ENGLISH IN NURSING

GASTROINTESTINAL SYSTEM

By Group 4:

Desy Anwar Kusuma W. 131411131010

Lucy Kartika Dewi 131411131031
Rahendra Wahyu A. 131411131046
Retty Merdianti 131411131064
Senja Putrisia F. E. 131411131082
Ridha Cahya Prakhasita 131411131100
Thaliah Jihan N 131411133014
Prasetiya Wahyuni 131411133032

FACULTY OF NURSING
UNIVERSITAS AIRLANGGA
SURABAYA
2015
 PREFACE

We extend our gratitude to Allah SWT for all His mercy so that we can
complete the task group for Small Group Discussion (SGD) English In Nursing
course entitled "Gastrointestinal System” well.
We express gratitude to the deepest:

1. Setho Hadisuyatmana, S.Kep., Ns., MNs as a facilitator who gives

guidance and direction in the completion of this paper
2. Group 4 who have cooperated in this task.

The writers realize that this papers not perfect enough and there are still
many short comings. Therefore, the authors hope to get contructive criticism and
suggestions in the preparation of the papers so that the next will be better. Finally,
the authors hope that this paper is useful for us personally and for those who need
it.

Surabaya, May 15th, 2015

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 CONTENTS

ENGLISH IN NURSING......................................................................................... i
PREFACE ............................................................................................................... ii
CONTENTS ........................................................................................................... iii
CHAPTER 1 INTRODUCTION ............................................................................ 1
3.1 Background ................................................................................................. 1
3.2 Purpose ........................................................................................................ 1
3.3 Significance ................................................................................................. 2
CHAPTER 2 FUNDAMENTAL THEORIES ........................................................ 3
2.1 Anatomy & Physiology ............................................................................... 3
2.2 Types & Classification ................................................................................ 7
2.2.1 Alimentary Canal (Luminal GI) ........................................................... 7
2.2.2 Accessory Organs (Hepato-biliary-pancreatic GI) ............................... 7
2.3 Etiology ....................................................................................................... 8
NURSING CARE PLAN .............................................................................. 8
2.3.1 Acute Gastritis .................................................................................... 11
2.3.2 Chronic Gastritis ................................................................................ 11
2.3.3 Atrophic Gastritis ............................................................................... 12
2.4 Clinical Appearances ................................................................................. 13
2.4.1 Signs and Symtomps .......................................................................... 13
2.4.2 Interpreting Test Results .................................................................... 13
CHAPTER 3 SUMMARY .................................................................................... 14
3.1 Summary ................................................................................................... 14
BIBLIOGRAPHY ................................................................................................. 15

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 CHAPTER 1
INTRODUCTION

3.1 Background
The gastrointestinal (GI) system includes the gastrointestinal tract
(mouth, pharynx, esophagus, stomach, small intestine, and large intestine)
plus the accessory organs (salivary glands, liver, gallbladder, and pancreas)
that are not part of the tract but secrete substances into it via connecting
ducts. The overall fuction of the gastrointestinal system is to process
ingested foods into molecular forms that are than transferred, along with
salts and water to the body’s internal organs, where they can be distributed
to cells by the circulatory system.

Adult gastrointestinal tract consist of a tube approximately 15 ft long,

running through the body from mouth to anus. The lumen of the tract is like
hole of a doughnut. This fact is relevant to understanding some of the tract’s
properties. For example, the large intestine is inhabited by billions of
bacteria, most of which are normal flora even beneficial in this location.
However, if the same bacteria enter the internal organs, as may happen, for
example, in the case of a ruptured appendix, they may cause a severe
infection.

The function of the gastrointestinal system can be described in terms

of these four processes digestion, secretion, absorption, and mobilityband
the mechanisms controlling them.

The gastrointestinal system is designed to maximize absorption, and

within fairly wide limits it will absorb as much of any particular substance
as ingested. With a few important exceptions, therefore, the gastrointestinal
system does not regulate the amount of nutrients absorbed or their
concentrations in the internal organs. The regulation of the plasma
concentration of the absorbed nutrients is primarily the function of the
kidneys.

