Ns.

Yulia Dewi
Prodi S1 Keperawatan
STIKES KEPANJEN
 Stomach
3 muscle layers
Oblique
Circular
Longitudinal
Regions
Cardiac sphincter
Fundus
Antrum (pylorus)
Pyloric sphincter
Vascular
Inner surface thrown into
folds Rugae
Contains enzymes that work
best at pH 1-2 3
Normal Stomach Anatomy
Stomach - Normal
Stomach - Normal
 Stomach
Functions Absorbs
Mix food Alcohol
Reservoir Water
Start digestion of
Lipophilic acid
Protein
B 12
Nucleic acids
Fats
Activates some enzymes
Destroy some bacteria
Makes intrinsic factor B
12 absorption
Destroys some bacteria

7
 Inflammatory
Disease of Stomach
 Definition
The term gastritis is used to denote
inflammation associated with
mucosal injury.
Gastritis is mostly a histological term that
needs biopsy to be confirmed.
Gastritis is usually due to infectious
agents (such as Helicobacter pylori) and
autoimmune and hypersensitivity
reactions.
 Definition
Epithelial cell damage and regeneration
without associated inflammation is
properly referred to as "gastropathy.
Gastropathy may be referred without
histological evidence and just according to
gross appearance in endoscopy or radiology
Gastropathy is usually caused by irritants such
as drugs (e.g., nonsteroidal anti-inflammatory
agents and alcohol), bile reflux, hypovolemia,
and chronic congestion.
 Sex:

Male-to-female ratio of gastritis is approximately1:1

 Pathophysiology
The mechanisms of mucosal injury in gastritis is thought
to be an imbalance of
aggressive factors

acid production or pepsin

and
defensive factors

mucus production
bicarbonate
and blood flow
Protective factors vs. hostile factors
 Gastritis

Acute Chronic
 Acute & Chronic Difference

Acute refers to short term inflammation

Acute refering to neurophilic infiltrate

Chronic referring to long standing forms

Chronic referring to mononuclear cell
infiltrate especially lymphocyte and
macrophages
 Acute Gastritis

Definition

An acute mucosal inflammatory

process, with neutrophilic infiltrate,
that is usually transient.
There may be hemorrhage into the
mucosa or sloughing of the mucosa.
Severe erosive form is an important
cause of severe GI bleeding
 Etiology
Frequently associated with, among others:
heavy use of NSAIDS, especially aspirin

excessive alcohol consumption

heavy smoking

severe stress e.g. trauma, burns,

surgery
Ischemia

Systemic infection

Often, idiopathic
 NSAIDs

NSAIDs and aspirin also

interfere with the protective
mucus layer by inhibiting
mucosal cyclooxygenase activity,
reducing levels of mucosal
prostaglandins
 Smoking
Promotes gastritis & ulcer occurrence
Increases the likelihood of
ulcer complications

Mechanisms
Stimulate gastric acid secretion
Stimulate bile salt reflux
Causes alteration in mucosal blood flow
Decrease mucus secretion
Reduces prostaglandin synthesis
Decrease pancreatic bicarbonate secretion
 Effects of Diet and Stress

Diet and Stress Action

Diet Dyspepsia, may pain - not believed

to cause ulcer or assist healing

Physiologic mucosal blood flow, tissue hypoxia,

stress mucosal lining degradation; e.g. ICU,
sepsis, burn, trauma. Associated with
multiple erosions & significant bleeding
Etiology of
Gastritis
A) Normal
B) Increased
Attack
*Hcl
*Pepsin.
*NSAIDs.
C) Weak defense
*Helicobacter pylori
*Stress, drugs, smoking
 Acute Gastritis - Pathogenesis

Acid secretion + Bicarbonate

All above Factor
+ back diffusion buffer

Direct Disruption
Mucosal + of Blood flow
Injury Mucus layer

Acute Gastritis
 Stages of Acute Gastritis

Acute superficial Acute erosive

gastritis gastritis
Inflammation of Destruction of multiple
superficial gastric small zones of
mucosa. superficial mucosa.

