NCM 112 (Lecture): Anatomy and
Physiology of GIT
I. Alimentary Canal/
Tract/Passageway
- The GIT is a 23-26-foot-long (7m- 7.9m
but will depend on the stature of the
patient) pathway that extends from the
mouth to the esophagus, stomach, small
intestines and large intestines, and
rectum to the terminal structure, the
anus.
- Passageway of the food.
- Food stays in the stomach for 1-2 hours
for starchy foods, 3 hours for proteins or
depending in the food you have eaten.
Functions
1. Digestion
2. Absorption
3. Elimination
Organs of the Alimentary Canal
1. Mouth
a) Lips (most external)
o Structure that keeps the food
inside the mouth so that the
nutrients from the food will be
kept inside and be chewed then
transport it to the next part of
GIT.
o When the patient has cleft lip, it
is difficult for them to chew, keep
the food inside the mouth, and to
talk.
o Lips will keep the mouth moist.
Mouth is best functional when it
is moist.
GI
b) Teeth
o This is important for mastication.
o Complete set of teeth is
important for teeth alignment
and for chewing of food.
o Embedded in the mandible and
jaw bone.
o Normal adult: 32 Teeth
§ Upper: 16
§ Lower: 16
o Four kinds of teeth
a. Incisors (central and lateral
for biting food)
§ Upper: 4
§ Lower: 4
b. Canines (for biting tough and
hard food)
§ Upper: 2
§ Lower: 2
c. Premolars (for grinding food)
§ Upper: 4 (R-2, L2)
§ Lower: 4 (R-2, L2)
d. Molars (grinding, chewing
tough and hard food)
§ Upper: 6 (R-3, L3)
§ Lower: 6 (R-3, L3)
§ Wisdom teeth: Last 3
molars and sometimes
impacted
c) Tongue
o Most powerful muscle of the
body.
o Can push down food from
oropharynx to esophagus.
o Responsible for appreciating
flavors.
o Four Basic Receptors
a. Sweet (how do you eat ice
cream cone and lollipops?)
§ At the front area or
anterior tongue
b. Sour (Seen Indian Mango)
§ Sides of the tongue.
c. Salty (Pringles)
§ Middle area
d. Bitter (when drinking meds)
§ Back or posterior
tongue.
 d) salivary glands
o release saliva to moisten food
for easy chewing and mixed with
enzymes for easy digestion and
easy swallowing of food bolus.
o Types of salivary glands
a. Sublingual
§ Below the tongue
§ Produces ample
amount of saliva.
b. Submandibular
§ Below the mandible
§ Associated with sour
receptor so it reacts to
sour taste.
c. Parotid
§ Parotitis- inflammation
of the parotid gland, can
sometimes be mistaken
as mumps.
e) buccal mucosa
o inner cheeks
o keeps the food moist
o keeps salivary glands and
enzymes to mix properly.
o Act as walls
2. Esophagus
- Connects mouth and stomach
- Very long passageway for food from the
mouth to the stomach.
- Food moves here with specific
contraction that alternates called
peristalsis.
3. Stomach
- A large organ that stores food
- Reservoir or storage area of food until
the small intestine is ready to digest the
food.
- It is a J-shaped organ.
- The bolus from the mouth will be
transported in the stomach and be
mixed with a lot of enzymes and acids,
making it more acidic and now be called
a chime.
Accessory organs (Liver, gallbladder,
pancreas)
- when damaged they play a great role on
the abdominal cavity affecting all areas
of the GI system.
4. Small Intestine
- Major organ for digestion
- Accessory organs secrete specific acids
and fluids that help alkalinize the food
because food coming from the stomach,
the chime, is so acidic.
- Open up a small portion of duodenum
and will allow secretions from the liver
and pancreas to alkalinize the food.
- Move down further for absorption of
nutrients and in preparation for
excretion.
- Three parts
a. Duodenum
b. Jejunum
c. Ileum
5. Large Intestine
- Attached to the small intestine via the
ileoceccal valve (terminal area of ileum
which is the last part of the small
intestine going to the cecum which is the
first part of the large intestine)
- Comprised of 5 major areas
a. Ascending colon
b. Transverse colon
c. Descending colon
d. Sigmoid colon
e. Rectum
o Last part of internal elimination
area
Anus
o Has a communication externally.
Note:
Any problems with the anatomy and
physiology that causes disorders of these
organs should be catered immediately.
Functions of the GIT
Absorptio hormone
Digestion Elimination
n gastrin.
Mouth Carbohydr Ileum
- masticati ates - wet or
on or - abso loose
chewing, rbed becau
biting, in se
grinding JEJU fluids
- amylase NUM are
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n starch absor
Duodenum Vitamins Transverse
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ne.
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turning NUM a. amylas
- Hydrochl e to
oric acid breakdo
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(crude- ng
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with not yet
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s, ph will d.
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3.6. It to
needs to breakdo
be acidic wn
to kill triglycer
bacteria ides to
that is fatty
present in acids.
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- Protease ptidase
will digest will
CHON digest
into peptide
simpler s to
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(polypepti acids
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Regulate enter
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 body’s Minerals Descending
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n books
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) it’s
- Liver will mush
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a. Bile Fluids Sigmoid
salts - Abso - Solid
will rbed or
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act or large d
react intest stools
with the ine
fat Fatty Acids Rectum
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Digestion o juices (pancreatic juices like

amylase, lipase)
a. Mechanical- types of digestion that
o fluids (contain chemicals like the
uses body parts, muscles, each organ
saliva)- H2O with the presence
of the body to properly breakdown food
of hydrogen and oxygen.
into smaller pieces like the mouth.
Mouth has both mechanical (chewing) Absorption
and chemical (salivary enzymes)
a. Duodenum
digestion.
o most of the absorption takes
b. Chemical- does not use body part in
place in the duodenum. Major
breaking down food. It uses acids,
organ for digestion. Only allow
enzymes, hormones, juices, and fluids
some carbohydrates to be
to aid in the breakdown of food into their
absorbed.
simplest forms.
b. Jejunum
o Acids (Hydrochloric acid)
o Absorbs all nutrients.
o enzymes (amylases)
o Major organ for absorption.
o hormones (in releasing of
c. ileum
enzymes and acids like secretin
o site of elimination
and cholecystokinin)
Control of Gastrointestinal Motility preparing for digestion, pancreas will
increase insulin and decrease glucagon.
1. Peristalsis
Once insulin has produced, it will stop
- Coordinated (from one point to another)
the stored glycogen.
sequential (1-2-1-2) contraction and
relaxation of smooth muscles.
2. Rhythmic Movements
- Intermittent contractions that are
responsible for mixing and moving food
along the digestive tract. Prominent in
the stomach.
3. Tonic Movements
- Consists of constant level contraction
without periods of relaxation found in the
lower esophagus, upper region of the Secretory Glands serve two basic
stomach (to avoid backflow of food), functions:
ileocecal valve (once it enters here, food
a. Production of mucus to lubricate and
cannot backflow anymore) and internal
protect the mucosal layer of the GI tract
anal sphincter. External sphincter can
wall. Without mucus if it is too acidic
be controlled but internal anal sphincter
and no neutralization the food that will
cannot be controlled.
go through mucosal linings they will
pass through the walls without
neutralization and can cause
inflammation. With presence of mucus
this will protect the mucosal layer and
facilitate easy and smooth transition of
food.
b. Secretion of fluids and enzymes to aid
in the digestion and absorption of
nutrients.

Gastrointestinal secretions
NCM 112 Lecture: Prioritization of Nursing
- Happens because when we think about Problems
food, the sensation of food and the smell > 3 things to consider in Prioritizing the
of food will stretch receptors send signal Nursing problem:
to the brain, which triggers secretion of • The client needs – identify which is need
digestive juices (in stomach and small by the patient right now.
intestine). Stomach will then release o Is it blood, water, education,
gastrin (even with the thought of food) oxygen, nutrition
which promotes production of stomach • ABC’s and safety – These are the
acids (prepares your body for eating). immediate threat to safety for the patients
Intestine releases secretin and o A-Airway
cholecystokinin (CCK), stimulating o B – breathing
secretion of pancreatic juice and bile (in o C- circulation
preparation for eating). o Safety
- When we are not eating yet, pancreas • Nursing Process – use the ADPIE
secretes glucagon to send signals to o A – Assessment
liver to release stored glycogen to o D – Diagnosis
increase blood sugar to maintain vital o P – Planning
functions and activities. Body is o I – Intervention
 o E – Evaluation
1. CLIENT NEEDS
• Uses Maslow’s Hierarchy of
needs – it is created by Abraham
Maslow
A. Physiologic needs – these are the
physical needs of the person that is going
to support the basic life function.
