Gastric Disorder

1. SMS 2044

4. Mucous: Mucus, Pepsinogen Ii
Chief: Pepsinogen I
Parietal: Acid
Enteroendocrine: Histamine, Somatostatin,
Endothelin

5. 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
Stomach

6. 6
Gastric heterotopia

7.  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.

8. 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

11. 11

12. 12

13.  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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15. 15
Histopathology usually demonstrates
increased numbers of eosinophils

16.  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.

17.  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
17

18. 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.

19.  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

20. Commonly seen with bile reflux (toxic to cells)
Prominent hyperplastic response
(inflammatory cells scanty)

21.  Common infection
 10% 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 lymphoma
 Reflux Oesophagitis.
 Non ulcer dyspepsia

22. 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.

23.  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

24. Peptic ulcer disease (Helicobacter)
Adenocarcinoma (all types)

25. 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
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.

26. 26
Chronic gastritis with lymphoid follicle formation in the gastric mucosa (arrow)
Some gastric glands are still found (arrowhead).

27. 27
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)

28. 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.

29. Normal
Acute gastritis
Chronic gastritis
Atrophic gastritis
Intestinal
metaplasia
Dysplasia Cancer

30.  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

31.  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

32. Neurogenic or catecholamine-induced vasoconstriction
Mucosal ischemia
Damage the mucosal
barrier
Directly injure mucosal cells by
oxygen or metabolic deprivation

33. Fig. 40-14

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36.  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

37.  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)
 Oesophagus
 Gastro-enterostomy stoma
 Related to ectopic gastric mucosa (e.g. in Meckel’s
diverticulum)

38.  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.

39. Etiology of PUD
Normal
Increased Attack
Hyperacidity,Zollinger Ellison
syndrome.
Weak defense
Stress, drugs, smoking
Helicobacterpylori*

40. 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

41. 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 neutralized
 Second, 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

42.  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

43. 43

44. 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.

45. Bacteria over
epithelial cells

47.  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.

48.  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.

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

50. 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.

51.  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.

54. 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

55. 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.

58. 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 tissue
o (4) a zone of active nonspecific inflammatory infiltration with
neutrophils predominating
Histologic Appearance

59. (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.

60. 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

61. (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
(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

62.  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.

63.  Pain or discomfort
 A 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 present
 Obstruction of the pyloric channel is rare.
63

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

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

69.  Neutralize stomach acid
 Calcium
 Tums, Rolaids
 Aluminum + Magnesium
 Maalox, Riopan, Mylanta, Gelusil
 Sodium
 Alka-Seltzer
 Magnesium
 Milk of Magnesia

70.  Standard Therapy
 14-16 days
 Bismuth subsalicylate (Pepto Bismol)
 Metronidazole
 Tetracycline
 Newest Treatment
 Helidac (three antibiotic regimen)

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