COLLEGE OF HEALTH SCIENCES

2nd SEM: 2021-2022

BSN-3

COURSE TITLE:

(NCM 116A)

CARE OF CLIENTS WITH PROBLEMS IN NUTRITION,

GASTRO-INTESTINAL, METABOLISM AND ENDOCRINE,
PERCEPTION AND COORDINATION, ACUTE AND CHRONIC

Sub-Topic

NURSING CARE OF AT RISK AND SICK ADULT CLIENTS WITH

ALTERATIONS/PROBLEMS IN NUTRITION & GASTROINTESTINAL,
ACUTE AND CHRONIC

Prepared by:

MARICHU N. GUYGUYON, MAN

Faculty

CHAPTER I.
 THE NURSING PROCESS

OVERVIEW OF THE GASTROINTESTINAL SYSTEM

Main organs of the Gastrointestinal system

a. Mouth
b. Pharynx
c. Esophagus
d. Stomach
e. Small intestine
f. Large intestine
The accessory organs
a. Tongue
b. Salivary glands
c. Pancreas
d. Liver
e. Gallbladder
f. Appendix

Figure1. A. Organs of the GI system. B. Anatomy of the stomach

Major functions of the Digestive System:

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 • Breakdown of food particles into the molecular form for digestion.
• Absorption into the bloodstream of small nutrient molecules produced
by digestion.
• Elimination of undigested unabsorbed foodstuffs and other waste
products.

Phases of Gastric Secretion

Stimulus to secretion Secretion
Cephalic (nervous)
Sight, smell, taste of food HCl acid, pepsinogen, mucus
(before food enters stomach).
Initiated in the CNS and
mediated by the vagus nerve.
Gastric (hormonal and
nervous)
Food in antrum of stomach, Release of gastrin from antrum into
vagal stimulation. circulation to stimulate gastric
secretions and motility

Intestinal (hormonal)
Presence of chyme in small Acidic chyme (pH <2): Release of secretin,
intestine. gastric inhibitory polypeptide,
cholecystokinin into circulation to
decrease HCl acid secretion
Chyme (pH >3): Release of gastrin from
duodenum to increase acid secretion

N.B. Specific nursing management (nursing process) are provided in the

succeeding topics of diseases

ASSESSMENT OF THE GASTROINTESTINAL SYSTEM

A. Patient History
1. Past Health History.
a) Data collection on GI functioning:
▪ abdominal pain, nausea and vomiting, diarrhea, constipation,
abdominal distention, jaundice, anemia, heartburn, dyspepsia,
changes in appetite, hematemesis, food intolerance or allergies,
indigestion, excessive gas, bloating, lactose intolerance, melena,
trouble swallowing, hemorrhoids, or rectal bleeding.
b) History of past or present diseases
▪ reflux, gastritis, hepatitis, colitis, gallstones, peptic ulcer, cancer,
diverticuli, or hernias.
c) Weight history
▪ Weight loss/gain that is unplanned or unexplained within the past 6
to 12 months
▪ History of dieting and repeated weight loss and gain.
2. Medications
a) Note patient’s previous and current use of medications:

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 ▪ Drug name, frequency of use, and duration of use (how long)
▪ over-the-counter (OTC) drugs, prescription drugs, herbal products,
vitamins, and nutritional supplements
▪ Hepatotoxic drugs such as: high doses of acetaminophen and
nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin that may
lead to upper GI bleeding.
▪ Other medications:
➢ Antibiotics – may alter the normal flora of the GI system causing
diarrhea
➢ Antacids and laxatives - affect the absorption of some
medications.
3. Surgery or Other Treatments
a) obtain data related to any abdominal or rectal surgery
▪ year, reason for surgery, postoperative course, and possible blood
transfusions.
4. Health Perception–Health Practices
a) patient’s health practices related to the GI system
▪ maintenance of normal body weight, proper dental care, adequate
nutrition, and effective elimination habits.
b) recent travel abroad with possible exposure to hepatitis or parasitic
infestation (hepatitis C) and if the patient received hepatitis A and B
vaccines.
c) Chronic alcoholism – can cause fatty infiltration of the liver → cirrhosis
and hepatocellular carcinoma.
d) cigarette smoking – Nicotine irritates the mucosal lining of the GI tract
while smoking can lead to GI cancers (mouth and esophageal cancers),
esophagitis, and ulcers and delays the healing of ulcers.

