BACHELOR OF SCIENCE IN NURSING

NCMB 316 - CARE OF CLIENTS WITH PROBLEMS IN

NUTRITIONAL AND GASTROINTESTINAL METABOLISM AND
ENDOCRINE, PERCEPTION AND COORDINATION (ACUTE AND CHRONIC)
COURSE MODULE COURSE UNIT WEEK
1 1 1

DISTURBANCES IN INGESTION, DIGESTION, AND ABSORPTION

 Read course and unit objectives

 Read study guide prior to class attendance z
 Read required learning resources; refer to unit
terminologies for jargons
 Proactively participate in classroom discussions
 Participate in weekly discussion board (Canvas)
 Answer and submit course unit tasks

At the end of this unit, the students are expected to:

Cognitive:
1. Describe the structure and function of the organs of the gastrointestinal (GI) tract.
2. Describe the mechanical and chemical processes involved in digesting and absorbing foods and
eliminating waste products.
3. Use assessment parameters appropriate for determining the status of GI function.
4. Describe the appropriate preparation, teaching, and follow-up care for patients who are
undergoing diagnostic testing of the GI tract.
 Psychomotor:
1. Practice beginning skills in promoting healthy physiologic and psychosocial responses.
2. Participate actively during class discussions
3. Confidently express opinion and thoughts in front of the class.

Affective:
1. Exemplify caring attitude(s) in the performance of procedures in a simulated scenario.
2. Demonstrate caring as the core of nursing, love of God, love of country, love of people.

Hinkle, J. L., & Cheever, K. H. (2018). Brunner & Suddarth's textbook of medical-surgical
nursing (Edition 14.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.

I. Functions of the Digestive System:

1. Ingestion. Food must be placed into the mouth before it can

be acted on; this is an active, voluntary process called
ingestion.
2. Propulsion. If foods are to be processed by more than one
digestive organ, they must be propelled from one organ to the
next; swallowing is one example of food movement that
depends largely on the propulsive process called peristalsis
(involuntary, alternating waves of contraction and relaxation
of the muscles in the organ wall).
3. Food breakdown: mechanical digestion. Mechanical
digestion prepares food for further degradation by enzymes
by physically fragmenting the foods into smaller pieces, and
examples of mechanical digestion are: mixing of food in the
mouth by the tongue, churning of food in the stomach, and
segmentation in the small intestine.
4. Food breakdown: chemical digestion. The sequence of steps in which the large food molecules are broken
down into their building blocks by enzymes is called chemical digestion.
5. Absorption. Transport of digested end products from the lumen of the GI tract to the blood or lymph is
absorption, and for absorption to happen, the digested foods must first enter the mucosal cells by active or passive
transport processes.
6. Defecation. Defecation is the elimination of indigestible residues from the GI tract via the anus in the form of
feces.

II. Anatomy of the Digestive System

The organs of the digestive system can be separated into two main groups: those forming the alimentary canal and
the accessory digestive organs.
Organs of the Alimentary Canal
The alimentary canal, also called the gastrointestinal tract, is a continuous, hollow muscular tube that winds through
the ventral body cavity and is open at both ends. Its organs include the following:

A. Mouth
Food enters the digestive tract through the mouth, or oral cavity, a mucous membrane-lined cavity.

 Lips. The lips (labia) protect its anterior opening.

 Cheeks. The cheeks form its lateral walls.
 Palate. The hard palate forms its anterior roof, and the soft palate forms its posterior roof.
 Uvula. The uvula is a fleshy finger-like projection of the soft palate, which extends inferiorly from the
posterior edge of the soft palate.
 Vestibule. The space between the lips and the cheeks externally and the teeth and gums internally is the
vestibule.
 Oral cavity proper. The area contained by the teeth is the oral cavity proper.
 Tongue. The muscular tongue occupies the floor of the mouth and has several bony attachments- two of
these are to the hyoid bone and the styloid processes of the skull.
 Lingual frenulum. The lingual frenulum, a fold of mucous membrane, secures the tongue to the floor
of the mouth and limits its posterior movements.
 Palatine tonsils. At the posterior end of the oral cavity are paired masses of lymphatic tissue, the
palatine tonsils.
 Lingual tonsil. The lingual tonsils cover the base of the tongue just beyond.

B. Pharynx
From the mouth, food passes posteriorly into the oropharynx and laryngopharynx.

 Oropharynx. The oropharynx is posterior to the oral cavity.

 Laryngopharynx. The laryngopharynx is continuous with the esophagus below; both of which are
common passageways for food, fluids, and air.

C. Esophagus
The esophagus or gullet, runs from the pharynx through the diaphragm to the stomach.

 Size and function. About 25 cm (10 inches) long, it is essentially a passageway that conducts food by
peristalsis to the stomach.
 Structure. The walls of the alimentary canal organs from the esophagus to the large intestine are made up of
the same four basic tissue layers or tunics.
 Mucosa. The mucosa is the innermost layer, a moist
membrane that lines the cavity, or lumen, of the organ; it
consists primarily of a surface epithelium, plus a small
amount of connective tissue (lamina propria) and a
scanty smooth muscle layer.
 Submucosa. The submucosa is found just beneath the
mucosa; it is a soft connective tissue layer containing blood
vessels, nerve endings, lymph nodules, and lymphatic
vessels.
 Muscularis externa. The muscularis externa is a muscle
layer typically made up of an inner circular layer and an
outer longitudinal layer of smooth muscle cells.
 Serosa. The serosa is the outermost layer of the wall that consists of a single layer of flat serous fluid-
producing cells, the visceral peritoneum.
 Intrinsic nerve plexuses. The alimentary canal wall contains two important intrinsic nerve plexuses- the
submucosal nerve plexus and the myenteric nerve plexus, both of which are networks of nerve
fibers that are actually part of the autonomic nervous system and help regulate the mobility and secretory
activity of the GI tract organs.