3.2 Purpose
1. General Purpose
After this group discussion, students are expected to understand anatomy
physiology, types and classification, etiology, and clinical appearance of
Gastritis illness.
2. Specific Purpose
After this group discussion, students are expected to implemented the
nursing care plan of Gastritis illness.
3.3 Significance
1. Advancing knowledge and experience about gastrointestinal system.
2. Adding more vocabularies and grammar.
3. Implemented the nursing care plan of Gastritis illness.

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 CHAPTER 2
FUNDAMENTAL THEORIES

2.1 Anatomy & Physiology

The digestive system, also known as the gastrointestinal (GI) tract
or the alimentary system, is responsible for breaking down complex food
into simple nutrients the body can absorb and convert into energy. The GI
system consists of the mouth, pharynx, esophagus, stomach, small and large
intestine, and rectum. The accessory organs (salivary glands, liver,
gallbladder, and pancreas) secrete digestive catalysts (a substance that
speeds up a chemical reaction) into the GI tract through connecting ducts.
1. Mouth
Mechanical digestion in the mouth with mastication, where the
teeth break down into smaller pieces by chewing and mixing it with
saliva. There are three pairs of salivary glands: Parotid,
submandibular, and sublingual. Saliva is mostly water that dissolves
food for tasting and moistens it for swallowing. Chemical breakdown
of cooked starches begins in the mouth with the help of the enzyme
ptyain, a salivary amylase.
The tongue assists with chewing by keeping food between the
teeth. The food is formed into a bolus as the tongue compresses it
against the hard palate. Sensory receptors are activated as the bolus
enters the oropharynx, stimulating the swallowing reflex. The larynx
pulls upward as the epiglottis closes over the glottis, thus preventing
food from entering the trachea.
2. Throat
The throat is part of both the digestive and respiratory systems
and is responsible for coordinating the functions of breathing and
swallowing. From superior to inferior, the throat is subdivided into 3
sections: oropharynx, hypopharynx, and larynx. Together, the
oropharynx, hypopharynx, and larynx function to sense and propel a
food bolus from the mouth to the esophagus in a coordinated fashion
while protecting the airway.
3. Pharynx
The pharynx consists of the oropharynx and the laryngopharynx.
Both structures provide passageways for food, fluids and air. The
pharynx is made of skeletal muscles and is lined with mucous
membranes. The skeletal muscles move food to the oesophagus via the
pharynx through peristalsis (alternating waves of contraction and
relaxation of involuntary muscle). The mucosa of the pharynx contains
mucus-producing glands that provide fluid to facilitate the passage of
the bolus of food as it is swallowed.

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4. Esophagus
Peristalsis, coordinated rhythmic contractions of the muscles,
pushes the bolus through the esophagus. The esophagus is a hollow,
mucular tube approximately 10 inches long that goes hrough the
diaphragm at the hiatus and enters the stomach at the gastroesophageal
junction.The cardiac sphincter, also called the lower esophageal
sphincter (LES) or gastroesophageal sphincter, located at the distal
end of esophagus, relaxes ad allows t food to pass into the stomach.
5. Abdomen
The first layer mucosa is the innermost layer, and it consist of
an epithelium, the lamina, and the muscularis mucosae. In the
epithelium, it contains exocrine gland cells and endocrine gland cells,
which secrete mucus and digestive enzymes into the lumen, and
release GI hormones into the blood, respectively. In the lamina
propri, it contains small blood vessels, nerve fibers, and lymphatic
cells/tissues. In addition, a thin muscle layer called muscularis
mucosae is also found and the activity of its muscle is responsible for
controlling mucosal blood flow and GI secretion.
The second layer submucosa is a connective tissue with major
blood and lyphatic vessels, along with a network of nerve cells, called
the submucosal nerve plexus, passing through.
The third layer muscularis externa is a thick muscle and its
contraction contributes to major gut motility (segmentation and
peristaltis). This muscle layer typically consist of two substansial
layers of smooth muscle cells; an inner circular layer and an outer
longitudinal layer. A prominent network of nerve cells, called the
myenteric nerve plexus.
The fourth layer serosa is the outermost layer, which mainly
consist of connective tissues and it connects to the abdominal wall,
thus supporting the GI tract in the abdominal cavity.
6. Stomach
The peristaltic movement of the stomach mixes the partially
digested food and digestive enzymes into a semiliquid mass called
chyme. The chyme will not pass the small intestine until it is proper
consistency and particles are 1 milimeter or less. When the chyme has
reached the proper consistency, the pyloric sphincter relaxes, releasing
a portion at a time of the chyme into the small intestine and then
contracts, preventing the backup of intestinal contents into the
stomach.
7. Small Intestine
The small intestine begins at the pyloric sphincter and ends at
the ileocaecal junction at the entrance of the large intestine. The small

