4. Mucous: Mucus, Pepsinogen Ii
Chief: Pepsinogen I, Ii
Parietal: Acid
Enteroendocrine: Histamine, Somatostatin,
Endothelin
5. Stomach
Condition Comment
Pyloric 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 newborn
Gastric 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
8. 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
9. 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.
10. 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
12. Suicide attempts with acids and alkali
Mechanical trauma (e.g., nasogastric intubation)
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.
14. 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.
Concurrent erosion and hemorrhage is readily visible
by endoscopy and is termed acute erosive
gastritis.
14
18. 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 patient
vomiting, or may present as overt hematemesis, melena,
and potentially fatal blood loss.
19. 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
19
21. 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.
22. 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
23. A – autoimmune
B – bacterial (helicobacter)
C - chemical
Autoimmune chronic gastritis
Autoantibodies to gastric parietal cells
Hypochlorhydria/achlorhydria
Loss of gastric intrinsic factor leads to malabsorption of
vitamin B12 with macrocytic, megaloblastic anaemia
24. Commonly seen with bile
reflux (toxic to cells)
Prominent hyperplastic
response (inflammatory
cells scanty)
26. 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.
27. 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
29. Histological F.
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. A Steiner silver stain
The inflammation may be demonstrates the numerous darkly
stained H. pylori organisms along
accompanied by variable gland loss the luminal surface of the gastric
and mucosal atrophy. epithelial cells. Note that there is
no tissue invasion by bacteria.
30. In the autoimmune variant, loss of parietal cells is
particularly prominent.
Intestinal metaplasia refers to the replacement of gastric
epithelium with columnar and goblet cells of intestinal
variety.
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
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32. Chronic gastritis with lymphoid follicle formation in the gastric mucosa
(arrow)
Some gastric glands are still found (arrowhead). 32
33. Chronic gastritis with chronic inflammatory cell infiltration and lymphoid
follicle formation (arrowhead) in the gastric mucosa.
Atrophy of the gastric glands is seen.(arrow). (M: mucosa, and SM:
submucosa)
33
35. Normal Acute gastritis
Atrophic gastritis
Chronic gastritis
Intestinal Dysplasia Cancer
metaplasia
36. GASTRIC ULCERATION
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.
37. 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
38. Neurogenic or catecholamine-induced vasoconstriction
Mucosal ischemia
Damage the mucosal Directly injure mucosal cells by
barrier oxygen or metabolic deprivation
41. MORPHOLOGY
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
Multiple stress ulcers of the
Microscopically, acute stress ulcers are stomach, highlighted by the
abrupt lesions, with essentially dark digested blood in their
unremarkable adjacent mucosa. bases.
43. Etiology of PUD
Normal
Increased Attack
Hyperacidity, Zollinger
Ellison syndrome.
Weak defense
Stress, drugs, smoking
Helicobacter pylori*
44. 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
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46. Pathogenesis
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.
47. 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.
48. 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.
The possible mechanisms are as follows:
Although H. pylori don’t invade the tissues, it induces
an intense inflammatory and immune response.
51. 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.
52. H. pylori enhances gastric acid secretion and impairs
duodenal bicarbonate production, thus reducing
luminal pH in the duodenum.
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.
53. 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.
54. 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.
55. 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.
56.
57.
58. All peptic ulcers, whether gastric or duodenal, have an
identical gross and microscopic appearance.
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.
59. 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.
60.
61.
62. Histologic Appearance
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
o (2) a zone of active nonspecific inflammatory infiltration with neutrophils
predominating,
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.
63. FIgure 2).
(
Four zones of active peptic ulcer.
The necrotic fibrinoid debris and nonspecific
inflammatory infiltrate are labeled by arrowhead.
Figure 3). Necrotic fibrinoid debris
Beneath the necrotic and inflammatory zones, and inflammatory infiltrate in the
there is granulation tissue (arrow).
Below the granulation tissue, fibrotic tissue is
ulcer base.
seen (F).
64. Figure 4). Granulation tissue in the ulcer
base.
New blood vessels lined by plump (Figure 5). Fibrotic tissue beneath
endothelial cells (arrow). Edema and the ulcer base
inflammatory infiltrate are also seen.
65. (Figure 7) Chronic gastritis with (Figure 8) Intestinal metaplasia in chronic
intestinal metaplasia (arrow) seen in gastritis. The gastric foveolar epithelium
the mucosa around the peptic ulcer. (arrowhead) is replaced by intestinal type
The mucinous gastric foveolar of epithelium (arrow). The intestinal
epithelium (arrowhead) is replaced epithelium has goblet cells. Chronic
by intestinal type of epithelium inflammatory cell infiltration is also
66. 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.