- Fundamental life needs
- Included:
o Water/fluids – the number 1 because
our body is composed of 75% of water
o Food – this talk about the nutrition and
diet . The ability of the body to
function (since the body needs
energy) from the nutrition in the food
intake of the person.
§ Without a proper food intake,
there will be a problem in the
body of the person
§ Based on plate: there should
be CHO, CHON, Fats
(regardless of the type of
fats). All of these should be in
equal number and
proportions. Also, add the
vitamins and minerals, and
fiber.
§ Types of fats:
monounsaturated,
polyunsaturated and
unsaturated fats and
saturated fats. All of these fats
are needed by the body but of
different proportions.
§ Monounsaturated (somehow
difficult to breakdown) and
unsaturated (it will not cause
any blockages in the body)
fats are the healthier ones.
§ Polyunsaturated fats – kind of
fats that are most difficult to
breakdown and it may cause
problems to the blood
vessels. This could lead to
atherosclerosis, stenosis, etc.
§ Review notes on fats intake
§ Note: that it is not true to
minimize your carbohydrate
all the time, it depends on the
metabolic needs of the body.
If the patient is a hyperthyroid
patient, you need to meet the
metabolic requirements since
the body of the patient has an
increase metabolism. Which
id why high caloric diet is
given to the patient. This is
opposite to the diabetic plate
o Sex – it is need according
to Sigmund Freud theory of
the conscious mind.
• According to the theory,
all of us are one big ID.
Our body is comprised
of one big ID. It
o The ID will give
you your wants,
desires, grit (ability
to fight), fantasies,
great push, libido
• Sex is important
because even after the
disease process,
usually (esp. the male
patient), they would ask
if they can still be
intimate/perform the
activity with his wife
o Oxygenation – most
important. It is needed by
the body for the cells to
function
• Without oxygenation,
the body will cease to
exists.
o ABC’s – Airway,
Breathing, Circulation
• Airway - If there is no
problem with the airway
of the patient, the
exchange of the gases
is free flowing. There is
no obstruction. The O2
can come in and CO2
can go out
• Breathing – the ability of
intake/inhale of O2 and
the ability to exhale or
release of the CO2.
• Circulation
o Major circulation:
Cerebral,
coronary,
abdominal, renal,
peripheral.
o If there is a
problem in the
circulation,
different parts of
the body will be
affected.
o Blood – person needs
blood to live
• If there is a decrease of
blood in the body, it
would intel that there
would be lose of focus,
dizziness, incomplete
activities of daily living,
immunocompromise,
prone to bleeding
o Temperature – this is
specific to pedia and
geria patients. It could
be a serious problem
when it happened to the
youngest or oldest of the
population.
• Pediatric patients - they
do not have the
capacity yet to
thermoregulate (ex. In
preterm neonates)
• Geriatric patients – they
lost their insulating
capacity of the body.
Because when the
patient starts to age,
there is a
decomposition of their
adipose tissue. With the
decomposition of the
adipose tissue (which
helps in the
insulation/trapping of
heat in the body), the
patient will have a
problem in
thermoregulation.
B. Safety and Security
- Included:
o Clothing – this is an added
protection and insulation to
the body like for example,
from frost bite
• When you have a frost,
their can be a problem with
your breathing especially if it
is in the nose
o Shelter- is under the safety
and security
• Even though a person
doesn’t have a shelter,
they can still live like in the
homeless persons
§ These shelter and
clothing can help you in
your nursing diagnosis
during community
nursing,
§ Example: for stroke
patients, you must install
handrails, bathroom bars,
etc. in their homes
§ We do not have these
kind of problem when the
patient is in the hospital
because we can provide
a temporary shelter for
them but how about if
they will go home? Which
is why installation of
these things are
important
C. Love and Belongingness
- more of psyche
 - these 3, the love and belongingness, - You have transcendence, you know
self-esteem, and self-transcendence – that it is impossible if there is no God
they all use psyche/ psychological who will help, that you need the help of
balance of a person other people, it is impossible if there is
- it is believed that if there is an unmet no medicine used, etc.
need in either physiological, safety and - Readiness of being part of the
security and physiological needs of a community
person’s totality, there would be a - You have the readiness, involvement,
problem with coping mechanism, receptive
defense mechanism, relationships.
- These will result in a problem with love
and belongingness. They cannot not
stay in one relationship, they problems 2. Nursing process
with coping. They have a problem with - Nursing process is the ability of the
their defense mechanism: they would nurse to identify or to perform nursing
over rationalized things, and they tasks that are going to help in the
would always be angry. recuperation, and rehabilitation of the
- These problems can lead to suicide patient while under the nurse’s care
- The patient had a second stroke, as a
D. Self-Esteem nurse what will you do first?
- Usually related to achievement, and - This is more on nursing action because
goals this is related to nursing care plan
- If a person met her physiologic needs, - 5 stages of the nursing Process: ADPIE
safety and security, and love and
belongingness, usually the person can a. A – Assessment – you are:
achieve his/her goals easily. § checking (normal vs abnormal
- It is where EGO is found VS),
§ observing (if this is acceptable or
E. Self- Actualization non-acceptable),
- This is the fulfillment § looking (for additional signs and
- There is a sense of fulfillment symptoms and manifestations)
- Where Ego is found also § This is important because it will
- Example: in Stroke patients, cancer guide you in checking and
patients, colostomy patients, etc. if that knowing what will be the priority
person has a self-actualization, even if and should done first in your
the disease is irreversible, they can still patient
overcome that challenge in their life. § In here, you already have the
And there is a sense of fulfillments to subjective and objective cues
push them to still do many things, like OBJECTIVE
a leader in a prayer group, leader of SUBJECTIVE (will validate the
support group, etc. subjective cues)
- Verbalized - IAPP
F. Self- Transcendence (nurse kasakit (Inspection,
- Overall awareness of all surroundings na gid ya sang Auscultation,
akun tiyan) Percussion,
including nature, God and fellow
palpation)
- You are being one with everything (you
- Felt - Use of scale
have involvement) (nurse ang (like pain
- Aware of having one creator, aware in sakit nagalatay scale)
your environment, community, you pakadtu sa
have spiritual belief, etc. likod ko)
- Claimed - Laboratories § Intermediate – within your time
(inde nurse ah, result/findings frame (like in one shift, within 4,6,
naga sakit gd - 8 -12 hours)
ya ang akun § Short-term goals- it can be an
sulok2x) intermediate goal. It can be used
- Reported - Imaging like interchangeably, but not if you
( nurse kagabe X-ray, CT have a time element. Because
ang sakit sang scan this can be done within 24 hours-
akun tiyan ari
a week
lang sa
tubang, § Long-term goals – example:
subong ari na weight gain, fluid volume
sa likod) excess/deficit
• It could be as short as 1
• week, up to 6 months
b. D- Diagnosing – you are going to § The short-term and long term
identify the problem plan are usually done by the
§ Is it existing – Example: Acute nursing managers.
pain related to rupture of the § Nursing care plan should be
peritoneum as evidence by SMART: Specific, Measurable,
guarding behavior Attainable, Realistic, Time-
§ Is it foreseeable – you already bound.
have the signs and symptoms,
and somehow that there are d. I- Interventions
things that is acceptable now, but § This talks about actions
in a couple of hours is not going § In here, you are taking
to be acceptable anymore. consideration the needs of the
• It is going to happen very patient. Especially in the
soon Maslow’s theory
• Example: Pupillary dilation § First thing to put is the
– you have to close monitor assessment, then so on and so
the patient forth
§ Is it a risk - these are problems § Actions should be related to
that there are existing risk factor subjective and objective cues,
in patient client needs (physiologic – self-
• Example: patient has a actualization)
fever and the WBC are § Identify if your nursing actions
raising, meaning the are: independent, dependent,
patient had an infection. collaborative
Therefore, there can be risk • Dependent – this is an
for dehydration related to... intervention that is given
directly from a doctor’s
c. P- Planning order. It needs prescription
§ Where you are going to set goals o It is where
§ These goals can either be: long- medication used can
term, short-term, intermediate, be found
immediate o Restraints, either
§ There is a time frame chemicals or
§ Immediate (like in cardio patient physicals or
like performing CPR) mechanical
§ Chemical –
valium like
 diazepam department
when patient prescription
is violent
§ This restraint e. E – Evaluation – you are going to
should be recheck, redo, refine
raised/renewe § You are checking for the
d every 24 effectiveness of the interventions
hours § You are going to go back to the
§ It’s effectivity plan and evaluate by using the
is every 24 objectives and objective cues
hours. You § Goal met, goal partially met, goal
have to not met.
assess if the • This is a guide if you are
patient is still going to endorse your NCP
violent after to the next shift or it is
this 24 hours. needed some alteration
§ Physical (modified) or it is needed to
restraints – be renewed (terminate)
when we are
tying the ESOPHAGEAL DISORDERS
patient when Chapter 45: Management of Patients with
they are Esophageal Disorders
violent like a
GLOSSARY
strait jacket.