D. Stomach
Different regions of the stomach have been named, and they include the following:

 Location. The C-shaped stomach is on the left side of the abdominal cavity, nearly hidden by the liver
and the diaphragm.
 Function. The stomach acts as a temporary “storage tank” for food as well as a site for food
breakdown.
 Cardiac region. The cardiac region surrounds the cardioesophageal sphincter, through which
food enters the stomach from the esophagus.
 Fundus. The fundus is the expanded part of the stomach lateral to the cardiac region.
 Body. The body is the midportion, and as it narrows inferiorly, it becomes the pyloric antrum, and then the
funnel-shaped pylorus.
 Pylorus. The pylorus is the terminal part of the stomach and it is continuous with the small intestine through
the pyloric sphincter or valve.
 Size. The stomach varies from 15 to 25 cm in length, but its diameter and volume depend on how much
food it contains; when it is full, it can hold about 4 liters (1 gallon) of food, but when it is empty it collapses
inward on itself.
 Rugae. The mucosa of the stomach is thrown into large folds called rugae when it is empty.
 Greater curvature. The convex lateral surface of the stomach is the greater curvature.
 Lesser curvature. The concave medial surface is the lesser curvature.
 Lesser omentum. The lesser omentum, a double layer of peritoneum, extends from the liver to the greater
curvature.
 Greater omentum. The greater omentum, another extension of the peritoneum, drapes downward and
covers the abdominal organs like a lacy apron before attaching to the posterior body wall, and is riddled
with fat, which helps to insulate, cushion, and protect the abdominal organs.
 Stomach mucosa. The mucosa of the stomach is a simple columnar epithelium composed entirely of
mucous cells that produce a protective layer of bicarbonate-rich alkaline mucus that clings to the stomach
mucosa and protects the stomach wall from
being damaged by acid and digested by enzymes.
 Gastric glands. This otherwise smooth lining is dotted
with millions of deep gastric pits, which lead into
gastric glands that secrete the solution called
gastric juice.
 Intrinsic factor. Some stomach cells produce intrinsic
factor, a substance needed for the absorption of vitamin
b12 from the small intestine.
 Chief cells. The chief cells produce protein-digesting
enzymes, mostly pepsinogens.
 Parietal cells. The parietal cells produce corrosive
hydrochloric acid, which makes the stomach contents
acidic and activates the enzymes.
 Enteroendocrine cells. The enteroendocrine cells
produce local hormones such as gastrin, that are
important to the digestive activities of the stomach.
 Chyme. After food has been processed, it resembles heavy cream and is called chyme.

E. Small Intestine
The small intestine is the body’s major digestive organ.

 Location. The small intestine is a muscular tube extending from the pyloric sphincter to the large intestine.
 Size. It is the longest section of the alimentary tube, with an average length of 2.5 to 7 m (8 to 20 feet) in a
living person.
 Subdivisions. The small intestine has three subdivisions: the duodenum, the jejunum, and the
ileum, which contribute 5 percent, nearly 40 percent, and almost 60 percent of the small intestine,
respectively.
 Ileocecal valve. The ileum meets the large intestine at the ileocecal valve, which joins the large and small
intestine.
 Hepatopancreatic ampulla. The main pancreatic and bile ducts join at the duodenum to form the flasklike
hepatopancreatic ampulla, literally, the ” liver-pacreatic-enlargement”.
 Duodenal papilla. From there, the bile and pancreatic
juice travel through the duodenal papilla and enter the
duodenum together.
 Microvilli. Microvilli are tiny projections of the plasma
membrane of the mucosa cells that give the cell surface a
fuzzy appearance, sometimes referred to as the brush
border; the plasma membranes bear enzymes (brush border
enzymes) that complete the digestion of proteins and
carbohydrates in the small intestine.
 Villi. Villi are fingerlike projections of the mucosa that give
it a velvety appearance and feel, much like the soft nap
of a towel.
 Lacteal. Within each villus is a rich capillary bed and a
modified lymphatic capillary called a lacteal.
 Circular folds. Circular folds, also called plicae
circulares, are deep folds of both mucosa and submucosa
layers, and they do not disappear when food fills the small
intestine.
 Peyer’s patches. In contrast, local collections of lymphatic
tissue found in the submucosa increase in number toward the
end of the small intestine.

F. Large Intestine
The large intestine is much larger in diameter than the small
intestine but shorter in length.

 Size. About 1.5 m (5 feet) long, it extends from the ileocecal

valve to the anus.
 Functions. Its major functions are to dry out indigestible
food residue by absorbing water and to eliminate these
residues from the body as feces.
 Subdivisions. It frames the small intestines on three sides
and has the following subdivisions: cecum, appendix,
colon, rectum, and anal canal.
 Cecum. The saclike cecum is the first part of the large intestine.
 Appendix. Hanging from the cecum is the wormlike appendix, a potential trouble spot because it is an ideal
location for bacteria to accumulate and multiply.
 Ascending colon. The ascending colon travels up the right side of the abdominal cavity and makes a turn,
the right colic (or hepatic) flexure, to travel across the abdominal cavity.
 Transverse colon. The ascending colon makes a turn and continuous to be the transverse colon as it
travels across the abdominal cavity.
 Descending colon. It then turns again at the left colic (or splenic) flexure, and continues down the
left side as the descending colon.
 Sigmoid colon. The intestine then enters the pelvis, where it becomes the S-shaped sigmoid colon.
 Anal canal. The anal canal ends at the anus which opens to the exterior.
 External anal sphincter. The anal canal has an external voluntary sphincter, the external anal
sphincter, composed of skeletal muscle.
 Internal involuntary sphincter. The internal involuntary sphincter is formed by smooth muscles.

Accessory Digestive Organs

Other than the intestines and the stomach, the following are also part of the digestive system:

G. Teeth
The role the teeth play in food processing needs little introduction; we masticate, or chew, by opening and closing
our jaws and moving them from side to side while continuously using our tongue to move the food between our
teeth.

 Function. The teeth tear and grind the food, breaking it down into smaller fragments.
 Deciduous teeth. The first set of teeth is the deciduous teeth, also called baby teeth or milk teeth, and
they begin to erupt around 6 months, and a baby has a full set (20 teeth) by the age of 2 years.
 Permanent teeth. As the second set of teeth, the deeper permanent teeth, enlarge and develop, the roots of
the milk teeth are reabsorbed, and between the ages of 6 to 12 years they loosen and fall out.
 Incisors. The chisel-shaped incisors are adapted for cutting.
 Canines. The fanglike canines are for tearing and piercing.
 Premolars and molars. Premolars (bicuspids) and molars have broad crowns with round cusps (tips) and
are best suited for grinding.
 Crown. The enamel-covered crown is the exposed part of the tooth above the gingiva or gum.
 Enamel. Enamel is the hardest substance in the
body and is fairly brittle because it is heavily
mineralized with calcium salts.
 Root. The outer surface of the root is covered by a
substance called cementum, which attaches the
tooth to the periodontal membrane
(ligament).
 Dentin. Dentin, a bonelike material, underlies the
enamel and forms the bulk of the tooth.
 Pulp cavity. It surrounds a central pulp cavity,
which contains a number of structures (connective
tissue, blood vessels, and nerve fibers) collectively
called the pulp.
 Root canal. Where the pulp cavity extends into
the root, it becomes the root canal, which provides
a route for blood vessels, nerves,
 and other pulp structures to enter the pulp cavity of the tooth.