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 intestine is about 6 m long but only about 2.5 cm in diameter. This
long tube hangs in coils in the abdominal cavity, suspended by the
mesentery and surrounded by the large intestine. The small intestine
has three regions: the duodenum, the jejunum and the ileum. The
duodenum begins at the pyloric sphincter and extends around the head
of the pancreas for about 25 cm. Both pancreatic enzymes and bile
from the liver enter the small intestine at the duodenum. The jejunum,
the middle region of the small intestine, extends for about 2.4 m. The
ileum, the terminal end of the small intestine, is approximately 3.6 m
long and meets the large intestine at the ileocaecal valve.
Food is chemically digested, and most of it is absorbed, as it
moves through the small intestine. Circular folds (deep folds of the
mucosa and submucosa layers), villi (finger-like projections of the
mucosa cells) and microvilli (tiny projections of the mucosa cells)
increase the surface area of the small intestine to enhance absorption
of food. Although up to 10 L of food, liquids and secretions enter the
GI tract each day, less than 1 L reaches the large intestine.
Enzymes in the small intestine break down carbohydrates,
proteins, lipids and nucleic acids. Pancreatic amylase acts on starches,
converting them to maltose, dextrins and oligosaccharides; the
intestinal enzymes dextrinase, glucoamylase, maltase, sucrose and
lactase further break down these products into monosaccharides.
Pancreatic enzymes (trypsin and chymotrypsin) and intestinal
enzymes continue to break down proteins into peptides. Pancreatic
lipases digest lipids in the small intestine. Triglycerides enter as fat
globules and are coated by bile salts and emulsified. Nucleic acids are
hydrolysed by pancreatic enzymes and then broken apart by intestinal
enzymes. Both pancreatic enzymes and bile are excreted into the
duodenum in response to the secretion of secretin and cholecystokinin,
hormones produced by the intestinal mucosa cells when chyme enters
the small intestine.
8. Large Intestine
The large intestine is a tube 2.5 in. in diameter and about 4 ft
long. Its first portion, the cecum, forms a blind-ended pouch from
which extends the appendix, a small fingerlike projection having no
known essential function. The colon consists of three relatively
straight segments-the ascending, transverse, and descending portions.
The terminal portion of descending colon is S-shaped, forming the
sigmoid colon, which empties into a relatively straight segment of the
large intestine, the rectum, which ends at the anus.
The primary absorptive process in the large intestine is the
active transport of sodium from lumen to blood, with the