§ Mechanical 1. achalasia: absent or ineffective
restrains – it is peristalsis (wavelike contraction) of the
used in post distal esophagus accompanied by
orif, post- failure of the esophageal sphincter to
surgical relax in response to swallowing
procedure 2. Boerhaave syndrome: spontaneous
o Laboratory and esophageal rupture due to forceful
diagnostic, imaging vomiting or straining
procedures 3. dysphagia: difficulty swallowing
• Collaborative – this still 4. dysplasia: abnormal change in cells
needed a prescribed by the 5. Frey syndrome: a rare syndrome
doctor, but it is characterized by undesirable sweating
interdepartmental and flushing occurring on the cheek,
o Scenario: what’s temporal region, and behind the ears
written in doctors after eating certain foods; also called
order are: refer to auriculotemporal syndrome
doc. X for rehab, for 6. gastroesophageal reflux disease
dietary instruction (GERD): disorder marked by backflow
care of dietary of gastric or duodenal contents into the
department, refetc. esophagus that causes troublesome
o In here must call the symptoms and/or mucosal injury to the
rehab and set a esophagus
schedule 7. gingivitis: inflammation of the gums;
o In collaborative, you change in color from pink to red, with
are making an associated swelling, bleeding, and
intervention that are sensitivity/tenderness
related to other
 8. halitosis: foul odor from the oral cavity;
in laymen’s terms, “bad breath”
9. hernia: protrusion of an organ or part of
an organ through the wall of the cavity
that normally contains it
10. lithotripsy: the use of shock waves to
break up or disintegrate stones
11. odynophagia: pain on swallowing
12. parotitis: inflammation of the parotid
gland
13. periapical abscess: abscessed tooth
14. pyrosis: a burning sensation in the
stomach and esophagus that moves up
to the mouth; commonly called
heartburn
15. sialadenitis: inflammation of the
salivary glands
16. stomatitis: inflammation of the oral
mucosa
17. temporomandibular disorders: a
group of conditions that cause pain or
dysfunction of the temporomandibular
joint and surrounding structures
18. vagotomy syndrome: dumping
syndrome; gastrointestinal symptoms,
such as diarrhea and abdominal
cramping, resulting from rapid gastric
emptying
19. xerostomia: dry mouth
DISORDERS OF THE ESOPHAGUS
The esophagus is a mucus-lined, muscular
tube that carries food from the mouth to the
stomach. It begins at the base of the pharynx
and ends about 4 cm below the diaphragm. Its
ability to transport food and fluid is facilitated
by two sphincters. The upper esophageal
sphincter, also called the hypopharyngeal
sphincter, is located at the junction of the
pharynx and the esophagus. The lower
esophageal sphincter, also called the
gastroesophageal sphincter or cardiac
sphincter, is located at the junction of the
esophagus and the stomach. An incompetent
lower esophageal sphincter allows reflux
(backward flow) of gastric contents. Because
there is no serosal layer of the esophagus, if
surgery is necessary, it is more difficult to
perform suturing or anastomosis. Disorders of
the esophagus include motility disorders
(achalasia, spasms), hiatal hernias,
diverticula, perforation, foreign bodies,
chemical burns, gastroesophageal reflux
disease (GERD), Barrett esophagus (BE),
benign tumors, and carcinoma. Dysphagia,
the most common symptom of esophageal
disease, may vary from an uncomfortable
feeling that a bolus of food is caught in the
upper esophagus to acute odynophagia (pain
on swallowing). Obstruction of food (solid and
soft) and even liquids may occur anywhere
along the esophagus. Often, the patient can
indicate that the problem is located in the
upper, middle, or lower third of the esophagus.
A. Hiatal Hernia
In the condition known as hiatal hernia, the
opening in the diaphragm through which the
esophagus passes becomes enlarged, and
part of the upper stomach moves up into the
lower portion of the thorax. Hiatal hernia
occurs more often in women than in men.
There are two main types of hiatal hernias:
sliding and paraesophageal. Sliding, or type I,
hiatal hernia occurs when the upper stomach
and the gastroesophageal junction are
displaced upward and slide in and out of the
thorax (see Fig. 45-7A). About 95% of patients
with esophageal hiatal hernia have a sliding
hernia. A paraesophageal hernia occurs when
all or part of the stomach pushes through the
diaphragm beside the esophagus (see Fig. 45-
7B). Paraesophageal hernias are further
classified as types II, III, or IV, depending on
the extent of herniation. Type IV has the
greatest herniation, with other intra-abdominal
viscera such as the colon, spleen, or small
bowel evidencing displacement into the chest
along with the stomach (Oleynikov & Jolley,
2015).
Clinical Manifestations
The patient with a sliding hernia may have
pyrosis, regurgitation, and dysphagia, but
many patients are asymptomatic. The patient
may present with vague symptoms of
intermittent epigastric pain or fullness after
eating. Large hiatal hernias may lead to
intolerance to food, nausea, and vomiting.
Sliding hiatal hernias are commonly
associated with GERD. Hemorrhage,
obstruction, and strangulation can occur with
any type of hernia (Oleynikov & Jolley, 2015).
Assessment and Diagnostic Findings
Diagnosis is typically confirmed by x-ray
studies; barium swallow;
esophagogastroduodenoscopy (EGD), which
is the passage of a fiberoptic tube through the
mouth and throat into the digestive tract for
visualization of the esophagus, stomach, and
small intestine; esophageal manometry; or
chest CT scan (Kohn, Price, Demeester, et al.,
2013).
Management
Management for a hiatal hernia includes
frequent, small feedings that can pass easily
through the esophagus. The patient is advised
not to recline for 1 hour after eating, to prevent
reflux or movement of the hernia, and to
elevate the head of the bed on 4- to 8-inch (10-
to 20-cm) blocks to prevent the hernia from
sliding upward. Surgical hernia repair is
indicated in patients who are symptomatic,
although the primary reason for the surgery is
typically to relieve GERD symptoms and not
repair the hernia. Current guidelines
recommend a laparoscopic approach, with an
open transabdominal or transthoracic
approach reserved for patients with
complications such as bleeding, dense
adhesions, or injury to the spleen. Up to 50%
of patients may experience early
postoperative dysphagia; therefore, the nurse
advances the diet slowly from liquids to solids,
while managing nausea and vomiting, tracking
nutritional intake, and monitoring weight. The
nurse also monitors for postoperative
belching, vomiting, gagging, abdominal
distension, and epigastric chest pain, which
may indicate the need for surgical revision;
these should be reported immediately to the
primary provider. Surgical repair is often
reserved for patients with more extreme cases
that involve gastric outlet obstruction or
suspected gastric strangulation, which may
result in ischemia, necrosis, or perforation of
the stomach (Kohn et al., 2013).
B. Barrett Esophagus
BE is a condition in which the lining of the
esophageal mucosa is altered. It affects 5.6%
of the population in the United States, occurs
predominantly in white men aged 50 or older,
and occurs in association with GERD
(Sharma, Katzka, Gupta, et al., 2015). Reflux
eventually causes changes in the cells lining
the lower esophagus. The cells that are laid to
cover the exposed area no longer form the
normal, squamous mucosa, but instead form
columnar-lined epithelium that resembles the
intestines. BE is the only known precursor to
esophageal adenocarcinoma (EAC).
Clinical Manifestations
The patient complains of symptoms of GERD,
notably frequent heartburn. The patient may
also complain of symptoms related to peptic
ulcers or esophageal stricture, or both.
Assessment and Diagnostic Findings
An EGD is performed. This usually reveals an
esophageal lining that is red rather than pink.
Biopsies are performed, and high-grade
dysplasia (HGD; abnormal changes in cells) is
evidenced by the squamous mucosa of the
esophagus replaced by columnar epithelium
that resembles that of the stomach or
intestines.