H. Salivary Glands
Three pairs of salivary glands empty their secretions into the mouth.

 Parotid glands. The large parotid glands lie anterior to the ears and empty their secretions into the mouth.
 Submandibular and sublingual glands. The submandibular and sublingual glands empty their
secretions into the floor of the mouth through tiny ducts.
 Saliva. The product of the salivary glands, saliva, is a mixture of mucus and serous fluids.
 Salivary amylase. The clear serous portion contains an enzyme, salivary amylase, in a
bicarbonate-rich juice that begins the process of starch digestion in the mouth.

I. Pancreas
Only the pancreas produces enzymes that break down all categories of digestible foods.

 Location. The pancreas is a soft, pink triangular gland that extends across the abdomen from the spleen to
the duodenum; but most of the pancreas lies posterior to the parietal peritoneum, hence its location is
referred to as retroperitoneal.
 Pancreatic enzymes. The pancreatic enzymes are secreted into the duodenum in an alkaline fluid that
neutralizes the acidic chyme coming in from the stomach.
 Endocrine function. The pancreas also has an endocrine function; it produces hormones
insulin and glucagon.

J. Liver
The liver is the largest gland in the body.

 Location. Located under the diaphragm, more to the right side of the body, it overlies and almost
completely covers the stomach.
 Falciform ligament. The liver has four lobes and is suspended from the diaphragm and abdominal wall by
a delicate mesentery cord, the falciform ligament.
 Function. The liver’s digestive function is to produce bile.
 Bile. Bile is a yellow-to-green, watery solution containing bile salts, bile pigments, cholesterol,
phospholipids, and a variety of electrolytes.
 Bile salts. Bile does not contain enzymes but its bile salts emulsify fats by physically breaking large fat
globules into smaller ones, thus providing more surface area for the fat-digesting enzymes to work on.

K. Gallbladder
While in the gallbladder, bile is concentrated by the removal of water.

 Location. The gallbladder is a small, thin-walled green sac that snuggles in a shallow fossa in the inferior
surface of the liver.
 Cystic duct. When food digestion is not occurring, bile backs up the cystic duct and enters the gallbladder
to be stored.

III. Physiology of the Digestive System

Specifically, the digestive system takes in food (ingests it), breaks it down physically and chemically into nutrient
molecules (digests it), and absorbs the nutrients into the bloodstream, then, it rids the body of indigestible remains
(defecates).
A. Activities Occurring in the Mouth, Pharynx, and Esophagus
The activities that occur in the mouth, pharynx, and esophagus are food ingestion, food breakdown, and food
propulsion.
Food Ingestion and Breakdown
Once food is placed in the mouth, both mechanical and chemical digestion begin.
 Physical breakdown. First, the food is physically broken down into smaller particles by chewing.
 Chemical breakdown. Then, as the food is mixed with saliva, salivary amylase begins the chemical
digestion of starch, breaking it down into maltose.
 Stimulation of saliva. When food enters the mouth, much larger amounts of saliva pour out; however, the
simple pressure of anything put into the mouth and chewed will also stimulate the release of saliva.
 Passageways. The pharynx and the esophagus have no digestive function; they simply provide
passageways to carry food to the next processing site, the stomach.
Food Propulsion – Swallowing and Peristalsis
For food to be sent on its way to the mouth, it must first be swallowed.
 Deglutition. Deglutition, or swallowing, is a complex process that involves the coordinated activity of
several structures (tongue, soft palate, pharynx, and esophagus).
 Buccal phase of deglutition. The first phase, the voluntary buccal phase, occurs in the mouth; once the
food has been chewed and well mixed with saliva, the bolus (food mass) is forced into the pharynx by the
tongue.
 Pharyngeal-esophageal phase. The second phase, the involuntary pharyngeal-esophageal phase,
transports food through the pharynx and esophagus; the parasympathetic division of the autonomic nervous
system controls this phase and promotes the mobility of the digestive organs from this point on.
 Food routes. All routes that the food may take, except the desired route distal into the digestive tract, are
blocked off; the tongue blocks off the mouth; the soft palate closes off the nasal passages; the larynx rises so
that its opening is covered by the flaplike epiglottis.
 Stomach entrance. Once food reaches the distal end of the esophagus, it presses against the
cardioesophageal sphincter, causing it to open, and food enters the stomach.

B. Activities of the Stomach

The activities of the stomach involve food breakdown and food propulsion.
Food Breakdown
The sight, smell, and taste of food stimulate parasympathetic nervous system reflexes, which increase the
secretion of gastric juice by the stomach glands
 Gastric juice. Secretion of gastric juice is regulated by both neural and hormonal factors.
 Gastrin. The presence of food and a rising pH in the stomach stimulate the stomach cells to release the
hormone gastrin, which prods the stomach glands to produce still more of the protein- digesting enzymes
(pepsinogen), mucus, and hydrochloric acid.
 Pepsinogen. The extremely acidic environment that hydrochloric acid provides is necessary, because it
activates pepsinogen to pepsin, the active protein-digesting enzyme.
 Rennin. Rennin, the second protein-digesting enzyme produced by the stomach, works primarily on milk
protein and converts it to a substance that looks like sour milk.
 Food entry. As food enters and fills the stomach, its wall begins to stretch (at the same time as the gastric
juices are being secreted).
 Stomach wall activation. Then the three muscle layers of the stomach wall become active; they compress
and pummel the food, breaking it apart physically, all the while continuously mixing the food with the
enzyme-containing gastric juice so that the semifluid chyme is formed.
Food Propulsion
Peristalsis is responsible for the movement of food towards the digestive site until the intestines.
 Peristalsis. Once the food has been well mixed, a rippling peristalsis begins in the upper half of the
stomach, and the contractions increase in force as the food approaches the pyloric valve.
 Pyloric passage. The pylorus of the stomach, which holds about 30 ml of chyme, acts like a meter that
allows only liquids and very small particles to pass through the pyloric sphincter; and because the pyloric
sphincter barely opens, each contraction of the stomach muscle squirts 3 ml or less of chyme into the small
intestine.
 Enterogastric reflex. When the duodenum is filled with chyme and its wall is stretched, a nervous reflex,
the enterogastric reflex, occurs; this reflex “puts the brakes on” gastric activity and slows the emptying of the
stomach by inhibiting the vagus nerves and tightening the pyloric sphincter, thus allowing time for intestinal
processing to catch up.