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 accompanying osmotic absorption of water. If fecal material remains
in the large intestine for a long time, almost all the water is absorbed,
leaving behind hard fecal pellets. There is normally a net movement of
potassium from blood into the large-intestine lumen, and severe
depletion of total-body potassium can result when large volumes of
fluid are excreted in the feces. There is also a net movement of
bicarbonate ions into the lumen, and loss of this bicarbonate (a base)
in patients with prolonged diarrhea can cause the blood to become
acidic.
9. Pancreas
The pancreas, a gland located between the stomach and small
intestine, is the primary enzyme-producing organ of the digestive
system. It is a triangular gland extending across the abdomen, with its
tail next to the spleen and its head next to the duodenum. The body
and tail of the pancreas are retroperitoneal, lying behind the greater
curvature of the stomach. The pancreas is actually two organs in one,
having both exocrine and endocrine structures and functions. The
exocrine portion of the pancreas, through secretory units called acini,
secretes alkaline pancreatic juice containing many different enzymes.
The acini, cluster of secretory cells surrounding ducts, drain into the
pancreatic duct. The pancreatic duct joins with the common bile duct
just before it enters the duodenum.
The pancreas produces from 1 to 1.5 L of pancreatic juice daily.
Pancreatic juice is clear and has high bicarbonate content. This
alkaline fluid neutralizes the acidic chyme as it enters the duodenum,
optimizing the pH for intestinal and pancreatic enzyme activity. The
secretion of pancreatic juice is controlled by the vagus nerve and the
intestinal hormones secretin and cholecystokinin. Pancreatic juice
contains enzymes that aid in the digestion of all categories of food:
lipase promote fat breakdown and absorption; amylase completes
starch digestion; and trypsin, chymotrypsin and carboxypeptidase are
responsible for half of all protein digestion. Nuclease break down
nucleic acids.
10. Liver and Gallbladder
The liver weights about 1.4 kg in the average size adult. It is
located in the right side of the abdomen, inferior to the diaphragm and
anterior to the stomach. The liver has four lobes: right, left, caudate
and quadrate. A mesenteric ligament separates the right and left lobes
and suspends the liver from the diaphragm and anterior abdominal
wall. The liver is encased in a fibroelastic capsule, called the glisson
capsule. This capsule contains blood vessels, lymphatic and nerves.

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 When the liver is diseased or swollen, distension causes pain and the
lymphatics may ooze fluid into the peritoneal cavity.
Liver tissue consist of units called lobules, which are composed
of plates of hepatocytes. A branch of the hepatic artery, a branch of
the hepatic portal vein and bile dust communicate with each lobule.
Sinusoids, blood-filled spaces within the lobules, are lined with
kupffer cells. These phagocytic cells remove debris from the blood.
Bile production is the liver’s primary digestive function. Bile is
a greenish, watery solution containing bile salts, cholesterol, bilirubin,
electrolytes, water and phospholipids. These subtances are necessary
to emulsify and promote the absorption of fats. Liver cells make from
700 to 1200 mL of bile daily. When bile is not needed for digestion,
the sphincter of Oddi (located at the point at which bile enters the
duodenum) is closed and the bile backs up the cystic duct into the
gallbladder for storage.
Bile is concentrated and stored in the gallbladder, a small sac
cupped in the inferior surface of the liver. When food containing fats
enters the duodenum, hormones stimulate the gallbladder to secrete
bile into the cystic duct into the gallbladder for storage.
Bile is concentrated and stored in the gallbladder, a small sac
cupped in the inferior surface of the liver. When food containing fats
enters the duodenum, hormones stimulate the gallbladder to secrete
bile into the cystic duct. The cystic duct joins the hepatic duct to form
the common bile duct, from which bilw enters into the duodenum.

2.2 Types & Classification

Gastrointestinal system is divided into two parts: theLuminary
GI(alimentary canal) and hepato-biliary-pancreatic GI.
2.2.1 Alimentary Canal (Luminal GI)
The alimentary canal is a hollow tube lined with mucous
membrane. The alimentary canal includes mouth, esophagus, stomach,
small intestine, large intestine, rectum. The GI tract is a muscular tube
of about 5 m long when one is alive; however, after person dies and
during autopsy or postmortem examination, the lenght of the tract can
be doubled to 10 m. This is due the loss of muscle tone. The motor
and secretory activities of the GI system are highly controlled and
integrated by the gut endocrine and enteric nervous systems (ENS).
2.2.2 Accessory Organs (Hepato-biliary-pancreatic GI)
The accessory organs includes salivary glands (parotid,
sublingual, and submandibular glands), liver, pancreas, gallbladder.
The salivary glands secrete saliva for digestion and lubrication; the
pancreas produces hydrolytic enzymes for the digestion of our daily
foostuff and bicarbonate for the neutralizations of our gastric contents;

7
 the liver secretes bile, which is stored temporarily in the gallbladder
and susequenly delivered to the duodenum for that digestion and
absorption.

