid backing up into the

throat)BelchingOccasionally, symptoms of GERD are present

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Obstruction of the pyloric channel is rare. Malignant transformation is unknown with duodenal

ulcers and is very rare with gastric ulcers. The latter event is always open to the possibility that

carcinoma was present from the outset.

Peptic ulcers are notoriously chronic, recurrent lesions-they more often impair the quality of life than shorten it. When untreated, the average individual requires 15 years for healing of a peptic ulcer.

Nevertheless, with present-day therapies (including antibiotics active against H. pylori), most ulcer victims can be helped if not cured, and they usually escape the surgeon's knife.


Diagram of aggravating causes of, and defense mechanisms against, peptic ulceration.

Stomach is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression.

Ulcer margins are perpendicular and present chronic gastritis.

During the active phase, the base of the ulcer shows 4 zones : Inflammatory exudate, Fibrinoid necrosis, Granulation tissue and Fibrous tissue.

The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis. (H&E, ob. x7)

Sharp edges, converging folds of mucosa in the upper half. The ulcer bed is covered by fibrinopurulent exudate.

Chronic peptic ulcer (stomach)

During the active phase, the base of the ulcer shows 4 zones :

inflammatory exudate - at the lumen(cell debrisand, neutrophils)

fibrinoid necrosis (yellow in van Gieson staining and pink in H&E)

granulation tissue

mature fibrous tissue (abundant collagen - red in van Gieson staining and pink in H&E, profound, spreading beneath ulcers margins, producing mucosal retraction - radiating folds).

This fibrous layer may contain vessels with thickened walls or with thrombosis (H&E, ob. x10)



(Figure 1) Peptic ulcer of stomach (arrow). The whole mucosa and part of submucosa are denuded.(M: mucosa, SM: submucosa, MP: muscularis propria)

Pancreas

Pancreas

Ulcer

Ulcer

MucosaMucosa

(Figure 6). Fibrosis in the muscularis propria (arrow). Chronic inflammatory cell infiltration is also noted (arrowhead).

(Figure 8) Intestinal metaplasia in chronic gastritis. The gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow). The intestinal epithelium has goblet cells. Chronic inflammatory cell infiltration is also seen.

(Figure 7) Chronic gastritis with intestinal metaplasia (arrow) seen in the mucosa around the peptic ulcer. The mucinous gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow).


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Lect 4- gastric disord

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