Gastric disorder

SMS 2044

Mucous: Mucus, Pepsinogen Ii

Chief: Pepsinogen I

Parietal: Acid

Enteroendocrine: Histamine, Somatostatin, Endothelin

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,blood quickly congeals and turns brown in the acid

environment of the stomach lumen.Vomited blood hence has the appearance of coffee

grounds.

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).

Pathogenesis: The pathogenesis is poorly understood, in part because normal mechanisms for gastric mucosal protection are not totally clear.

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

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All variants are marked by :Mucosal edema Inflammatory infiltrate of

neutrophils and possibly by chronic inflammatory cells.

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

Erosion and hemorrhage is readily visible by endoscopy and is termed acute erosive gastritis.

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,

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 patientvomiting, or may present as overt hematemesis, melena,

and potentially fatal blood loss.

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 Endoscopy, to check for stomach lining inflammation and

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

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Chronic Gastritis is defined as the presence of chronic mucosal

inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia.

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

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

Autoimmune chronic gastritis

Autoantibodies to gastric parietal cellsHypochlorhydria/achlorhydriaLoss of gastric intrinsic factor leads to malabsorption of vitamin B12 with macrocytic, megaloblastic anaemia

Commonly seen with bile reflux (toxic to cells)Prominent hyperplastic response

(inflammatory cells scanty)

Common infection10% of men, 4% women develop PUD *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

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.

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

Causes cell damage and inflammatory cell infiltration

In most countries the majority of adults are infected

Peptic ulcer disease (Helicobacter)Adenocarcinoma (all types)

1. Lymphocytic and plasma cell infiltrate in the lamina propria, occasionally accompanied by neutrophilic inflammation of the neck region of the mucosal pits.

2. Gland loss and mucosal atrophy.

3. Intestinal metaplasia refers to the replacement of gastric epithelium with columnar and goblet cells of intestinal variety.

4. lymphoid tissue within the gastric mucosa has been implicated as a precursor of gastric lymphoma

5.

Histological F.

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.

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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. Hypochlorhydria or achlorhydria (referring to levels of gastric luminal hydrochloric acid) Hypergastrinemia are characteristically present.

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

Normal Acute gastritis

Chronic gastritis Atrophic gastritis

Intestinal metaplasia

Dysplasia Cancer

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.

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

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

Neurogenic or catecholamine-induced vasoconstriction

Mucosal ischemia

Damage the mucosal barrier

Directly injure mucosal cells by oxygen or metabolic deprivation

Fig. 40-14


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.

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

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)

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.

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.

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

Etiology of PUD

Normal

Increased AttackHyperacidity, Zollinger Ellison syndrome.

Weak defenseStress, drugs, smokingHelicobacter pylori*

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

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

mucosal exposure to gastric acid and pepsin. • At pH level 3.5 or more, stomach acid is neutralizedSecond, there is a very strong causal association with H.

pylori infection.

Mucosa can continually repair itself except in extreme instances

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

Pathogenesis

The array of host mechanisms that prevent the gastric mucosa from being digested like a piece of meat include the following:

1. Secretion of mucus by surface epithelial cells include the water-insoluble mucous gel layer.

2. Secretion of bicarbonate into the surface mucus, to create a buffered surface microenvironment.

3. 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

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4. 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

5. Mucosal elaboration of prostaglandins (Vasodilation ), which help maintain mucosal blood flow.

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

an intense inflammatory and immune response.

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.

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.

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

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.

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

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.

1. defects in the mucosa that penetrate at least into the submucosa, and often into the muscularis propria or deeper.

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

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

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

Morphology

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

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

7. If the ulcer crater penetrates through the duodenal or gastric wall, a localized or generalized peritonitis may develop and adjacent structure such as adherent omentum, liver, or pancreas could be affect.

o In open ulcer, four zones can be distinguished:

o (1) The base and margins have a thin layer of necrotic fibrinoid debris.

o (2) Fibrous, collagenous scar that fans out widely from the margins of the ulcer.

o (3) Granulation tissueo (4) a zone of active nonspecific inflammatory infiltration with

neutrophils predominating

Histologic Appearance

(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).

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 discomfortA 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)Occasionally, symptoms of GERD are presentObstruction of the pyloric channel is rare.

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


(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

Neutralize stomach acidCalcium

Tums, RolaidsAluminum + Magnesium

Maalox, Riopan, Mylanta, GelusilSodium

Alka-SeltzerMagnesium

Milk of Magnesia

Standard Therapy14-16 daysBismuth subsalicylate (Pepto Bismol)MetronidazoleTetracycline

Newest TreatmentHelidac (three antibiotic regimen)


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Health & Medicine

Gastric disorder