Management
Monitoring varies depending on the extent of
cell changes. Follow-up biopsies are
recommended no sooner than 3 to 5 years
after a biopsy shows no evidence of dysplasia
(Sharma et al., 2015). Treatment is
individualized for each patient.
Recommendations include surveillance with
biopsies, use of proton pump inhibitors (PPIs)
(see Table 45-2) to control reflux symptoms,
endoscopic resection, radiofrequency ablation
(high-frequency heat energy that kills
surrounding cells and tissues), and
consideration of metal stents for severe
dysphagia palliation (Sharma et al., 2015)
C. Diverticular Disease
A diverticulum is a saclike herniation of the
lining of the bowel that extends through a
defect in the muscle layer. Diverticula may
occur anywhere in the GI tract, from the
esophagus to the colon, but occur most
commonly in the colon, particularly in the
sigmoid colon (DiMarino, 2013; Shahedi, Dea,
Chudasama, et al., 2016). However, Asian
Americans may develop diverticula in the right
colon, probably because of genetic differences
(Shahedi et al., 2016).
Diverticulosis is defined by the presence of
multiple diverticula without inflammation or
symptoms. Diverticular disease of the colon is
very common in developed countries, and its
prevalence increases with increasing age;
indeed, it is present in half of all adults over 65
years of age, and nearly all adults by 90 years
of age (DiMarino, 2013). Diverticulosis is the
most common pathologic incidental finding on
colonoscopy. Approximately 80% of patients
with diverticulosis never develop any
complications or symptoms of disease. A low
intake of dietary fiber is considered a risk
factor, as well as obesity, a history of cigarette
smoking, regular use of nonsteroidal anti
inflammatory drugs (NSAIDs) and
acetaminophen (Tylenol), and a positive family
history. Although there is an equal prevalence
of diverticulosis between men and women,
complications related to diverticulosis more
commonly happen in men younger than 44
years of age, and in women older than 54
years of age (Razik & Nguyen, 2015).
Diverticulitis occurs when a diverticulum
becomes inflamed, causing perforation, and
potential complications such as obstruction,
abscess, fistula (abnormal tract) formation,
peritonitis, and hemorrhage (DiMarino, 2013).
Pathophysiology
Diverticula form when the mucosal and
submucosal layers of the colon herniate
through the muscular wall because of high
intraluminal pressure, low volume in the colon
(i.e., fiber-deficient contents), and decreased
muscle strength in the colon wall (i.e.,
muscular hypertrophy from hardened fecal
masses). Bowel contents can accumulate in
the diverticulum and decompose, causing
inflammation and infection. The diverticulum
can also become obstructed and then
inflamed if the obstruction continues. The
inflammation of the weakened colonic wall of
the diverticulum can cause it to perforate,
giving rise to irritability and spasticity of the
colon (i.e., diverticulitis). In addition,
abscesses may develop and may eventually
perforate, leading to peritonitis and erosion of
the arterial blood vessels, resulting in
bleeding. When a patient develops symptoms
of diverticulitis, microperforation of the colon
has occurred (DiMarino, 2013; Shahedi et al.,
2016).
Clinical Manifestations
Chronic constipation sometimes precedes the
development of diverticulosis by many years.
Most commonly, no problematic symptoms
occur with diverticulosis. Some patients may
have mild signs and symptoms that include
bowel irregularity with intervals of alternating
constipation and diarrhea, with nausea,
anorexia, and bloating or abdominal distention
(Shahedi et al., 2016). With diverticulitis, up to
70% of patients report an acute onset of mild
to severe pain in the left lower quadrant. This
may be accompanied by a change in bowel
habits, most typically constipation, with
nausea, fever, and leukocytosis. Acute
complications of diverticulitis may include
abscess formation, bleeding, and peritonitis. If
an abscess develops, the associated findings
are tenderness, a palpable mass, fever, and
leukocytosis. Inflamed diverticula may erode
areas adjacent to arterial branches, causing
massive rectal bleeding. An inflamed
diverticulum that perforates results in
abdominal pain localized over the involved
segment, usually the sigmoid; local abscess or
peritonitis follows (see previous discussion)
(DiMarino, 2013; Shahedi et al., 2016).
Recurrent episodes of diverticulitis may cause
chronic complications that include fistula
formation, including colovesicular fistulas (i.e.,
between the colon and bladder) and, in
women, colovaginal fistulas (i.e., between the
colon and vagina). As a response to repeated
inflammation, the colon may narrow with scar
tissue and fibrotic strictures, leading to
cramps, narrow stools, and increased
constipation, or, at times, intestinal obstruction
(DiMarino, 2013; Shahedi et al., 2016) (see
later discussion).
Assessment and Diagnostic Findings
Diverticulosis is typically diagnosed by
colonoscopy, which permits visualization of
the extent of diverticular disease (DiMarino,
2013; Shahedi et al., 2016). Laboratory tests
that assist in diagnosis of diverticulitis include
a CBC, revealing an elevated white blood cell
count; if the patient has frank blood in the
stool, a hemoglobin level should also be
analyzed. Urinalysis and urine cultures should
be analyzed in patients with suspected
colovesicular fistulas. An abdominal CT scan
with contrast agent is the diagnostic test of
choice to confirm diverticulitis; it can also
reveal perforation and abscesses. Abdominal
x-rays may demonstrate free air under the
diaphragm if a perforation has occurred from
the diverticulitis. Results from these radiologic
tests confirm whether or not the patient has
uncomplicated diverticulitis or complicated
diverticulitis that could require surgical
intervention. The Hinchey classification is
used as a guide to determine treatment
(DiMarino, 2013; Shahedi et al., 2016) (see
Table 47-3).
Gerontologic Considerations
The incidence of diverticular disease
increases with age because of degeneration
and structural changes in the circular muscle
layers of the colon and because of cellular
hypertrophy. The symptoms are less
pronounced in the older adult than in other
adults. Older adults may not have abdominal
pain until infection occurs. They may delay
reporting symptoms because they fear surgery
or are afraid that they may have cancer
(Eliopoulos, 2018).
Medical Management
Medical management is guided by the
presence of complications. Treatment for
patients with uncomplicated diverticulitis or
with Hinchey Stage I diverticulitis (see Table
47-3) is on an outpatient basis with diet and
medication. This is the typical treatment for
80% of patients with diagnosed diverticulitis
(DiMarino, 2013). Rest, oral fluids, and
analgesic medications are recommended.
Initially, a clear liquid diet is consumed until the
inflammation subsides; then a high fiber, low-
fat diet is recommended. This type of diet
helps increase stool volume, decrease colonic
transit time, and reduce intraluminal pressure.
Although antibiotics are typically prescribed for
7 to 10 days, results from a systematic review
did not find that the use of antibiotics improved
outcomes (Shabanzadeh & Wille-Jorgensen,
2012).
In acute cases of diverticulitis with significant
symptoms, hospitalization is required.
Hospitalization is often indicated for those who
are older, immunocompromised, or taking
corticosteroids. Patients with Hinchey Stage 2
diverticulitis (see Table 47-3) can require
hospitalization; those with higher stages
require surgery and hospitalization (see later
discussion). Withholding oral intake,
administering IV fluids, and instituting
nasogastric (NG) suctioning if vomiting or
distention occurs are used to rest the bowel.
Broad-spectrum antibiotics (e.g.,
ampicillin/sulbactam [Unasyn],
ticarcillin/clavulanate [Timentin]) (Shahedi et
al., 2016) are prescribed. An opioid (e.g.,
oxycodone) or other analgesic agents may be
prescribed for pain relief. Oral intake is
increased as symptoms subside. A low-fiber
diet may be necessary until signs of infection
decrease.
