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

NURSING FACULTY
AIRLANGGA UNIVERSITY
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. Ira Suarilah, S.Kep., M.Sc., as a facilitator who gives guidance and

direction in the completion of this paper
2. 4th group who have cooperated in this task.

The writersrealizethatthis paperis not perfectandthere are still

manyshortcomings.Therefore, theauthorshopeto
getconstructivecriticismandsuggestionsin thepreparation of thepaperso thatthe
nextwill be better. Finally theauthorshope thatthispaper isusefulfor
uspersonallyandfor those whoneed it.

Surabaya, May 15th, 2015

ii
 CONTENTS

COVER .................................................................................................................... i
PREFACE ............................................................................................................... ii
CONTENTS ........................................................................................................... iii
CHAPTER 1 INTRODUCTION ............................................................................ 1
3.1 Background .............................................................................................. 1
3.2 Purpose ..................................................................................................... 1
3.3 Benefit ...................................................................................................... 2
CHAPTER 2 FUNDAMENTAL THEORIS .......................................................... 3
2.1 Anatomy & Physiology ............................................................................ 3
2.2 Types & Classification ............................................................................. 8
1 Alimentary Canal (Luminal GI) ............................................................... 8
2 Accessory Organs (Hepato-biliary-pancreatic GI) ................................... 8
2.3 Etiology .................................................................................................... 9
CHAPTER 3 CONCLUSION ............................................................................... 18
3.1 Conclusion .............................................................................................. 18
BIBLIOGRAPHY ................................................................................................. 19

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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 environment, where they can be
distributed to cells by the circulatory system.

The adult gastrointestinal tract is a tube approximately 15 ft long,

running through the body from mouth to anus. The lumen of the tract, like
the hole in a doughnut, is continuous with the external environment, which
means that its contents are technically outside the body. 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 harmless and
even beneficial in this location. However, if the same bacteria enter the
internal environment, 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 is ingested. With a few important exceptions, therefore, the
gastrointestinal system does not regulate the amount of nutrients absorbed
or their concentrations in the internal environment. 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
Gastrointestinal System.
2. Specific Purpose
After this group discussion, students are expected to implemented the
nursing process of Gastrointestinal System.
3.3 Benefit
1. Advancing knowledge and experience about gastrointestinal system.
2. Adding more vocabularies and grammar.

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 CHAPTER 2
FUNDAMENTAL THEORIS

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

3
 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.
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

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 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
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.

5
 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
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.

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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.
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

7
 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.

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

8
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.
Treatment
a. Administer antacids: Maalox, Mylanta, Tums, Gaviscon
b. Administer sucralfate to protect gastric lining.
c. Administer histamine 2 blockers: ranitidine, famotidine, nizatidine,
cimetidine
d. Administer proton pump inhibitors: omeprazole, esomerazole,
pantoprazole, raberprazole, lansoprazole
e. Eradicate Helicobacter pyroli infection if present
f. Diet modification
g. Monitor hemoglobin and hematocrit.

Nursing Diagnoses
a. Risk for imbalanced nutrition: Less than what body requires
b. Risk for imbalanced fluid volume
c. Nausea

Nursing Intervention
a. Monitor vital signs
b. Monitor intake and output
c. Monitor stool for occult blood
d. Assess abdomen for bowel sounds, tenderness
e. Teach patient about:
 Diet restrictions (avoid alcohol, caffeine, acidic foods)
 Medications
 Avoid smoking
 Avoid NSAIDs.

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1. Acute Gastritis
 Gnawing or burning epigastric distress, occasionally accompanied
by nausea and/or vomiting. The pain may improve or worsen with
eating.
 Previous mucosal injury (eg, gastritis, peptic ulcer disease,
endoscopic injury caused by polypectomy, injury caused by any
surgery)
 History of eating raw fish
 Exposure to potentially noxious drugs or chemical agents. This
includes corticosteroids or other prescription medications that can
cause gastritis.
 Routine use of aspirin or NSAIDs, especially at high doses
The physical examination findings are often normal with
occasional mild epigastric tenderness. The examination tends to
exhibit more abnormalities as the patient develops complications in
relation to 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

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  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. Chronic Gastritis
Acute H pylori infection usually is not detected clinically, but
persistence of the organism causes H pylori chronic gastritis, which is
usually asymptomatic but may manifest as epigastric pain, nausea,
vomiting, anorexia, early satiety or weight loss. Symptoms may occur
with the development of complications of chronic H pylori gastritis,
which include peptic ulcers, gastric adenocarcinoma, and mucosa-
associated lymphoid tissue (MALT) lymphoma.

Autoimmune gastritis
The clinical manifestations of autoimmune gastritis are
primarily related to the deficiency in cobalamin, which is not
adequately absorbed because of intrinsic factor (IF) deficiency
resulting from severe gastric parietal cell atrophy. The disease has an
insidious onset and progresses slowly. Cobalamin deficiency affects
the hematologic, gastrointestinal (GI), and neurologic systems.