2.3 Etiology
Gastritis is an inflammation of the stomach lining due to either erosion
or atrophy. Erosive causes include stresses such as physical illness or
medication such as nonsteroial anti-inflammatory drugs (NSAID’s).
Atrophic causes include a history of prior surgery (such as gastrectomy),
pernicious anemia, alcohol use, or Helicobacter pylori infection.
Prognosis
Gatritis may causes changes within the cells of the stomach lining
leading to malnutrition, lymphoma, or gastric cancer. Hospitalized patients,
especially in critical care settings, should have preventive medications to
avoid the development of gastritis.

NURSING CARE PLAN

Assessment:
1. Does the patient complains of heartburn, can not eat, nausea and
vomiting?
2. When the occurrence of symptoms, whether before eating, after eating,
after ingesting spicy foods, certain drugs or alcohol?
3. What are the symptoms associated with anxiety, Stress, allergies, eating
and drinking too much or eating too fast?
4. What are the symptoms diminish or disappear?
5. Is there a history of previous gastric disease?
6. Does the patient have vomiting blood?
7. Is there any abdominal tenderness?
8. Dehydration or change in skin turgor or dry mucous membranes?
Diagnosis:
1. Acute pain
2. Imbalanced Nutrition Less Than Body Requirements
3. Risk for fluid volume deficit
4. Anxiety
Intervention:
1. Relief of pain:
 Encourage clients to learn relaxation techniques
 Encourage clients to avoid foods and beverages that irritate the
stomach, such as alcohol
 Encourage clients to use diet pd regular intervals.
2. Maintaining adequate nutrition remains
 Provide eat small but frequent meals and do not irritate.
 Give solid foods as soon as possible
 Provide a drink that contains no caffeine
3. Maintain body fluid volume
 Observation of fluid intake and output

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  Observe for signs of dehydration
4. Reduce anxiety
 Encourage clients to express their problems and fears
 Help clients identify situations that cause anxiety
 Teach stress management strategies
Nursing Interventions
No. Diagnoses Interventions
1 Acute • Review the level of pain.
Pain • Provide information
Purpose: about the different
Pain is strategies chosen to reduce
gone / no pain.
pain • Encourage clients to use
the chosen strategy to
reduce pain.
• Encourage clients to
avoid eating foods that
stimulate an increase in
stomach acid.
• Collaboration with the
medical team for
the administration of anti-
analgesic.
2 Imbalanc • Describe the client and
ed family about the
Nutrition importance of food for the
Less body.
Than • Monitor the amount of
Body food intake.
Require • Monitor and record the
ments number of vomiting,
Purpose: frequency and color
Nutrition • Provide a
balanced. varied diet according to his
diet to stimulate appetite.
• Provide food in small
portions but frequently.
• Collaboration with the
medical team for the
administration of anti-
emetic drugs.
Rational
• In order to determine the
level of pain experienced by
the client.
• Able to learn methods of
pain reduction and can do
it.
• Assist in menurunhkan
experienced pain threshold.
• In order for clients to find
foods that stimulate
stomach acid and does not
consume them.
• Reduce the level of pain
experienced by the client.
• Clients and families can
learn the importance of
• To know the food is
consumed.
• As the data to perform
nursing actions and
subsequent treatment.
• To klirn be motivated and
stimulates appetite.
• To reduce the feelings and
needs food for patients.
• As a therapy for inhibiting
/ stimulating nausea and
vomiting.
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3. Risk  Assess the possibility of  Detecting theearly signs
for Fluid signs of dehydration and of dehydration.
Volume record intake and output.  Detecting early indicator
Deficit  Assess the balance of of fluid and electrolyte
Purpose: fluids and electrolytes imbalance.
volume of every 24 hours.  In order for the client's
body fluid  Encourage clients to body fluid balance can be
s are met keep the peroral intake is maintained
to eat and drink a little  Caffeine is a central
but often. nervous system stimulant
 Encourage clients to that can increase the
avoid consuming foods activity of gastric and
and beverages that pepsin secretion leading to
contain caffeine. increased secretion of
gastric acid that can cause
reactions of nausea and
vomiting.
4. Anxiety • Assess the client's • As the initial data to
Purpose: anxiety. determine the client's
No • Give the client an anxiety level.
Anxiety opportunity to express his • In order to determine the
anxiety. cause of anxiety is
• Explain to clients that experienced as well as
can challenge reduce the psychological
dijalankankan diet after burden of the client.
recovery. • The client can adhere to
• Explain to the client diet and avoid disease
about medical procedures relapse again.
/ treatments will be done • Able to understand and
and encouraged accept all the measures
cooperative therein. taken to cure the disease
• Provide motivation to the process.
client about his recovery. • Clients and families are
optimistic for the healing of
disease and comply with all
recommended clients are
given.