Surgical Management
Although acute diverticulitis usually subsides
with medical management, immediate surgical
intervention is necessary if complications
(e.g., perforation, peritonitis, hemorrhage,
obstruction) occur. In particular, patients with
Hinchey Stage III or IV diverticulitis are
considered surgical candidates (Shahedi,
2016). In cases of abscess formation without
peritonitis, hemorrhage, or obstruction, CT-
guided percutaneous drainage may be
performed to drain the abscess, and IV
antibiotics are given. After the abscess is
drained and the acute episode of inflammation
has subsided (after approximately 6 weeks),
surgery may be recommended to prevent
repeated episodes. Two types of surgery are
typically considered either to treat acute
complications or prevent further episodes of
inflammation:
• One-stage resection, in which the
inflamed area is removed and a primary
end-to-end anastomosis is completed
• Multiple-stage procedures for
complications such as obstruction or
perforation (see Fig. 47-4)
The type of surgery performed depends on the
extent of complications found during the
procedure. When possible, the area of
diverticulitis is resected and the remaining
bowel is joined end to end (i.e., primary
resection and end-to-end anastomosis). This
is performed using traditional surgical or
laparoscopically assisted colectomy with
lavage. A two-stage resection may be
performed in patients with Hinchey Stage IV
diverticulitis; the diseased colon is resected
(as in a one-stage procedure) but no
anastomosis is performed. In this procedure,
one end of the bowel is brought out to the
abdominal wall and the distal end is closed
over and left in the abdomen (Hartmann
procedure), or if the blood supply to the distal
colon is questionable, both ends of the bowel
are brought out to the abdominal wall (double-
barrel) (Hupfeld, Burcharth, Pommergaard, et
al., 2014). Both Hartmann procedures and
double-barrel colostomies are usually
reanastomosed at a later time.
Nursing Management
The nurse recommends a fluid intake of 2
L/day (within limits of the patient’s cardiac and
renal reserve) and suggests foods that are soft
but have increased fiber, such as prepared
cereals or soft-cooked vegetables, to increase
the bulk of the stool and facilitate peristalsis,
thereby promoting defecation. An
individualized exercise program is encouraged
to improve abdominal muscle tone. It is
important to review the patient’s daily routine
to establish a schedule for meals and a set
time for defecation and to assist in identifying
habits that may have suppressed the urge to
defecate. The nurse encourages daily intake
of bulk laxatives such as psyllium, which helps
propel feces through the colon. Some people
with diverticulosis may have food triggers such
as nuts and popcorn that bring on a
diverticulitis attack, whereas others may not
report food triggers. If triggers are identified,
patients should be urged to avoid them.
For the patient who has had a colostomy
placed, refer to the later section on Nursing
Management of the Patient Requiring an
Ostomy.
D. Gastroesophageal Reflux Disease
- Gastroesophageal reflux disease
(GERD) is a fairly common disorder
marked by backflow of gastric or
duodenal contents into the esophagus
that causes troublesome symptoms
and/or mucosal injury to the
esophagus. Excessive reflux may occur
because of an incompetent lower
esophageal sphincter, pyloric stenosis,
hiatal hernia, or a motility disorder. The
incidence of GERD seems to increase
with aging and is seen in patients with
irritable bowel syndrome and
obstructive airway disorders (asthma,
 COPD, cystic fibrosis) (Robinson & cause esophageal irritation. The patient
DiMango, 2014), BE (see later is instructed to eat a low-fat diet; avoid
discussion), peptic ulcer disease, and caffeine, tobacco, beer, milk, foods
angina. GERD is associated with containing peppermint or spearmint,
tobacco use, coffee drinking, alcohol and carbonated beverages; avoid
consumption, and gastric infection with eating or drinking 2 hours before
Helicobacter pylori bedtime; maintain normal body weight;
avoid tight-fitting clothes; and elevate
Clinical Manifestations the head of the bed by at least 30
- Symptoms may include pyrosis degrees (Hart, 2013). See Table 45-2
(heartburn, specifically more commonly for a list of medications commonly used
described as a burning sensation in the to manage GERD.
esophagus), dyspepsia (indigestion),
regurgitation, dysphagia or
odynophagia, hypersalivation, and
esophagitis. The symptoms may mimic
those of a heart attack. GERD can
result in dental erosion, ulcerations in
the pharynx and esophagus, laryngeal
damage, esophageal strictures,
adenocarcinoma, and pulmonary
complications (Hart, 2013).

Assessment and Diagnostic Findings

- The patient’s history aids in obtaining
an accurate diagnosis. Diagnostic
testing may include an endoscopy or
barium swallow to evaluate damage to
the esophageal mucosa (Hart, 2013).
Ambulatory 12- to 36-hour esophageal
pH monitoring is used to evaluate the
degree of acid reflux. Esophageal pH
monitoring was historically an
uncomfortable procedure, but the
advent of wireless capsule pH
monitoring is better tolerated and quite
accurate (Singhal & Khaitan, 2015)

Management
- Management begins with educating the
patient to avoid situations that decrease
lower esophageal sphincter pressure or
GASTRIC DISORDERS
Chapter Readings: Gastric Disorders
A. Peptic Ulcer Disease
- Peptic ulcer disease affects
approximately 4.5 million Americans
annually, and it requires inpatient
hospitalization for an estimated 30 out
of every 100 patients (Anand, 2015). A
peptic ulcer may be referred to as a
gastric, duodenal, or esophageal ulcer,
depending on its location. A peptic ulcer
is an excavation (hollowed-out area)
that forms in the mucosa of the
stomach, in the pylorus (the opening
between the stomach and duodenum),
in the duodenum or in the esophagus.
Erosion of a circumscribed area of
mucosa is the cause (see Fig. 46-2).
This erosion may extend as deeply as
the muscle layers or through the muscle
to the peritoneum (thin membrane that
lines the inside of the wall of the
abdomen) (Grossman & Porth, 2014;
NIDDK, 2014).
- Peptic ulcers are more likely to occur in
the duodenum than in the stomach. As
a rule they occur alone, but they may
occur in multiples. Chronic gastric
ulcers tend to occur in the lesser
curvature of the stomach, near the
pylorus. Esophageal ulcers occur as a
result of the backward flow of HCl from
the stomach into the esophagus
(gastroesophageal reflux disease
[GERD]). Women and men have about
equivalent lifetime risk of developing
peptic ulcers (Anand, 2015). The rates
of peptic ulcer disease among middle-
aged adults have diminished over the
past several decades, whereas the
rates among older adults have
increased (Anand, 2015; Pilotto &
Franceschi, 2014). Those who are 65
years and older present to both
outpatient and inpatient settings for
treatment of peptic ulcers more than
any other age group. This trend may be
explained, at least in part, by higher
rates of NSAID use and H. pylori
infections in older adult populations
(Anand, 2015; Pilotto & Franceschi,
2014). In the past, stress and anxiety
were thought to be causes of peptic
ulcers, but research has documented
that most peptic ulcers result from
infection with the gram-negative
bacteria H. pylori, which may be
acquired through ingestion of food and
water. Person-to-person transmission
of the bacteria also occurs through
close contact and exposure to emesis.
Although H. pylori infection is common
in the United States, most infected
people do not develop ulcers. It is not
known why H. pylori infection does not
cause ulcers in all people, but most
likely the predisposition to ulcer
formation depends on certain factors,
such as the type of H. pylori and other
as yet unknown factors (Anand, 2015;
Ruggiero & Censini, 2014; Grossman &
Porth, 2014). The use of NSAIDs such
as ibuprofen and aspirin is also a major
risk factor for peptic ulcers.
Furthermore, infection with H. pylori
and concomitant use of NSAIDs are
synergistic risks (Anand, 2015). It is
believed that smoking and alcohol
consumption may be risks, although the
evidence is inconclusive. There is no
evidence that the ingestion of milk,
caffeinated beverages, and spicy foods
are associated with the development of
peptic ulcers (Anand, 2015; NIDDK,
2014). Familial tendency also may be a
significant predisposing factor. People
with blood type O are more susceptible
to the development of peptic ulcers than
are those with blood type A, B, or AB.
There also is an association between
peptic ulcer disease and chronic
obstructive pulmonary disease,
cirrhosis of the liver, and chronic kidney
disease (Anand, 2015). Peptic ulcer
disease is also associated with
Zollinger–Ellison syndrome (ZES). ZES
is a rare condition in which benign or
malignant tumors form in the pancreas
and duodenum that secrete excessive
amounts of the hormone gastrin
(Anand, 2015; NIDDK, 2014). The
excessive amount of gastrin results in
extreme gastric hyperacidity and
severe peptic ulcer disease. While the
exact cause of ZES is unknown, 25% of
cases are linked to an inherited, genetic
condition called multiple endocrine
neoplasia, type 1 (MEN 1) (Epelboy &
Mazeh, 2014)
Pathophysiology
- Peptic ulcers occur mainly in the
gastroduodenal mucosa because this
tissue cannot withstand the digestive
action of gastric acid (HCl) and pepsin.
The erosion is caused by the increased
concentration or activity of acid–pepsin
or by decreased resistance of the
normally protective mucosal barrier. A
damaged mucosa cannot secrete
enough mucus to act as a barrier
against normal digestive juices.