Acute Gastric Ulceration

Destruction of full thickness of mucosa

ACUTE GASTRITIS -
MORPHOLOGY
Mucosal congestion ,edema
inflammation & ulceration
 Acute Gastritis - Morphology
Ranges from edema with neutrophil infiltration, vascular congestion,&
an intact epithelium, to erosion (mucosal defect that does not cross
the muscularis mucosa) and hemorrhage.
 Acute Gastritis

Gastric mucosa
demonstrates
infiltration by
Neutrophils
 Acute Gastritis

diffusely hyperemic
gastric mucosa
causes for acute
gastritis
alcoholism
drugs
infections, etc.
 Acute Gastritis
Clinical Features
broad range of signs and symptoms that depend
on the severity of the condition
Asymptomatic

Epigastric pain, nausea & vomiting

Hemorrhage, massive hematemesis, melena, or
fatal blood loss
One of the major causes of massive
hematemesis, particularly in alcoholics.
~25% patients taking aspirin for rheumatoid
arthritis will develop acute gastritis, and some
will bleed
 Complications:

Malignancy

Hemorrhage

Perforation

Obstruction
 Chronic Gastritis
Definition

Chronic mucosal inflammatory changes leading

to atrophy and metaplasia (usually without
erosions)

Dysplasia and ultimate neoplasia are

complications.
 Chronic
Gastritis

Type B Type A
Antral Autoimmune
Gastritis gastritis
 Type B (Antral Gastritis)
90% of patients with antral chronic gastritis:
Helicobacter pylori infected
Motile, gram negative curvilinear rods that
elaborate urease (buffers gastric acid) & toxins
and have adhesins to bind to the epithelium.
Pathogenesis
H. pylori (urease NH4+ + toxins) + Host (acid
+ peptic enzymes) Chronic Inflammation
Antibodies Gland destruction + Mucosal
atrophy acid intrinsic factor (which can
lead to pernicious anemia)
 Helicobacter gastritis
2 patterns of infection
Diffuse involvement of body and antrum (pan
gastritis associated with diminishing acid
output)
Infection confined to antrum (antral gastritis,
associate with increased acid output)
 Helicobacter pylori

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
H. pylori Gastritis - Morphology

H. pylori organisms along

superficial mucus layer of
antral biopsy

Web Path
 Bile reflux gastropathy
Bile reflux gastropathy typically results from the
regurgitation of bile into the stomach because
of an operative stomach, an incompetent
pyloric sphincter, or abnormal duodenal motility.

The effect of bile salts on gastric mucosa is

comparable to that seen after chronic NSAID
use
 Chemical gastritis

Commonly seen with bile

reflux (toxic to cells)
Prominent hyperplastic
response (inflammatory
cells scanty)
With time intestinal
metaplasia
 Clinical Features
Usually only a few symptoms:

nausea, vomiting, upper abdominal discomfort

Most infected person have gastritis, but

are asymptomatic
Hypochlorhydria, but NOT achlorhydria
and pernicious anemia (parietal cells
never completely destroyed)
Gastrin normal to slightly elevated
Antibiotics are treatment of choice
 Clinical Complications
H. pylori
H. pylori predisposes to peptic ulcers
in duodenum and stomachMost
patients with a peptic ulcer are
infected.
Risk of gastric carcinoma and
lymphoma
 Type A (Auto immune)
Etiology

Autoimmune - antibodies to parietal cells,

gastrin receptor, intrinsic factor, and H+,K+
ATPase
<10% of cases of chronic gastritis

Possible autosomal dominant

inheritance
 Morphology of chronic gastritis

Chronic inflammatory cell

infiltration
Mucosal atrophy

Intestinal (goblet cell)

metaplasia
Seen in Helicobacter and
autoimmune gastritis (not
chemical)
 Autoimmune gastritis

Autoimmune gastritis -
pernicious anemia
Chronic atrophic
gastritis is associated
with Abs
- intrinsic factor
- patietal cell
bright green IF- in the
parietal cells of the
gastric mucosa.
Autoimmune Gastritis -Morphology
Diffuse mucosal damage of the body and fundic
mucosa. Antrum less involved.