C. Activities of the Small Intestine

The activities of the small intestine are food breakdown and absorption and food propulsion.
Food Breakdown and Absorption
Food reaching the small intestine is only partially digested.
 Digestion. Food reaching the small intestine is only partially digested; carbohydrate and protein digestion
has begun, but virtually no fats have been digested up to this point.
 Brush border enzymes. The microvilli of small intestine cells bears a few important enzymes, the so-
called brush border enzymes, that break down double sugars into simple sugars and complete protein
digestion.
 Pancreatic juice. Foods entering the small intestine are literally deluged with enzyme-rich pancreatic juice
ducted in from the pancreas, as well as bile from the liver; pancreatic juice contains enzymes that, along with
brush border enzymes, complete the digestion of starch, carry out about half of the protein digestion, and are
totally responsible for fat digestion and digestion of nucleic acids.
 Chyme stimulation. When chyme enters the small intestine, it stimulates the mucosa cells to produce
several hormones; two of these are secretin and cholecystokinin which influence the release of
pancreatic juice and bile.
 Absorption. Absorption of water and of the end products of digestion occurs all along the length of the
small intestine; most substances are absorbed through the intestinal cell plasma membranes by the process of
active transport.
 Diffusion. Lipids or fats are absorbed passively by the process of diffusion.
 Debris. At the end of the ileum, all that remains are some water, indigestible food materials, and large
amounts of bacteria; this debris enters the large intestine through the ileocecal valve.
Food Propulsion
Peristalsis is the major means of propelling food through the digestive tract.
 Peristalsis. The net effect is that the food is moved through the small intestine in much the same way
that toothpaste is squeezed from the tube.
 Constrictions. Rhythmic segmental movements produce local constrictions of the intestine that mix the
chyme with the digestive juices, and help to propel food through the intestine.

D. Activities of the Large Intestine

The activities of the large intestine are food breakdown and absorption and defecation.
Food Breakdown and Absorption
What is finally delivered to the large intestine contains few nutrients, but that residue still has 12 to 24 hours
more to spend there.
 Metabolism. The “resident” bacteria that live in its lumen metabolize some of the remaining
nutrients, releasing gases (methane and hydrogen sulfide) that contribute to the odor of feces.
 Flatus. About 50 ml of gas (flatus) is produced each day, much more when certain carbohydrate- rich
foods are eaten.
  Absorption. Absorption by the large intestine is limited to the absorption of vitamin K, some B
vitamins, some ions, and most of the remaining water.
 Feces. Feces, the more or less solid product delivered to the rectum, contains undigested food residues,
mucus, millions of bacteria, and just enough water to allow their smooth passage. Propulsion of the
Residue and Defecation
When presented with residue, the colon becomes mobile, but its contractions are sluggish or short- lived.
 Haustral contractions. The movements most seen in the colon are haustral contractions, slow segmenting
movements lasting about one minute that occur every 30 minutes or so.
 Propulsion. As the haustrum fills with food residue, the distension stimulates its muscle to contract, which
propels the luminal contents into the next haustrum.
 Mass movements. Mass movements are long, slow-moving, but powerful contractile waves that move
over large areas of the colon three or four times daily and force the contents toward the rectum.
 Rectum. The rectum is generally empty, but when feces are forced into it by mass movements and its wall is
stretched, the defecation reflex is initiated.
 Defecation reflex. The defecation reflex is a spinal (sacral region) reflex that causes the walls of the
sigmoid colon and the rectum to contract and anal sphincters to relax.
 Impulses. As the feces is forced into the anal canal, messages reach the brain giving us time to make a
decision as to whether the external voluntary sphincter should remain open or be constricted to stop passage
of feces.
 Relaxation. Within a few seconds, the reflex contractions end and rectal walls relax; with the next mass
movement, the defecation reflex is initiated again.

IV. Laboratory Assessments

A. BARIUM SWALLOW TEST

A barium swallow test is a special type
of imaging test that uses barium and X- rays
to create images of your upper
gastrointestinal (GI) tract. Your upper GI
tract includes the back of your mouth and
throat (pharynx) and your esophagus.

Barium is used during a swallowing test to

make certain areas of the body show up
more clearly on an X-ray. The radiologist
will be able to see size and shape of the
pharynx and esophagus. He or she will also
be able see how you swallow. These details
might not be seen on a standard X-ray.
Barium is used only for imaging tests for
the GI tract.

A barium swallow test may be used by itself or as part of an upper GI series. This series looks at your esophagus,
stomach, and the first part of the small intestine (duodenum). Fluoroscopy is often used during a barium swallow
test. Fluoroscopy is a kind of X-ray “movie.” Barium is a white liquid that is visible on X-rays. Barium passes
through the digestive system and does not cause a person any harm.
As it passes through the body, barium coats the inside of the food pipe, stomach, or bowel, causing the outlines of
the organs to appear on X-ray.

Why are barium swallow tests used?

A barium swallow can help a doctor identify problems in the food pipe, stomach, or bowel. A
barium swallow test may be used if someone has any of the following conditions:
 frequent, painful heartburn
 gastric reflux, where food or acid keeps coming back up the food pipe
 difficulty eating, drinking, or swallowing
This test can give a doctor information about how the person is swallowing.
It can also reveal if someone has any of the following in their food pipe, stomach, or the first part of the bowel:
 ulcers
 abnormal growths
 blockages
 narrowing
If someone has a tumor, this will show up on the X-ray as an irregular outline that extends from the wall of the
affected organ.

Procedure
 People who are undergoing a barium swallow should not eat or drink for a few hours before the test. In some
cases, the doctor may ask the person to stop taking medication before the test. Some hospitals recommend not
chewing gum, eating mints, or smoking cigarettes after midnight the night before a barium swallow test.
 The test takes around 60 minutes and will take place in the X-ray department of the hospital. A person will
need to change into a hospital gown.
 In the X-ray room, the person drinks the barium liquid. It often has a chalky taste but can sometimes be
flavored.
 A person will lie on a tilting table for part of the examination.
 In some cases, a person will be given an injection to relax their stomach.
 A person will be standing for some parts of the examination, and lying down on a tilting table for other parts.
This allows the liquid to travel through the body, and for the radiologist and radiographer to take a selection
of images.
 People do not have to stay in hospital after the test and are free to go home as soon as it is complete. The
results usually arrive within 1-2 weeks.

B. BARIUM ENEMA TEST

A barium enema is an X-ray procedure used to examine the

rectum and colon, often used as a complement to lower
gastrointestinal (GI) endoscopy.
 It is a diagnostic tool for patients with, for example,
lower GI bleeding, altered bowel habit or abdominal
pain, or to screen for polyps and colorectal cancer.
 Contraindications include: acute
colitis/diverticulitis, recent polypectomy or colonic
biopsy, older patients (>70 years old), pregnancy.
How does it work?
 Contrast is passed into the rectum to enhance X-ray pictures of the bowel. Barium enemas may use a
single contrast (barium only) or double contrast (barium and air). Double-contrast studies are more
common and successful.
 Patient Preparation
 Bowel preparation: this varies, but often involves a period of low-residue diet and oral/laxative washout.
Preparation is vital for good views of the bowel: the patient should receive full instructions on preparation
and the procedure.
 The radiologist should be supplied with a full patient history.