Exposure of the mucosa to gastric acid
(HCl), pepsin, and other irritating
agents (e.g., NSAIDs or H. pylori) leads
to inflammation, injury, and subsequent
erosion of the mucosa. Patients with
duodenal ulcers secrete more acid than
normal, whereas patients with gastric
ulcers tend to secrete normal or
decreased levels of acid. When the
mucosal barrier is impaired, even
normal or decreased levels of HCl may
result in the formation of peptic ulcers.
The use of NSAIDs inhibits
prostaglandin synthesis, which is
associated with a disruption of the
normally protective mucosal barrier.
Damage to the mucosal barrier also
results in decreased resistance to
bacteria, and thus infection from H.
pylori bacteria may occur (Anand, 2015;
Grossman & Porth, 2014).
- ZES is suspected when a patient has
several peptic ulcers or an ulcer that is
resistant to standard medical therapy. It
is identified by the following:
hypersecretion of gastrin, duodenal
ulcers, and gastrinomas (islet cell
tumors) in the pancreas or duodenum.
More than 80% of gastrinomas are
found in the “gastric triangle,” which
encompasses the cystic and common
bile ducts, the second and third portions
of the duodenum, and the junction of
the head and body of the pancreas
(Bonheur & Nachimuthu, 2014). Most
gastrinomas tend to grow slowly;
however, more than 50% of these
tumors are malignant (Epelboym &
Mazeh, 2014). The patient with ZES
may experience epigastric pain, pyrosis
diarrhea, and steatorrhea (fatty stools).
Patients with ZES associated with
MEN-1 syndrome may have coexisting
pituitary or parathyroid tumors. Fifty
percent of patients with ZES-
associated MEN-1 syndrome are
diagnosed with hyperparathyroidism
and therefore may exhibit signs of
hypercalcemia (Epelboym & Mazeh,
2014). Stress ulcer is the term given to
the acute mucosal ulceration of the
duodenal or gastric area that occurs
after physiologically stressful events,
such as burns, shock, sepsis, and
multiple organ dysfunction syndrome
(Clark et al., 2015). Stress ulcers, which
are clinically different from peptic
ulcers, are most common in patients
who are ventilator-dependent after
trauma or surgery. Fiberoptic
endoscopy within 24 hours of trauma or
surgery reveals shallow erosions of the
stomach wall; by 72 hours, multiple
gastric erosions are observed. As the
stressful condition continues, the ulcers
spread. When the patient recovers, the
lesions are reversed. This pattern is
typical of stress ulceration. Differences
of opinion exist as to the actual cause
of mucosal ulceration in stress ulcers.
Usually, the ulceration results from a
disruption of the normally protective
mucosal barrier and decreased
mucosal blood flow (ischemia).
Mucosal ischemia results in the reflux of
duodenal contents into the stomach,
which increases exposure of the
unprotected gastric mucosa to the
digestive effects of gastric acid (HCl)
and pepsin (Anand, 2015; Clark et al.,
2015; Frandah, Colmer-Hamood, &
Nugent, 2014; Grossman & Porth,
2014). The combination of mucosal
ischemia and increased gastric acid
and pepsin exposure creates an ideal
climate for ulceration. Specific types of
ulcers that result from stressful
conditions include Curling ulcers and
Cushing ulcers. Curling ulcer is
frequently observed about 72 hours
after extensive burn injuries and often
involves the antrum of the stomach or
the duodenum (Anand, 2015). Cushing
ulcer is common in patients with a
traumatic head injury, stroke, brain
tumor, or following intracranial surgery.
Cushing ulcer is thought to be caused
by increased intracranial pressure,
 which results in overstimulation of the
vagal nerve and an increased secretion
of gastric acid (HCl) (Grossman &
Porth, 2014). Curling ulcers and
Cushing ulcers may occur in the
esophagus, stomach, or duodenum
and are usually deeper and more
penetrating than typical stress ulcers
(Kemp, Bashir, Dababneh, et al., 2015).
Clinical Manifestations
- Symptoms of peptic ulcer disease may
last for a few days, weeks, or months
and may disappear only to reappear,
often without an identifiable cause.
Many patients with peptic ulcers have
no signs or symptoms. These silent
peptic ulcers most commonly occur in
older adults and those taking aspirin
and other NSAIDs (Anand, 2015). As a
rule, the patient with an ulcer complains
of dull, gnawing pain or a burning
sensation in the midepigastrium or the
back. There are few clinical
manifestations that differentiate gastric
ulcers from duodenal ulcers; however,
classically, the pain associated with
gastric ulcers most commonly occurs
immediately after eating, whereas the
pain associated with duodenal ulcers
most commonly occurs 2 to 3 hours
after meals. In addition, approximately
50% to 80% of patients with duodenal
ulcers awake with pain during the night,
whereas 30% to 40% of patients with
gastric ulcers voice this type of
complaint. Patients with duodenal
ulcers are more likely to express relief
of pain after eating or after taking an
antacid than patients with gastric ulcers
(Anand, 2015). Other nonspecific
symptoms of either gastric ulcers or
duodenal ulcers may include pyrosis
vomiting, constipation or diarrhea, and
bleeding. These symptoms are often
accompanied by sour eructation
(burping), which is common when the
patient’s stomach is empty. Although
vomiting is rare in an uncomplicated
peptic ulcer, it may be a symptom of a
complication of an ulcer. It results from
gastric outlet obstruction, caused by
either muscular spasm of the pylorus or
mechanical obstruction from scarring or
acute swelling of the inflamed mucous
membrane adjacent to the ulcer.
Vomiting may or may not be preceded
by nausea; usually, it follows a bout of
severe pain and bloating, which is
relieved by vomiting. Emesis may
contain undigested food eaten many
hours earlier. Constipation or diarrhea
may occur, probably as a result of diet
and medications. The patient with
bleeding peptic ulcers may present with
evidence of GI bleeding, such as
hematemesis (vomiting blood) or the
passage of melena (black, tarry stools)
(Anand, 2015). Between 30% and 50%
patients with bleeding peptic ulcers do
not experience abdominal pain at the
time of diagnosis (Gururatsakul,
Holloway, Bellon, et al., 2014). Peptic
ulcer perforation results in the sudden
onset of signs and symptoms. The
patient often reports severe, sharp
upper abdominal pain, which may be
referred to the shoulder; extreme
abdominal tenderness; and nausea or
vomiting. Hypotension and tachycardia
may occur, indicating the onset of
shock (Anand, 2015; Dimou &
Velanovich, 2015).
Assessment and Diagnostic Findings
- A physical examination may reveal
pain, epigastric tenderness, or
abdominal distention. Upper
endoscopy is the preferred diagnostic
procedure because it allows direct
visualization of inflammatory changes,
ulcers, and lesions. Through
endoscopy, a biopsy of the gastric
mucosa and any suspicious lesions can
be obtained. Endoscopy may reveal
lesions that, because of their size or
location, are not evident on x-ray
studies. H. pylori infection may be
determined by endoscopy and
histologic examination of a tissue
specimen obtained by biopsy, or a rapid
urease test of the biopsy specimen.
Other less invasive diagnostic
measures for detecting H. pylori include
serologic testing for antibodies against
the H. pylori antigen, stool antigen test,
and urea breath test (Anand, 2015).
The patient who has a bleeding peptic
ulcer may require periodic CBCs to
determine the extent of blood loss and
 whether or not blood transfusions are
advisable (see Chapter 32). Stools may
be tested periodically until they are
negative for occult blood. Gastric
secretory studies are of value in
diagnosing ZES and achlorhydria (lack
of hydrochloric acid [HCl],
hypochlorhydria (low levels of HCl), or
hyperchlorhydria (high levels of HCl)
Medical Management
- Once the diagnosis is established, the
patient is informed that the condition
can be managed. Recurrence may
develop; however, peptic ulcers treated
with antibiotics to eradicate H. pylori
have a lower recurrence rate than those
not treated with antibiotics. The goals
are to eradicate H. pylori as indicated
and to manage gastric acidity. Methods
used include medications, lifestyle
changes, and surgical intervention.
Pharmacologic Therapy
- Currently, the most commonly used
therapy for peptic ulcers is a
combination of antibiotics, proton pump
inhibitors, and sometimes bismuth salts
that suppress or eradicate H. pylori.