RISKS:
Colorectal Cancer
▪ 1st degree relatives (parents, siblings) or other family members
(grandparents, aunts, uncles) with previous colorectal cancer
Inflammatory Bowel Disease (IBD)
▪ People with IBD have a genetic predisposition or susceptibility to
the disease.
▪ First-degree relatives have a 5- to 20-fold increased risk of
developing IBD.
5. Nutritional-Metabolic Pattern.
a) Obtain a comprehensive nutritional assessment
▪ diet history – content, amount (portion size), food preferences and
preparation
▪ provide open-ended questions - allow patient to express beliefs and
feelings regarding diet.
▪ weekday and weekend dietary intake patterns including quality
and quantity of food. (Pinggang Pinoy)
▪ use of sugar and salt substitutes, caffeine, and amount of fluid and
fiber intake.
▪ Note any changes in appetite, food tolerance, and weight - Anorexia
and weight loss may indicate cancer or inflammation.
▪ dietary intolerances, food allergies and allergic response.

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6. Elimination Pattern.
a) Patient’s bowel elimination pattern
▪ frequency, time of day, and usual consistency of stool.
▪ use of laxatives and enemas, including type, frequency, and
results.
▪ Note any recent change in bowel patterns that may indicate colon
disease
- some foods and medications may alter the color of stool
b) Document the amount and type of fluid and fiber intake- these influence
the frequency and consistency of stools.
▪ Inadequate intake of fiber can be associated with constipation.
c) Investigate the possible connection between a skin problem and a GI
problem - food allergies can cause skin lesions, pruritus, and edema.
▪ Diarrhea can result in redness, irritation, and pain in the perianal
area.

7. Activity-Exercise Pattern.
a) Activity and Exercise affect GI motility while Immobility can lead to
constipation.
▪ Assess ambulatory status and ability/inability of patient in securing
and preparing food, self-feeding and if help is needed
▪ Assess accessibility to a toilet and if commode or ostomy supplies are
needed
8. Sleep-Rest Pattern.
a) GI symptoms can interfere with the quality of sleep.
▪ Presence of nausea, vomiting, diarrhea, indigestion, bloating, and
burning, epigastric pain.
b) Note sleep routines and follow individual’s preferences
▪ Provide easily digested snacks at night if hunger is a problem
(unless contraindicated).
9. Cognitive-Perceptual, Self-Concept/Esteem Pattern and Cultural
Beliefs
a) Alterations in sensory status can lead to problems in acquisition,
preparation, and ingestion of food
▪ Changes in taste or smell – may affect appetite and eating
pleasure.
▪ Vertigo
▪ Heat or cold sensitivity
▪ Determine a patient’s understanding of the illness and its
treatment.
▪ Overweight and underweight persons – may affect self-esteem and
body image.
▪ Determine stressors and coping mechanisms the patient uses.
- Stress may be manifested as anorexia, nausea, epigastric and
abdominal pain, or diarrhea.
- Some diseases of the GI system, such as peptic ulcer disease,
IBS, and IBD, may be exacerbated by stress.
▪ Assess the patient’s spiritual and cultural beliefs regarding food
and food preparation.

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 SAMPLE GUIDE QUESTIONS TO ASK DURING ASSESSMENT OF GI
SYSTEM (adapted from Lewis, 2014)
N.B. *If yes, describe.

Health Perception–Health Management

• Describe measures used to treat GI symptoms (diarrhea or vomiting)
• Do you smoke?* Do you drink alcohol?*
• Are you exposed to any chemicals regularly?* Did you have any
exposure in the past?*
• Have you recently traveled to other countries?*
Nutritional-Metabolic
• Describe your regular daily food and fluid intake.
• Do you take any supplemental vitamins or minerals?*
• Have you had any changes in appetite or food tolerance?*
• Any weight change in the past 6-12 mos?*
• Any allergies to any foods?*
Elimination
o Describe how long and time of day you usually have your bowel
movements. Consistency of the bowel movement?
o Do you use laxatives or enemas?* If so, how often?
o Have there been any recent changes in your bowel pattern?*
o Do you need any equipment, such as ostomy equipment, raised toilet
seat, commode?
Activity-Exercise
• Do you have difficulties in procuring and preparing food?*
Sleep-Rest
• Do you have any difficulties sleeping due to a GI problem?*
Cognitive-Perceptual
• Any changes in taste or smell affecting your appetite?*; pain affecting
food preparation, appetite, or chewing?*
• Do pain medications cause constipation, diarrhea, or appetite
suppression?*
Self-Perception/Relationships/Sexuality
• Describe any changes that affect your self-perception/relationships
(changes in bowel habits, weight, GI symptoms)
• Do you live alone? Describe how your family or others assist you with
your GI problems.
• Describe the effect of your GI problem on your sexual activity.
• How do cope with these problems?
• Describe any culturally health beliefs regarding food and food
preparation that may interfere with the treatment of your GI problem.