The Procedure
 The patient is cannulated and may be given intravenous antispasmodic medication (for example hyoscine
butylbromide) to make the procedure more comfortable and to aid the passage of barium.
 The patient is positioned in a left lateral position on an X-ray table.
 A digital rectal examination is then performed.
 A rectal catheter is lubricated and inserted into the rectum. This has two connectors. One connector is for
for passing barium and the other is for insufflating air.
 The patient is placed prone.
 Liquid barium is passed via a giving set into the catheter. It is passed slowly to prevent the patient
experiencing discomfort or an urge to defecate.
 X-ray screening takes place as the barium is passed so the radiologist can observe filling. The amount
instilled depends on the patient. The radiologist stops once the rectum is filled and the barium continues
to pass around the colon. The radiologist may change the patient’s position as necessary in order to aid
filling.
 Once the contrast reaches the splenic flexure, the patient returns to the prone position and air is
insufflated. As air enters, the colon inflates and the images of the mucosa become clearer.
 Radiography staff may assist in moving the patient to aid filling and to provide reassurance.
 Screening continues until the radiologist identifies the caecum, by seeing the appendix or by seeing
barium entering the small bowel.
 Once the entire colon is filled further pictures are taken in individual positions to obtain complete views.
 The radiographer ensures all pictures are valid.
 The rectum is emptied of barium and the catheter removed.
 The patient passes barium for several hours after the procedure.

Risks and side effects

 Patients may feel nauseous after a barium swallow test or become constipated. Drinking lots of fluids can help
to relieve constipation. Symptoms of nausea should improve as the barium passes through the system.
 It is normal for people to have white-colored stools the first few times they use the toilet after having a barium
swallow test.
 Some people might worry about being exposed to radiation as part of the X-ray process. However, the amount
of radiation a person is exposed to is minimal.
 Sometimes, the injection given to relax the stomach can cause temporary blurred vision.

Special considerations
 People should not have a barium swallow test if they are pregnant.
 If someone has glaucoma or heart problems and needs to have a barium swallow, the doctor may not give the
stomach-relaxing injection.
 If someone has diabetes then the doctor will schedule a morning appointment for the barium swallow.
 People who use insulin will be asked to miss their morning dose and maybe the previous evening’s dose.
They should bring their insulin and some food to have after the test. However, those who take long-acting
insulin should continue taking this.

Major Complications
- Colonic perforation.
- Haemorrhage.
- Oversedation.
- Cardiac arrhythmia.

Minor Complications
- Constipation.
- Abdominal discomfort.
- Rectal bleeding.
- Flatus.

C. GASTROSCOPY

A gastroscopy is a procedure where a thin,

flexible tube called an endoscope is used to
look inside the oesophagus (gullet), stomach and first part of the small intestine (duodenum). It's also sometimes
referred to as an upper gastrointestinal endoscopy. The endoscope has a light and a camera at one end. The
camera sends images of the inside of your oesophagus, stomach and duodenum to a monitor.

Why a gastroscopy may be used

A gastroscopy can be used to:
 investigate problems such as difficulty swallowing (dysphagia) or persistent abdominal
(tummy) pain
 diagnose conditions such as stomach ulcers or gastro-oesophageal reflux disease (GORD)
 treat conditions such as bleeding ulcers, a blockage in the oesophagus, non-cancerous growths
(polyps) or small cancerous tumours
A gastroscopy used to check symptoms or confirm a diagnosis is known as a diagnostic gastroscopy. A
gastroscopy used to treat a condition is known as a therapeutic gastroscopy.

The gastroscopy procedure

 A gastroscopy often takes less than 15 minutes, although it may take longer if it's being used to treat a
condition.
 It's usually carried out as an outpatient procedure, which means you won't have to spend the night in
hospital.
 Before the procedure, your throat will be numbed with a local anaesthetic spray. You can also choose to have
a sedative, if you prefer. This means you will still be awake, but will be drowsy and have reduced awareness
about what's happening.
 The doctor carrying out the procedure will place the endoscope in the back of your mouth and ask you to
swallow the first part of the tube. It will then be guided down your esophagus and into your stomach.
 The procedure shouldn't be painful, but it may be unpleasant or uncomfortable at times.

What are the risks?

A gastroscopy is a very safe procedure, but like all medical procedures it does carry a risk of
complications. Possible complications that can occur include:
 a reaction to the sedative, which can cause problems with your breathing, heart rate and blood pressure
 internal bleeding
 tearing (perforation) of the lining of your oesophagus, stomach or duodenum

D. Esophagogastroduodenoscopy
(EGD)

Esophagogastroduodenoscopy (EGD) is a
test to examine the lining of the esophagus,
stomach, and first part of the small intestine (the
duodenum).

How the Test is Performed

EGD is done in a hospital or medical center. The
procedure uses an endoscope. This is a flexible tube
with a light and camera at the end. The procedure is
done as follows:
 During the procedure, breathing, heart rate,
blood pressure, and oxygen level are
checked. Wires are attached to certain areas of the body and then to machines that monitor these vital signs.
 The patient receives medicine into a vein to help you relax. The patient should feel no pain and not
remember the procedure.
 A local anesthetic may be sprayed into the mouth to prevent you from coughing or gagging when the
scope is inserted.
 A mouth guard is used to protect the teeth and the scope. Dentures must be removed before the procedure
begins.
 The patient then lie on your left side.
 The scope is inserted through the esophagus (food pipe) to the stomach and duodenum. The duodenum
is the first part of the small intestine.
 Air is put through the scope to make it easier for the doctor to see.
 The lining of the esophagus, stomach, and upper duodenum is examined. Biopsies can be taken through
the scope. Biopsies are tissue samples that are looked at under the microscope.
 Different treatments may be done, such as stretching or widening a narrowed area of the
esophagus.
 After the test is finished, the client will not be able to have food and liquid until their gag reflex
returns (so you do not choke).
 The test lasts about 30 to 60 minutes.

Major Complications
- Colonic perforation.
- Haemorrhage.
- Oversedation.
- Cardiac arrhythmia.
 Minor Complications
- Constipation.
- Abdominal discomfort.
- Rectal bleeding.
- Flatus.