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2.3.1 Acute Gastritis
Acute gastritis has a number of causes, including certain drugs;
alcohol; bacterial, viral, and fungal infections; acute stress (shock);
radiation; allergy and food poisoning; bile; ischemia; and direct
trauma. The causes is:
 Drugs - NSAIDs, such as aspirin, ibuprofen, and naproxen;
cocaine; iron; colchicine, when at toxic levels, as in patients with
failing renal or hepatic function; kayexalate; chemotherapeutic
agents, such as mitomycin C, 5-fluoro-2-deoxyuridine, and
floxuridine
 Potent alcoholic beverages, such as whisky, vodka, and gin
 Bacterial infections -H pylori (most frequent), H heilmanii (rare),
streptococci (rare), staphylococci (rare), Proteus species
(rare), Clostridium species (rare), E coli (rare), tuberculosis (rare),
secondary syphilis (rare)
 Viral infections (eg, CMV)
 Fungal infections - Candidiasis, histoplasmosis, phycomycosis
 Parasitic infection (eg, anisakidosis)
 Acute stress (shock)
 Radiation
 Allergy and food poisoning
 Bile: The reflux of bile (an alkaline medium is important for the
activation of digestive enzymes in the small intestine) from the
small intestine to the stomach can induce gastritis.
 Ischemia: This term is used to refer to damage induced by
decreased blood supply to the stomach. This rare etiology is due to
the rich blood supply to the stomach.
 Direct trauma

2.3.2 Chronic Gastritis

Chronic gastritis may be caused by either infectious or
noninfectious conditions. Infectious forms of gastritis include the
following:
 Chronic gastritis caused by H pylori infection – This is the most
common cause of chronic gastritis
 Gastritis caused by Helicobacter heilmannii infection.
 Granulomatous gastritis associated with gastric infections in
mycobacteriosis, syphilis, histoplasmosis, mucormycosis, South
American blastomycosis, anisakiasis, or anisakidosis
 Chronic gastritis associated with parasitic infections -
Strongyloides species, schistosomiasis, or Diphyllobothrium latum
 Gastritis caused by viral (eg, CMV or herpesvirus) infection.

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 Noninfectious forms of gastritis include the following:
 Autoimmune gastritis
 Chemical gastropathy- usually related to chronic bile reflux, NSAID
and aspirin intake
 Uremic gastropathy
 Chronic noninfectious granulomatous gastritis– This may be
associated with Crohn disease, sarcoidosis, Wegener granulomatosis,
foreign bodies, cocaine use, isolated granulomatous gastritis, chronic
granulomatous disease of childhood, eosinophilic granuloma,
allergic granulomatosis and vasculitis, plasma cell granulomas,
rheumatoid nodules, tumoral amyloidosis and granulomas associated
with gastric carcinoma, gastric lymphoma, or Langerhans cell
histiocytosis
 Lymphocytic gastritis, including gastritis associated with celiac
disease (also called collagenous gastritis)
 Eosinophilic gastritis
 Radiation injury to the stomach
 Graft-versus-host disease (GVHD)
 Ischemic gastritis
 Gastritis secondary to drug therapy (NSAIDs and aspirin)