PJ Goldblatt, MD
 Chronic Gastritis
Clinical Features
Usually only a few symptoms: nausea,
vomiting, upper abdominal discomfort

Autoimmune
Hypo to achlorhydria (severe loss of
parietal glands)
Hypergastrinemia
10% have pernicious anemia
 Clinical Complications

Autoimmune:
Often seen in association with other
autoimmune disorders (Hashimoto
thyroiditis, Addison disease, and type I
diabetes)
Significant risk for the development of
gastric carcinoma (2-4%) and
endocrine tumors (carcinoid tumor)
 Chronic Gastritis
Morphology
Varying degrees of mucosal damage
possible
Mucosal lesions are reddened, with
thickened rugae
Atrophied rugae in long-standing cases
Lymphocytes and plasma cell infiltrate;
neutrophils indicate active inflammation
(may or may not be present)
 Regeneration - constant feature
Metaplasia - mucosa of antral and
body-fundic regions converts to
columnar absorptive cells and goblet
cells (intestinal metaplasia)
Atrophy - marked loss of glands
Dysplasia precursor lesion to
gastric cancer in atrophic gastritis
 Hypertrophic gastritis
Three variants are recognized

Menetriers disease

Hypersecretory gastropathy

Gastric gland hyperplasia

[the Zollinger-Ellison syndrome]
 Hyperplastic gastropathies

proliferative,
inflammatory, and
infiltrative
conditions are
associated with
large folds due to
excessive number
of mucosal
epithelial cells
 Mntrier's disease
Epithelial hyperplasia
involving the surface
and foveolar mucous
cells (i.e., foveolar
hyperplasia); the
oxyntic glands can be
normal or atrophic.
 Zollinger-Ellison syndrome

Increased numbers
of parietal cells
with no change in
surface and
foveolar mucous
cells.
 Hyperplastic gastropathies
mixed-type in which
both mucous and
oxyntic glandular
cells show
hyperplasia, may be
seen in as
lymphocytic and H.
pylori gastritis.
 Stomach
Acute Gastritis= inflammation of gastric mucosa
acute presence of neutrophils
Chronic lymphocytes and plasma cells
Caused by ingestion of strong acids or alkalies, NSAIDs,
cancer chemotherapy, irradiation, alcohol, uremia, severe
stress & shock states
Proposed mechanisms: acid production with surface
bicarbonate buffer
Morphology: Mucosal edema, hyperemia, PML infiltration,
erosions (not deeper than muscularis mucosa) &
hemorrhages
 Stomach
Chronic Gastritis = Chronic mucosal inflammation
Leading to mucosal atrophy, intestinal metaplasia &
dysplasia.
Pathogenesis:
Chronic infection by Helicobacter pylori (90%): MCC of
chronic gastritis, Elaboration of urease produces
ammonia that buffers gastric acid, protecting organism from
acid
Other diseases associated with H. pylori Infection
Peptic ulcer disease
Gastric carcinoma
Gastric lymphoma
Autoimmunity (>10%): Antibodies to parietal cells cause
parietal cell destruction (HCl & intrinsic factor)
 Stomach
Chronic Gastritis
Morphology:
Autoimmune diffuse mucosal damage of the body-fundic
mucosa
H. pylori affect antral mucosa
Histology: Lymphocytic & plasma cell infiltrate of the lamina propria
atrophy, regeneration, metaplasia (to intestinal type mucosa) &
dysplasia.
H. pylori detected on the mucosal surface
Clinically:
Mild abdominal discomfort, nausea, vomiting; hypochlorhydria,
hypergastrinemia & rarely
Overt pernicious anemia (in autoimmune) gastritis).
Long-term risk of cancer is 2-4%