Recommended combination drug
therapy is typically prescribed for 10 to
14 days and may include triple therapy
with two antibiotics (e.g., metronidazole
[Flagyl] or amoxicillin [Amoxil] and
clarithromycin [Biaxin]) plus a proton
pump inhibitor (e.g., lansoprazole
[Prevacid], omeprazole [Prilosec], or
rabeprazole [AcipHex]), or quadruple
therapy with two antibiotics
(metronidazole and tetracycline) plus a
proton pump inhibitor and bismuth salts
(Pepto-Bismol) (Anand, 2015; Marcus
& Greenwald, 2014). Research is
currently being conducted to develop a
vaccine against H. pylori (Ruggiero &
Censini, 2014). H2 blockers and proton
pump inhibitors that reduce gastric acid
secretion are used to treat ulcers not
associated with H. pylori infection.
Table 46-3 provides information about
the medication regimens for peptic
ulcer disease. The patient is advised to
adhere to and complete the medication
regimen to ensure complete healing of
the ulcer. The patient is advised to
avoid the use of aspirin and other
NSAIDs. Because most patients
become symptom free within a week,
the nurse stresses to the patient the
importance of following the prescribed
regimen so that the healing process can
continue uninterrupted and the return of
chronic ulcer symptoms can be
prevented. Maintenance dosages of H2
blockers are usually recommended for
1 year.
- For patients with ZES, hypersecretion
of gastrin stimulates the release of
gastric acid (HCl), which may be
controlled with high doses of H2
blockers. These patients may require
twice the normal dose, and dosages
usually need to be increased with
prolonged use (Epelboym & Mazeh,
2014). Octreotide (Sandostatin), a
medication that suppresses gastrin
levels, also may be prescribed. Patients
at high risk for stress ulcers (e.g.,
patients who are mechanically
ventilated for more than 48 hours) may
be treated prophylactically with either
H2 blockers or proton pump inhibitors,
and cytoprotective agents (e.g.,
misoprostol, sucralfate) because of the
increased risk of upper GI tract
hemorrhage (Clarke et al., 2015;
Plummer, Blaser, & Deane, 2014).
Smoking Cessation
- Smoking decreases the secretion of
bicarbonate from the pancreas into the
duodenum, resulting in increased
acidity of the duodenum. Continued
smoking is also associated with
delayed healing of peptic ulcers (Li et
al., 2014). Therefore, the patient is
encouraged to stop smoking. Refer to
Chapter 27 for information on how the
nurse may promote cessation of
tobacco use.
Dietary Modification
- The intent of dietary modification for
patients with peptic ulcers is to avoid
oversecretion of acid and hypermotility
in the GI tract. These can be minimized
by avoiding extremes of temperature in
food and beverages and
overstimulation from the consumption
 of alcohol, coffee (including 3443
decaffeinated coffee, which also
stimulates acid secretion), and other
caffeinated beverages. In addition, an
effort is made to neutralize acid by
eating three regular meals a day. Small,
frequent feedings are not necessary as
long as an antacid or an H2 blocker is
taken. Diet compatibility becomes an
individual matter: The patient eats
foods that are tolerated and avoids
those that produce pain.
postoperative bleeding, pain, infection,
and recovery time (American College of
Gastroenterology, 2015). The choice of
using an open abdominal approach or
laparoscopy is determined by the
surgeon’s preference and expertise as
well as clinical factors, such as the
patient’s current health status; the
presence of coexisting medical
conditions; and a history of previous
abdominal surgery.

Surgical Management Follow-Up Care

- The introduction of antibiotics to - Recurrence of peptic ulcer disease
eradicate H. pylori and of H2 blockers within 1 year may be prevented with the
as treatment for ulcers has greatly prophylactic use of H2 blockers taken at
reduced the need for surgical a reduced dose. Not all patients require
intervention (Epelboym & Mazeh, 2014; maintenance therapy; it may be
Soreide, Thorsen, & Soreide, 2014). prescribed only for those with two or
However, surgery is usually three recurrences per year, those who
recommended for patients with have had a complication such as
intractable ulcers (those failing to heal bleeding or gastric outlet obstruction, or
after 12 to 16 weeks of medical those for whom gastric surgery poses
treatment), life-threatening too high a risk. The likelihood of
hemorrhage, perforation, or obstruction recurrence is reduced if the patient
and for those with ZES that is avoids smoking, coffee (including
unresponsive to medications (Anand, decaffeinated coffee) and other
2015; Epelboym & Mazeh, 2014; caffeinated beverages, alcohol, and
Soreide et al., 2014). Surgical ulcerogenic medications (e.g.,
procedures include vagotomy, with or NSAIDs).
without pyloroplasty (transecting
nerves that stimulate acid secretion and
opening the pylorus), and antrectomy,
which is removal of the pyloric (antrum)
portion of the stomach with
anastomosis (surgical connection) to
either the duodenum
(gastroduodenostomy or Billroth I) or
jejunum (gastrojejunostomy or Billroth
II) (see Table 46-4.) Surgery may be
performed using a traditional open
abdominal approach (requiring a long
abdominal incision) or through the use
of laparoscopy (only requiring small
abdominal incisions). Laparoscopy is a
type of minimally invasive surgery that
involves the indirect visualization of the
abdominal cavity through the use of a
laparoscope (a thin flexible tube)
attached to a camera. The laparoscope
is placed into the abdomen through
small “keyhole” incisions (0.5 to 1.5 cm
in length). Laparoscopy has been
associated with decreased
 most often includes an infection with H.
B. Gastritis pylori (Marcus & Greenwald, 2014).
Chronic H. pylori gastritis is implicated
- Gastritis (inflammation of the gastric or in the development of peptic ulcers,
stomach mucosa) is a common GI gastric adenocarcinoma (cancer), and
problem, accounting for approximately gastric mucosa-associated lymphoid
2 million visits to outpatient clinics tissue lymphoma (Ruggiero & Censini,
annually in the United States (Wehbi, 2014; Yazbek, Trindade, Chin, et al.,
Yang, Sarver, et al., 2014). It affects 2015). Chronic gastritis may also be
women and men about equally and is caused by a chemical gastric injury
more common in older adults. Gastritis (gastropathy) as the result of long-term
may be acute, lasting several hours to drug therapy (e.g., aspirin and other
a few days, or chronic, resulting from NSAIDs) or reflux of duodenal contents
repeated exposure to irritating agents into the stomach, which most often
or recurring episodes of acute gastritis. occurs after gastric surgery (e.g.,
Acute gastritis may be classified as gastrojejunostomy and
erosive or nonerosive, based upon gastroduodenostomy). Autoimmune
pathologic manifestations present in disorders such as Hashimoto
the gastric mucosa (Wehbi et al., 2014). thyroiditis, Addison disease, and
The erosive form of acute gastritis is Graves’ disease are also associated
most often caused by local irritants with the development of chronic
such as aspirin and other nonsteroidal gastritis (see Chapter 52) (Grossman &
anti-inflammatory drugs (NSAIDs) (e.g., Porth, 2014; Marcus & Greenwald,
ibuprofen [Motrin]); alcohol 2014)
consumption; and gastric radiation
therapy (Grossman & Porth, 2014;
NIDDK, 2015; Wehbi et al., 2014). The
nonerosive form of acute gastritis is
most often caused by an infection with
Helicobacter pylori (H. pylori) (Wehbi et
al., 2014). It is estimated that 70% of
individuals in developing countries and
between 30% and 40% of individuals in
the United States and other
industrialized countries are infected
with H. pylori (Centers for Disease
Control and Prevention [CDC], 2016). A
more severe form of acute gastritis is
caused by the ingestion of strong acid
or alkali, which may cause the mucosa
to become gangrenous or to perforate
(see Chapter 72). Scarring can occur,
resulting in pyloric stenosis (narrowing
or tightening) or obstruction. Acute
gastritis also may develop in acute
illnesses, especially when the patient
has had major traumatic injuries; burns;
severe infection; hepatic, kidney, or
respiratory failure; or major surgery.
This type of acute gastritis is often
referred to as stress-related gastritis
(Clark, Gbadehan, Dim, et al., 2015;
NIDDK, 2015). Chronic gastritis is often
classified according to the underlying
3428 causative mechanism, which
 Clinical Manifestations
- The patient with acute gastritis may
have a rapid onset of symptoms, such
as epigastric pain or discomfort,
dyspepsia (indigestion), anorexia,
hiccups, or nausea and vomiting, which
can last from a few hours to a few days.