DISEASES OF THE UPPER GASTROINTESTINAL TRACT

VI. Gastroesophageal Reflux Disease (GERD)

Some degree of gastroesophageal reflux (backflow of gastric or duodenal contents into the esophagus) is normal
in both adults and children. Excessive reflux may occur because of an incompetent lower esophageal sphincter,
pyloric stenosis, or a motility disorder. The incidence of GERD seems to increase with aging.

Clinical Manifestations
Symptoms may include
 pyrosis (burning sensation in the esophagus),
 dyspepsia (indigestion),
 regurgitation, dysphagia or odynophagia (pain on swallowing),
 hypersalivation, and
 esophagitis.

Assessment and Diagnostic Findings

Diagnostic testing may include an endoscopy or barium swallow to evaluate damage to the esophageal mucosa.
Ambulatory 12- to 36-hour esophageal pH monitoring is used to evaluate the degree of acid reflux. Bilirubin
monitoring (Bilitec) is used to measure bile reflux patterns. Exposure to bile can cause mucosal damage.

Management
 Management begins with teaching the patient to avoid situations that decrease lower esophageal sphincter
pressure or cause esophageal irritation.
 The patient is instructed to eat a low-fat diet; to avoid caffeine, tobacco, beer, milk, foods containing
peppermint or spearmint, and carbonated beverages; to avoid eating or drinking 2 hours before bedtime; to
maintain normal body weight; to avoid tight-fitting clothes; to elevate the head of the bed on 6- to 8-inch (15-
to 20-cm) blocks; and to elevate the upper body on pillows.
 If reflux persists, antacids or H2 receptor antagonists, such as famotidine (Pepcid), nizatidine (Axid), or
ranitidine (Zantac), may be prescribed.
 Proton pump inhibitors (medications that decrease the release of gastric acid, such as lansoprazole [Prevacid],
rabeprazole [AcipHex], esomeprazole [Nexium], omeprazole [Prilosec], and pantoprazole [Protonix]) may be
used; however, these products may increase intragastric bacterial growth and the risk of infection.
 In addition, the patient may receive prokinetic agents, which accelerate gastric emptying. These agents
include bethanechol (Urecholine), domperidone (Motilium), and metoclopramide (Reglan). Because
metoclopramide can have extrapyramidal side effects that are increased in certain neuromuscular disorders,
such as Parkinson’s disease, it should be used only if no other option exists, and the patient should be
monitored closely.
  If medical management is unsuccessful, surgical intervention may be necessary. Surgical management
involves a Nissen fundoplication (wrapping of a portion of the gastric fundus around the sphincter area of the
esophagus).
 A Nissen fundoplication can be performed by the open method or by laparoscopy.

VII. Gastritis
Gastritis is inflammation of the stomach mucosa.

Acute gastritis lasts several hours to a few days and is often caused by dietary indiscretion (eating irritating
food that is highly seasoned or food that is infected). Other causes include excessive use of aspirin and other
nonsteroidal anti-inflammatory drugs (NSAIDs), excessive alcohol intake, bile reflux, and radiation therapy. A
more severe form of acute gastritis is caused by strong acids or alkali, which may cause the mucosa to become
gangrenous or to perforate. Gastritis may also be the first sign of acute systemic infection.

Chronic gastritis is a prolonged inflammation of the stomach that may be caused either by benign or malignant
ulcers of the stomach or by bacteria such as Helicobacter pylori. Chronic gastritis may be associated with
autoimmune diseases such as pernicious anemia, dietary factors such as caffeine, the use of medications such as
NSAIDs or bisphosphonates (eg, alendronate [Fosamax], risedronate [Actonel], ibandronate [Boniva]), alcohol,
smoking, or chronic reflux of pancreatic secretions and bile into the stomach. Superficial ulceration may occur
and can lead to hemorrhage.

Clinical Manifestations

Acute Gastritis
May have rapid onset of symptoms: abdominal discomfort, headache, lassitude, nausea, anorexia, vomiting, and
hiccupping

Chronic Gastritis
• May be asymptomatic.
• Complaints of anorexia, heartburn after eating, belching, a sour taste in the mouth, or nausea and vomiting.
• Patients with chronic gastritis from vitamin deficiency usually have evidence of malabsorption of
vitamin B12.

Assessment and Diagnostic Findings

• Gastritis is sometimes associated with achlorhydria or hypochlorhydria (absence or low levels of
hydrochloric acid) or with high acid levels.
• Upper gastrointestinal (GI) x-ray series, endoscopy.
• Biopsy with histologic examination are performed.
• Serologic testing for antibodies to the H. pylori antigen and a breath test may be performed.

Medical Management

Acute Gastritis
The gastric mucosa is capable of repairing itself after an episode of gastritis. As a rule, the patient
recovers in about 1 day, although the appetite may be diminished for an additional 2 or 3 days. The patient should
refrain from alcohol and eating until symptoms subside. Then the patient can progress to a nonirritating diet. If
symptoms persist, intravenous fluids may be necessary. If bleeding is present, management is similar to that of
upper GI tract hemorrhage. If gastritis is due to ingestion of
 strong acids or alkali, dilute and neutralize the acid with common antacids (eg, aluminum hydroxide);
neutralize alkali with diluted lemon juice or diluted vinegar.
If corrosion is extensive or severe, avoid emetics and lavage because of danger of perforation.
Supportive therapy may include nasogastric intubation, analgesic agents and sedatives, antacids, and IV fluids.
Fiberoptic endoscopy may be necessary; emergency surgery may be required to remove gangrenous or
perforated tissue; gastric resection (gastrojejunostomy) may be necessary to treat pyloric obstruction. Chronic
Gastritis Diet modification, rest, stress reduction, avoidance of alcohol and NSAIDs, and pharmacotherapy are
key treatment measures. Gastritis related to H. pylori infection is treated with selected drug combinations.

Nursing Management

Reducing Anxiety
• Carry out emergency measures for ingestion of acids or alkalies.
• Offer supportive therapy to patient and family during treatment and after the ingested acid or alkali has
been neutralized or diluted.
• Prepare patient for additional diagnostic studies (endoscopy) or surgery.
• Calmly listen to and answer questions as completely as possible; explain all procedures and
treatments.

Promoting Optimal Nutrition

• Provide physical and emotional support for patients with acute gastritis.
• Help patient manage symptoms (eg, nausea, vomiting, heartburn, and fatigue).
• Avoid foods and fluids by mouth for hours or days until acute symptoms subside.
• Offer ice chips and clear liquids when symptoms subside.
• Encourage patient to report any symptoms suggesting a repeat episode of gastritis as food is introduced. •
Discourage caffeinated beverages (caffeine increases gastric activity and pepsin secretion), alcohol, and
cigarette smoking (nicotine inhibits neutralization of gastric acid in the duodenum).
• Refer patient for alcohol counseling and smoking cessation when appropriate.