2.3.3 Atrophic Gastritis

Atrophic gastritis usually is associated with either chronic H
pylori infection or with autoimmune gastritis. The environmental
subtype of atrophic gastritis corresponds mostly with H pylori–
associated atrophic gastritis, although other unidentified
environmental factors may play a role in the development of gastric
atrophy. Yagi et al used magnifying endoscopy to distinguish atrophic
gastritis caused by H pylori from autoimmune gastritis.
 Chronic gastritis caused by H pylori infection of the stomach
 H pylori infection of the stomach is by far the most common cause
of chronic atrophic gastritis.
 The risk of atrophic gastritis is increased by 10-fold if an H
pyloriinfection is present.
 Whether H pylori infection follows the multifocal atrophic gastritis
pathway or the nonatrophic antral gastritis pathway may be related
to genetic susceptibility factors, environmental factors that
modulate the host-bacterial interaction, or bacterial strains.
 Although H pylori possessing the cag (cytotoxin-associated gene)
pathogenicity island have been shown to have increased virulence,
to cause higher levels of mucosal inflammation, and to be present
more frequently in individuals infected with H pylori who develop
gastric cancer, no specific virulence factors have been identified
that might be useful to predict specific H pylori disease outcome.

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  Host factors or the effects of other environmental agents are likely
to be the determinant elements modulating patterns of disease
progression. For example, family relatives of individuals with
gastric cancer develop pangastritis more frequently in response
to H pyloriinfection and they also develop multifocal intestinal
metaplasia more often, a preneoplastic lesion of the stomach and a
component of H pylori– associated atrophic gastritis.
 Autoimmune atrophic gastritis
 Autoimmune atrophic gastritis is a type of chronic atrophic gastritis
limited to corpus-fundus mucosa and characterized by marked
diffuse atrophy of parietal and chief cells.
 Autoimmune gastritis is associated with serum antiparietal and
anti-IF antibodies that cause IF deficiency, which, in turn, causes
decreased availability of cobalamin and, eventually, pernicious
anemia in some patients.
 In some families, the disease appears to be transmitted with an
autosomal dominant pattern of inheritance.

2.4 Clinical Appearances

2.4.1 Signs and Symtomps

a. Nausea and vomiting
b. Anorexia
c. Epigastric area discomfort
d. Epigastric tenderness on palpitation due to gastric irritation
e. Bleeding from irritation of the gastric mucosa
f. Hematemesis possible coffee ground emesis due to partial
digestion of blood
g. Melena black, tarry stool.
Symtomps of acute gastritis usually include nausea, vomiting,
anorexia, a feeling of fullness, and pain in the stomach area. In people
who abuse alkohol, hemorrhage may be the only symtomp. Symptoms
of crhonic gastritis may be the same as acute gastritis. Some patients,
however, have only mild indigestion or no symptoms at all unless they
develop pernicious anemia.

2.4.2 Interpreting Test Results

a. Hemoglobin and hematocrit decrease
b. Anemia (iron deficiency) due to chronic, slow blood loss
c. Fecal occult blood positive
d. Helicobacter pylori shows inflammation, allows biopsy.

13
 CHAPTER 3
SUMMARY

3.1 Summary
The Gastrointestinal system consists of the mouth, pharynx,
esophagus, stomach, small and large intestine, and rectum. The accessory
organs (salivary glands, liver, gallbladder, and pancreas) secrete digestive
catalysts (a substance that speeds up a chemical reaction) into the GI tract
through connecting ducts. Gastritis is an inflammation of the stomach lining
due to either erosion or atrophy in the Gastrointestinal system. Gatritis may
causes changes within the cells of the stomach lining leading to
malnutrition, lymphoma, or gastric cancer.

14
 BIBLIOGRAPHY

Digiulio, M., Donna Jackson and Jim Koegh (2007). Medical Surgical Nursing
Demystified. United States, McGraw-Hill.

Lemone, P. a. B., Karen M (2011). Medical-Surgical Nursing: Critical Thinking

in Client Care Volume 2. Australia, Pearson.

Leung, P. S. (2014). The Gastrointestinal System (Gastrointestinal, Nutritional,

and Exportability Physiology). New York, Springers.
Linton. 2012. Introduction Medical Surgical Nursing 5th Edition. Canada,
Elsevier
Redeen, S. (2010). Chronic gastritis : diagnosis, natural history and consequences.
Linköping, Linköping University, Faculty of Health Sciences.

Vander, A. J. (2001). Human Physiology: The mechanisms of Body Function 8

Edition. New York, McGraw-Hill.

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