Erosive gastritis may cause bleeding,
which may manifest as blood in vomit or
as melena (black, tarry stools) or
hematochezia (bright red, bloody
stools) (NIDDK, 2015; Wehbi et al.,
Pathophysiology
2014). The patient with chronic gastritis
- Gastritis is characterized by a
may complain of fatigue, pyrosis (a
disruption of the mucosal barrier that
burning sensation in the stomach and
normally protects the stomach tissue
esophagus that moves up to the mouth;
from digestive juices (e.g., hydrochloric
heartburn) after eating, belching, a sour
acid [HCl] and pepsin). The impaired
taste in the mouth, early satiety,
mucosal barrier allows corrosive HCL,
anorexia, or nausea and vomiting.
pepsin, and other irritating agents (e.g.,
Some patients may have only mild
NSAIDs and H. pylori) to come in
epigastric discomfort or report
contact with the gastric mucosa,
intolerance to spicy or fatty foods or
resulting in inflammation. In acute
slight pain that is relieved by eating
gastritis, this inflammation is usually
(Marcus & Greenwald, 2014; NIDDK,
transient and self-limiting in nature.
2015). Patients with chronic gastritis
Inflammation causes the gastric
may not be able to absorb vitamin B12
mucosa to become edematous and
because of diminished production of
hyperemic (congested with fluid and
intrinsic factor by the stomach’s parietal
blood) and to undergo superficial
cells due to atrophy, which may lead to
erosion (see Fig. 46-1). Superficial
pernicious anemia (see Chapter 33)
ulceration may occur as a result of
(Zayouna & Piper, 2014). Some
erosive disease and may lead to
patients with chronic gastritis have no
hemorrhage. In chronic gastritis,
symptoms (Marcus & Greenwald,
persistent or repeated insults lead to
2014) (see Table 46-1).
chronic inflammatory changes, and
eventually atrophy (or thinning) of the
Assessment and Diagnostic Findings
gastric tissue (Grossman & Porth,
- The definitive diagnosis of gastritis is
2014).
determined by an endoscopy and
histologic examination of a tissue
specimen obtained by biopsy (Marcus
& Greenwald, 2014; Wehbi et al.,
2014). A complete blood count (CBC)
may be drawn to assess for anemia as
a result of hemorrhage or pernicious
anemia. Diagnostic measures for
detecting H. pylori infection may be
used and are discussed later in this
chapter in the Peptic Ulcer Disease
section.

Medical Management
- The gastric mucosa is capable of
repairing itself after an episode of acute
gastritis. As a rule, the patient recovers
in about 1 day, although the patient’s
 appetite may be diminished for an
additional 2 or 3 days. Acute gastritis is
also managed by instructing the patient
to refrain from alcohol and food until
symptoms subside. When the patient
can take nourishment by mouth, a
nonirritating diet is recommended. If the
symptoms persist, intravenous (IV)
fluids may need to be given. If bleeding
is present, management is similar to the
procedures used to control upper GI
tract hemorrhage discussed later in this
chapter
- Therapy is supportive and may include
nasogastric (NG) intubation, antacids,
histamine-2 receptor antagonists (H2
blockers) (e.g., famotidine [Pepcid],
ranitidine [Zantac]), proton pump
inhibitors (e.g., omeprazole [Prilosec],
lansoprazole [Prevacid]), and IV fluids
(NIDDK, 2015; Wehbi et al., 2014).
Fiberoptic endoscopy may be
necessary. In extreme cases,
emergency surgery may be required to
remove gangrenous or perforated
tissue. A gastric resection or a
gastrojejunostomy (anastomosis of
jejunum to stomach to detour around
the pylorus) may be necessary to treat
gastric outlet obstruction, also called
pyloric obstruction, a narrowing of the
pyloric orifice, which cannot be relieved
by medical management. Chronic
gastritis is managed by modifying the
patient’s diet, promoting rest, reducing
stress, recommending avoidance of
alcohol and NSAIDs, and initiating
medications that may include antacids,
H2 blockers, or proton pump inhibitors
(NIDDK, 2015). H. pylori may be treated
with selected drug combinations which
typically include a proton pump
inhibitor, antibiotics, and sometimes
bismuth salts (see Table 46-2).
Nursing Management
1. Reducing Anxiety
a. If the patient has ingested acids
or alkalis, emergency measures
may be necessary (see Chapter
72). The nurse offers supportive
therapy to the patient and family
during treatment and after the
ingested acid or alkali has been
neutralized or diluted. In some
cases, the nurse may need to
prepare the patient for additional
diagnostic studies
(endoscopies) or surgery. The
patient may be anxious because
of pain and planned treatment
modalities. The nurse uses a
calm approach to assess the
patient and to answer all
questions as completely as
possible.
2. Promoting Optimal Nutrition
a. For acute gastritis, the nurse
provides physical and emotional
support and helps the patient
manage the symptoms, which
may include nausea, vomiting,
and pyrosis (heartburn). The
patient should take no foods or
fluids by mouth—possibly for a
few days—until the acute
symptoms subside, thus
allowing the gastric mucosa to
heal. If IV therapy is necessary,
the nurse monitors fluid intake
and output along with serum
electrolyte values. After the
symptoms subside, the nurse
may offer the patient ice chips
followed by clear liquids.
Introducing solid food as soon as
possible may provide adequate
oral nutrition, decrease the need
for IV therapy, and minimize
irritation to the gastric mucosa.
As food is 3432 introduced, the
nurse evaluates and reports any
symptoms that suggest a repeat
episode of gastritis. The nurse
discourages the intake of
caffeinated beverages, because
caffeine is a central nervous
system stimulant that increases
gastric activity and pepsin
secretion. The nurse also
discourages alcohol use.
Discouraging cigarette smoking
is important because nicotine
reduces the secretion of
pancreatic bicarbonate, which
inhibits the neutralization of
gastric acid in the duodenum
(the first part of the small
intestine) (Hannah, 2014; Li,
Chan, Lu, et al., 2014). When
 appropriate, the nurse initiates
and refers the patient for alcohol
counseling and smoking
cessation program
3. Promoting Fluid Balance
a. Daily fluid intake and output are
monitored to detect early signs
of dehydration (minimal fluid
intake of 1.5 L/day, minimal urine
output of 0.5 mL/kg/h). If food
and oral fluids are withheld, IV
fluids (3 L/day) usually are
prescribed and a record of fluid
intake plus caloric value (1 L of
b. 5% dextrose in water = 170
calories of carbohydrate) needs
to be maintained. Electrolyte
values (sodium, potassium,
chloride) are assessed every 24
hours to detect any imbalance.
The nurse must always be alert
to any indicators of hemorrhagic
gastritis, which include
hematemesis (vomiting of
blood), tachycardia, and
hypotension. All stools should be
examined for the presence of
frank or occult bleeding. If these
occur, the primary provider is
notified and the patient’s vital
signs are monitored as the
patient’s condition warrants.
Guidelines for managing upper
GI tract bleeding are discussed
later in this chapter
4. Relieving Pain
a. Measures to help relieve pain
include instructing the patient to
avoid foods and beverages that
may irritate the gastric mucosa
as well as the correct use of
medications to relieve chronic
gastritis. The nurse must
regularly assess the patient’s
level of pain and the extent of
comfort achieved through the
use of medications and
avoidance of irritating
substances.
Promoting Home, Community-Based, and
Transitional Care
1. Educating Patients About Self-Care
a. The nurse evaluates the
patient’s knowledge about
gastritis and develops 3434 an
individualized education plan
that includes information about
stress management, diet, and
medications (see Table 46-2).
Dietary instructions take into
account the patient’s daily
caloric needs as well as cultural
aspects of food preferences and
patterns of eating. The nurse
and patient review foods and
other substances to be avoided
(e.g., spicy, irritating, or highly
seasoned foods; caffeine;
nicotine; alcohol). Consultation
with a dietitian may be
recommended (see Chart 46-1).
Providing information about
prescribed medications, which
may include antacids, H2
blockers, or proton pump
inhibitors, may help the patient to
better understand why these
medications assist in recovery
and prevent recurrence. The
importance of completing the
medication regimen as
prescribed to eradicate H. pylori
infection must be reinforced to
the patient and caregiver (see
later discussion). Continuing and
Transitional Care The nurse
reinforces previous instruction
and conducts ongoing
assessment of the patient’s
symptoms and progress.
Patients with malabsorption of
vitamin B12 need information
about lifelong vitamin B12
injections; the nurse may instruct
a family member or caregiver
how to administer the injections
or make arrangements for the
patient to receive the injections
from the primary provider.
Finally, the nurse emphasizes
the importance of keeping
follow-up appointments with the
primary provider
INTESTINAL DISORDERS