Promoting Fluid Balance

• Monitor daily intake and output for dehydration (minimal intake of 1.5 L/day and urine output of 30 mL/h).
Infuse intravenous fluids if prescribed.
• Assess electrolyte values every 24 hours for fluid imbalance.
• Be alert for indicators of hemorrhagic gastritis (hematemesis, tachycardia, hypotension), and notify
physician.

Relieving Pain
• Instruct patient to avoid foods and beverages that may be irritating to the gastric mucosa.
• Instruct patient in the correct use of medications to relieve chronic gastritis.
• Assess pain and attainment of comfort through use of medications and avoidance of irritating
substances

VIII. Peptic Ulcer

A peptic ulcer is an excavation formed in the mucosal wall of the stomach, pylorus, duodenum, or esophagus. It is
frequently referred to as a gastric, duodenal, or esophageal ulcer, depending on its location. It is caused by the
erosion of a circumscribed area of mucous membrane. Peptic ulcers are
more likely to be in the duodenum than in the stomach. They tend to occur singly, but there may be several
present at one time.

Chronic ulcers usually occur in the lesser curvature of the stomach, near the pylorus. Peptic ulcer has been
associated with bacterial infection, such as Helicobacter pylori. The greatest frequency is noted in people between
the ages of 40 and 60 years. After menopause, the incidence among women is almost equal to that in men.
Predisposing factors include family history of peptic ulcer, blood type O, chronic use of nonsteroidal anti-
inflammatory drugs (NSAIDs), alcohol ingestion, excessive smoking, and, possibly, high stress.

Esophageal ulcers result from the backward flow of hydrochloric acid from the stomach into the esophagus.
Zollinger–Ellison syndrome (gastrinoma) is suspected when a patient has several peptic ulcers or an ulcer that is
resistant to standard medical therapy. This syndrome involves extreme gastric hyperacidity (hypersecretion of
gastric juice), duodenal ulcer, and gastrinomas (islet cell tumors). About 90% of tumors are found in the gastric
triangle. About one third of gastrinomas are malignant. Diarrhea and steatorrhea (unabsorbed fat in the stool) may
be evident. These patients may have coexistent parathyroid adenomas or hyperplasia and exhibit signs of
hypercalcemia. The most frequent complaint is epigastric pain.

The presence of H. pylori is not a risk factor. Stress ulcer (not to be confused with Cushing’s or
Curling’s ulcers) is a term given to acute mucosal ulceration of the duodenal or gastric area that occurs after
physiologically stressful events, such as burns, shock, severe sepsis, and multiple organ trauma. Fiberoptic
endoscopy within 24 hours of trauma or injury shows shallow erosions of the stomach wall; by 72 hours,
multiple gastric erosions are observed, and as the stressful condition continues, the ulcers spread. When the
patient recovers, the lesions are reversed; this pattern is typical of stress ulceration.

Clinical Manifestations
 Symptoms of an ulcer may last days, weeks, or months and may subside only to reappear without cause.
Many patients have asymptomatic ulcers.
 Dull, gnawing pain and a burning sensation in the midepigastrium or in the back are characteristic.
 Pain is relieved by eating or taking alkali; once the stomach has emptied or the alkali wears off, the pain
returns.
 Sharply localized tenderness is elicited by gentle pressure on the epigastrium or slightly right of the midline.
 Other symptoms include pyrosis (heartburn) and a burning sensation in the esophagus and stomach, which
moves up to the mouth, occasionally with sour eructation (burping).
 Vomiting is rare in uncomplicated duodenal ulcer; it may or may not be preceded by nausea and usually
follows a bout of severe pain and bloating; it is relieved by ejection of the acid gastric contents.
 Constipation or diarrhea may result from diet and medications.
 Bleeding (15% of patients with gastric ulcers) and tarry stools may occur; a small portion of patients who
bleed from an acute ulcer have only very mild symptoms or none at all.

Assessment and Diagnostic Methods

• Physical examination (epigastric tenderness, abdominal distention).
• Endoscopy (preferred, but upper gastrointestinal [GI] barium study may be done).
• Diagnostic tests include analysis of stool specimens for occult blood, gastric secretory studies, and biopsy
and histology with culture to detect H. pylori (serologic testing, stool antigen tests, or a breath test may
also detect H. pylori)
 Medical Management
The goals of treatment are to eradicate H. pylori and manage gastric acidity.

Pharmacologic Therapy
• Antibiotics combined with proton pump inhibitors and bismuth salts to suppress H. pylori.
• H2-receptor antagonists (in high doses in patients with Zollinger–Ellison syndrome) to decrease stomach acid
secretion; maintenance doses of H2-receptor antagonists are usually recommended for 1 year. Proton pump
inhibitors may also be prescribed.
• Cytoprotective agents (protect mucosal cells from acid or NSAIDs).
• Antacids in combination with cimetidine (Tagamet) or ranitidine (Zantac) for treatment of stress ulcer
and for prophylactic use. Lifestyle Changes
• Stress reduction and rest are priority interventions. The patient needs to identify situations that are stressful or
exhausting (eg, rushed lifestyle and irregular schedules) and implement changes, such as establishing regular
rest periods during the day in the acute phase of the disease. Biofeedback, hypnosis, behavior modification,
massage, or acupuncture may also be useful.
• Smoking cessation is strongly encouraged because smoking raises duodenal acidity and significantly inhibits
ulcer repair. Support groups may be helpful.
• Dietary modification may be helpful. Patients should eat whatever agrees with them; small, frequent meals are
not necessary if antacids or histamine blockers are part of therapy. Oversecretion and hypermotility of the GI
tract can be minimized by avoiding extremes of temperature and overstimulation by meat extracts. Alcohol
and caffeinated beverages such as coffee (including decaffeinated coffee, which stimulates acid secretion)
should be avoided. Diets rich in milk and cream should be avoided also because they are potent acid
stimulators. The patient is encouraged to eat three regular meals a day

Surgical Management
• With the advent of H2-receptor antagonists, surgical intervention is less common.
• If recommended, surgery is usually for intractable ulcers (particularly with Zollinger–Ellison syndrome), life
threatening hemorrhage, perforation, or obstruction. Surgical procedures include vagotomy, vagotomy with
pyloroplasty, or Billroth I or II.