The most significant hematologic manifestation is megaloblastic

anemia, but on rare occasions, purpura due to thrombocytopenia may
develop. Symptoms of anemia include weakness, light-headedness,
vertigo, tinnitus, palpitations, angina and symptoms of congestive
heart failure.

11
 There are many gastrointestinal manifestations of cobalamin
deficiency. Patients sometimes report having soreness of the tongue-
called glossitis. Anorexia with moderate weight loss that is
occasionally associated with diarrhea may result from malabsorption
associated with megaloblastic changes of the small intestinal epithelial
cells.

Neurologic manifestations result from demyelination, followed

by axonal degeneration and neuronal death. Affected sites include the
peripheral nerves, posterior and lateral columns of the spinal cord, and
cerebrum. Signs and symptoms include numbness and paresthesias in
the extremities, weakness, and ataxia. Sphincter disturbances may
occur. Mental function disturbances range from mild irritability to
severe dementia or psychosis. Neurologic disease may occur in a
patient with hematocrit and red cell parameters within the reference
range.

As previously mentioned, patients with pernicious anemia have

an increased frequency of gastric polyps and gastric carcinoid, in
addition to an increase in the frequency of gastric adenocarcinoma.

Granulomatous Gastritis
In multisystemic diseases, specific symptoms related to gastric
involvement may be minor. Caseating granulomas secondary to
tuberculosis may be found in the absence of lung disease in patients
who are malnourished, immunosuppressed, or alcoholic.

Patients with Crohn disease and gastric involvement may report

gastric pain, nausea, and vomiting. Gastric involvement in Crohn
disease is almost invariably associated with intestinal disease, and
intestinal manifestations predominate.

Sarcoidosis of the stomach is usually associated with

granulomatous inflammation in other locations, especially the lungs,
hilar nodes, or salivary glands. About 10% of patients with sarcoid
involvement in the stomach are asymptomatic. Patients who are
symptomatic present with gastric ulcers, hemorrhage, pyloric stricture,
and gastric outlet obstruction.

Idiopathic Isolated Granulomatous Gastritis

The diagnosis of idiopathic isolated granulomatous gastritis is
established only when known entities associated with granulomas are
excluded. Patients who are symptomatic usually are older than 40

12
years at presentation and have epigastric pain, weight loss, and
vomiting secondary to pyloric obstruction.

Lymphocytic gastritis
Lymphocytic gastritis mostly affects middle-aged or elderly
patients. It may be associated with chronic H pylori infection, gluten-
sensitive enteropathy, and Menetrier disease. It may represent a
hypersensitivity reaction involving the gastric body. Lymphocytic
gastritis has been described as complicating MALT lymphoma and
gastric carcinoma.

Eosinophilic gastroenteritis
Some patients with eosinophilic gastroenteritis have underlying
connective tissue disorders. Those with predominant mucosal
involvement may report nausea, vomiting, and abdominal pain related
to the ingestion of specific foods. Those with involvement of the
muscularis propria and resulting thickening and rigidity may present
with outlet obstruction symptoms. Many patients have a history of
allergy, peripheral eosinophilia, asthma, eczema, or food sensitivity.
Some respond to removal of these items from the diet, and steroid
treatment is often helpful.

Gastritis in graft versus host disease

Graft versus host disease (GVHD) follows allogeneic bone
marrow transplantationor transfusions, especially in patients who are
immunocompromised. Patients with isolated gastric GVHD have
symptoms of nausea, vomiting, and upper abdominal pain without
diarrhea.

Physical Examination
The physical examination contributes relatively little to the
assessment and management of chronic gastritis. However, some
findings are specifically associated with the particular complications
of H pylori– associated gastritis and autoimmune gastritis.

In uncomplicated H pylori– associated atrophic gastritis, clinical

findings are few and nonspecific. Epigastric tenderness may exist. If
gastric ulcers coexist, guaiac-positive stool may result from occult
blood loss. Bad breath (ie, halitosis) and abdominal pain or discomfort
may occur, with bloating associated with bacterial overgrowth
syndrome.

13
 Physical findings may result from the development of pernicious
anemia and neurologic complications in patients with autoimmune
atrophic gastritis. With severe cobalamin deficiency, the patient is
pale and has slightly icteric skin and eyes. The pulse is rapid, and the
heart may be enlarged. Auscultation usually reveals a systolic flow
murmur.

3. Atrophic Gastritis
Atrophic gastritis represents the end stage of chronic gastritis,
both infectious and autoimmune. In both cases, the clinical
manifestations of atrophic gastritis are those of chronic gastritis, but
pernicious anemia is observed specifically in patients with
autoimmune gastritis and not in those with H pylori– associated
atrophic gastritis.