NURSING PROCESS
THE PATIENT WITH PEPTIC ULCER

Assessment
• Assess pain and methods used to relieve it; take a thorough history, including a 72-hour food intake history.
• If patient has vomited, determine whether emesis is bright red or coffee ground in appearance. This helps
identify source of the blood.
• Ask patient about usual food habits, alcohol, smoking, medication use (NSAIDs), and level of tension
or nervousness.
• Ask how patient expresses anger (especially at work and with family), and determine whether patient
is experiencing occupational stress or family problems.
• Obtain a family history of ulcer disease.
• Assess vital signs for indicators of anemia (tachycardia, hypotension).
• Assess for blood in the stools with an occult blood test.
• Palpate abdomen for localized tenderness.

Diagnosis Nursing Diagnoses

• Acute pain related to the effect of gastric acid secretion on damaged tissue
• Anxiety related to coping with an acute disease
• Imbalanced nutrition related to changes in diet
• Deficient knowledge about preventing symptoms and managing the condition

Collaborative Problems/Potential Complications

• Hemorrhage: upper GI
• Perforation
• Penetration
• Pyloric obstruction (gastric outlet obstruction)

Planning and Goals

The major goals of the patient may include relief of pain, reduced anxiety, maintenance of nutritional requirements,
knowledge about the management and prevention of ulcer recurrence, and absence of complications.

Nursing Interventions

Relieving Pain and Improving Nutrition

• Administer prescribed medications.
• Avoid aspirin, which is an anticoagulant, and foods and beverages that contain acid-enhancing caffeine (colas,
tea, coffee, chocolate), along with decaffeinated coffee.
• Encourage patient to eat regularly spaced meals in a relaxed atmosphere; obtain regular weights and encourage
dietary modifications.
• Encourage relaxation techniques.

Reducing Anxiety
• Assess what patient wants to know about the disease, and evaluate level of anxiety; encourage patient to express
fears openly and without criticism.
• Explain diagnostic tests and administering medications on schedule.
• Interact in a relaxing manner, help in identifying stressors, and explain effective coping techniques and
relaxation methods.
• Encourage family to participate in care, and give emotional support.

Monitoring and Managing Complications

If hemorrhage is a concern
• Assess for faintness or dizziness and nausea, before or with bleeding; test stool for occult or gross blood;
monitor vital signs frequently (tachycardia, hypotension, and tachypnea).
• Insert an indwelling urinary catheter and monitor intake and output; insert and maintain an IV line for
infusing f luid and blood.
• Monitor laboratory values (hemoglobin and hematocrit).
• Insert and maintain a nasogastric tube and monitor drainage; provide lavage as ordered.
• Monitor oxygen saturation and administering oxygen therapy.
• Place the patient in the recumbent position with the legs elevated to prevent hypotension, or place the
patient on the left side to prevent aspiration from vomiting.
• Treat hypovolemic shock as indicated.
If perforation and penetration are concerns
• Note and report symptoms of penetration (back and epigastric pain not relieved by medications that were
effective in the past).
• Note and report symptoms of perforation (sudden abdominal pain, referred pain to shoulders, vomiting and
collapse, extremely tender and rigid abdomen, hypotension and tachycardia, or other signs of shock).
1. Dyspepsia: Difficult digestion
2. Emesis (vomiting): Stomach contents expelled through the mouth
3. Eructation: Act of belching or raising gas from stomach
4. Gastric ulcer: Lesion on wall of stomach; also known as peptic ulcer
5. Gastritis: Inflammation of the stomach
6. Gastrodynia: Pain in the stomach
7. Hematemesis: Vomiting of blood
8. Hiatal hernia: Protrusion of part of the stomach through the esophageal opening into diaphragm
9. Hyperemesis: Excessive vomiting
10. Nasogastric: Pertaining to nose and stomach
11. Nausea: Urge to vomit
12. Regurgitation: Return of solids and fluids to mouth from stomach
13. Ulcer: Sore or lesion of mucous membrane or skin
14. The liver, pancreas, and gallbladder all experience their own specific conditions, the most common of which
is good, old-fashioned, often-painful gallstones.
15. Calculus (plural is calculi): Stones
16. Cholelithiasis: Condition of having gallstones
17. Duodenal ulcer: Erosion or ulceration in the lining of the duodenum (first portion of the small
intestine)
18. Gallstones: Hard collections of bile that form in gallbladder and bile ducts
19. Hepatomegaly: Enlargement of liver
20. Hepatoma: Tumor of liver

Ignatavicius, D.D., Workman, M.L., & Rebar, C.R. (2018). Medical-Surgical Nursing: Concepts for
Interprofessional Collaborative Care (9th ed.). St. Louis: Elsevier.
LeMone, P., Burke, K.M., Bauldoff, G., & Gubrud, P. (2015). Medical-Surgical Nursing: Critical
Reasoning in Patient Care (6th ed.). Upper Saddle River, NJ: Pearson/Prentice Hall.
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2. CASE STUDY: (40 POINTS)

A 55-year-old man is transferred to your unit from the intensive care unit following a head injury. During
your admission assessment, he complains of a burning sensation in his midepigastric area. On
examination, you note a distended abdomen with tenderness in the epigastric area.

A. What questions would you ask the patient?

B. What diagnostic tests would you anticipate and how would you prepare your patient for these?
C. Describe your plan of nursing care for this patient.

Yamada T; Alpers DH; et al. (2009). Textbook of gastroenterology (5th ed.). Chichester, West Sussex:
Blackwell Pub. pp. 2774–2784. ISBN 978-1-4051-6911-0.
"Esophagus Disorders". Medline Plus. U.S. National Library of Medicine. Retrieved 23
December 2013.
Nicki R. Colledge, Brian R. Walker, Stuart H. Ralston; illustrated by Robert Britton
(2010). Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill
Livingstone/Elsevier. ISBN 978-0-7020-3085-7.
Ali Nawaz Khan. "Small-Bowel Obstruction Imaging". Medscape. Retrieved 2017-03-07. Updated: Sep 22,
2016
Fernandes, Teresa; Oliveira, Maria I.; Castro, Ricardo; Araújo, Bruno; Viamonte, Bárbara; Cunha, Rui
(2014). "Bowel wall thickening at CT: simplifying the diagnosis". Insights into Imaging. 5 (2): 195–208.
doi:10.1007/s13244-013-0308-y. ISSN 1869-4101. PMC 3999365. PMID 24407923.
Sing, Ronald F.; Heniford, B. Todd; Augenstein, Vedra A. (1 March 2013). "Intestinal Angioedema
Induced by Angiotensin-Converting Enzyme Inhibitors: An Underrecognized Cause of Abdominal
Pain?". The Journal of the American Osteopathic Association. 113 (3): 221–
223. doi:10.7556/jaoa.2013.113.3.221. ISSN 0098-6151.
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