H pylori-associated atrophic gastritis

Acute H pylori infection usually is not detected clinically, but
experimental infection results in a clinical syndrome characterized by
epigastric pain, fullness, nausea, vomiting, flatulence, malaise, and,
sometimes, fever. The symptoms resolve in approximately a week,
regardless of whether H pylori organisms are eliminated.

Persistence of the organism causes H pylori chronic gastritis,

which usually is asymptomatic or may manifest as gastric pain and,
rarely, nausea, vomiting, anorexia, or significant weight loss.
Symptoms associated with complications of chronic H pylori–
associated atrophic gastritis may develop, including gastric ulcers and
gastric adenocarcinoma.

Autoimmune atrophic gastritis

Autoimmune atrophic gastritis clinical manifestations primarily
are related to deficiency in cobalamin, which is not absorbed
adequately because of IF deficiency resulting from severe gastric
parietal cell atrophy. The disease has an insidious onset and
progresses slowly. Cobalamin deficiency affects the hematological,
GI, and neurologic systems.

Hematologic manifestations
The most significant manifestation is megaloblastic anemia, but,
rarely, purpura due to thrombocytopenia may develop. Symptoms of
anemia include weakness, light-headedness, vertigo and tinnitus,
palpitations, angina, and symptoms of congestive failure.

14
GI manifestations
The lack of cobalamin is associated with megaloblastosis of the
GI tract epithelium. Patients sometimes complain of a sore tongue.
Anorexia with moderate weight loss occasionally associated with
diarrhea may result from malabsorption associated with megaloblastic
changes in the epithelium of the small intestine.

Neurologic manifestations
These result from demyelination, followed by axonal
degeneration and neuronal death. The affected sites include peripheral
nerves, posterior and lateral columns of the spinal cord, and the
cerebrum. Signs and symptoms include numbness and paresthesias in
the extremities, weakness, and ataxia. Sphincter disturbances may be
present. Mental function disturbances vary from mild irritability to
severe dementia or psychosis. Neurologic disease may occur in
patients with normal hematocrit and normal red cell parameters.

Anemia
Patients with pernicious anemia have an increased frequency of
gastric polyps and have a 2.9-fold increase in gastric cancer.

Additionally, patients with autoimmune atrophic gastritis and H

pylori infection may manifest iron deficient anemia that may be
refractory to oral iron treatment. H pylori eradication in combination
with continued oral iron therapy was shown to result in a significant
increase in hemoglobin levels.

Primary hyperparathyroidism
Massironi et al found evidence of a noncausal association
between chronic autoimmune atrophic gastritis (CAAG) and primary
hyperparathyroidism (PHPT). In a prospective study, they evaluated
the prevalence of PHPT in 107 patients with CAAG and the
prevalence of CAAG in 149 patients with sporadic PHPT. The results
indicated that PHPT is about three-fold more prevalent in patients
with CAAG than in the general population and that CAAG is about
four-fold more prevalent in patients with PHPT than in the general
population.

Physical
Physical examination is of little contributory value in atrophic
gastritis; however, some findings are associated specifically with the

15
complications of H pylori–associated atrophic gastritis and
autoimmune atrophic gastritis.

 In uncomplicated H pylori– associated atrophic gastritis, clinical

findings are few and nonspecific.
o Epigastric tenderness may be present.
o If gastric ulcers coexist, guaiac-positive stool may result from
occult blood loss.
 Findings in a patient with autoimmune atrophic gastritis result from
the development of pernicious anemia and neurologic
complications.
 With severe cobalamin deficiency, the patient is pale and has
slightly icteric skin and eyes. The pulse is rapid, and the heart may
be enlarged. Auscultation usually reveals a systolic flow murmur.
Causes
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.
 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

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 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.
A large population-based study by Zhang et al suggested that the
presence of antigastric parietal cell antibodies (APCAs) may
contribute to the development of chronic atrophic gastritis even in the
absence of H pylori infection. The study, which included 9684 persons
aged 50-74 years, reported an overall seroprevalence of APCA in this
population of 19.5%, with a strong association found between the
existence of APCAs and the presence of chronic atrophic gastritis.
The more severe the disease, the greater the association with APCA
was found to be. However, the link between APCAs and the severity
of chronic atrophic gastritis was greatest in persons who were negative
for H pylori.

2.4 Clinical Appearances

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.

Interpreting Test Results

a. Hemoglobin and hematocrit decrease
b. Anemia (iron deficiency) due to chronic, slow blood loss
c. Fecal occult blood pos n 8jitive
d. Helicobacter pylori shows inflammation, allows biopsy.

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 CHAPTER 3
CONCLUSION
3.1 Conclusion
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.

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 BIBLIOGRAPHY

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

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Leung, P. S. (2014). New York, Springer.

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

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

Edition. New York, McGraw-Hill.

White, L., Gena Duncan, Wendy Baumle (2013). Medical-Surgical Nursing (3rd
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