TABLE 39-8 HEALTH HISTORY

B. Physical Examination
1. Mouth
a) Inspection
▪ Inspect mouth for symmetry, color, and size.
▪ Observe for abnormalities such as pallor or cyanosis, cracking,
ulcers, or fissures.
▪ Observe for any lesions.

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 ▪ For teeth and gums, look for caries; loose teeth; abnormal shape
and position of teeth; and swelling, bleeding, discoloration, or
inflammation of the gingivae.
▪ Note any distinctive breath odor.
▪ Inspect the pharynx by tilting the patient’s head back and
depressing the tongue with a tongue blade.
▪ Observe the tonsils, uvula, soft palate, and anterior and posterior
pillars - Instruct the patient to say “ah.” The uvula and soft palate
should rise and remain in the midline.
b) Palpation
▪ Palpate any suspicious areas in the mouth
- Note ulcers, nodules, indurations, and areas of tenderness
- ability to swallow, the tongue, and lesions
- Let patient with dentures remove them when doing an oral
examination for proper visualization and palpation of the area.

2. Abdomen
▪ Provide good lighting
▪ The patient should be in supine position and relaxed (knees slightly
flexed and the head of the bed slightly raised)
▪ Empty bladder and nurse’s hands should be warm to avoid muscle
guarding.
▪ Let patient breathe slowly through the mouth.
a) Inspection
▪ Assess for skin changes - color, texture, scars, striae, dilated veins,
rashes, lesions, umbilicus (location and contour), symmetry, contour
(flat, rounded [convex], concave, protuberant, distention), observable
masses (hernias or other masses), and movement (pulsations and
peristalsis).
b) Auscultation
▪ Auscultate before percussion and palpation in abdominal examination
▪ Use the diaphragm of the stethoscope in auscultating bowel sounds.
▪ Listen for bowel sounds for at least 2 minutes (A very “silent
abdomen” is uncommon)
- If bowel sounds are not heard, note the amount of time you
listened in each quadrant without hearing bowel sounds.
- Note any decreased or absent bowel sounds
• Use these terms to describe bowel sounds - present,
absent, increased, decreased, high pitched, tinkling,
gurgling, and rushing
Normal bowel sounds – high pitched and gurgling
Hyperperistalsis - characterized by loud gurgles known as borborygmi
(stomach growling)
Intestinal Obstruction - bowel sounds are more high pitched (rushes and
tinkling) meaning the intestines are under tension
Bruit – use bell of the stethoscope when listening
- characterized by a swishing or buzzing sound and indicative of
turbulent blood flow.
c) Percussion

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 ▪ Performed to estimate the size of the liver and determine the presence
of fluid, distention, and masses.
▪ Sound waves depends on the density of underlying tissues.
Tympany - higher-pitched, hollow sound produced by air
Dullness – produced by fluid or masses resulting in a short, high-pitched
sound with little resonance

d) Palpation.
▪ Light palpation is performed to check for tenderness or cutaneous
hypersensitivity, muscular resistance, masses, and swelling
▪ Using 2 fingers together, depress the abdominal wall about 0.4 inches
(1 cm).
▪ Deep palpation - done to outline abdominal organs and masses (use
palmar surface of the fingers and note any facial expressions of pain)

*Refer to the organs of the different quadrants of the abdomen for your
reference in assessing.

Common signs/symptoms of the GI system (Lewis, 2014)

Finding Description Possible Etiology and
Significance
Mouth
Ulcer, plaque on lips Sore or lesion Carcinoma, viral
or in mouth infections
Cheilosis Softening, fissuring, and Riboflavin deficiency
cracking of lips at angles
of mouth
Cheilitis Inflammation of lips Often unknown
(usually lower) with
fissuring, scaling, crusting
Smooth tongue Red, slick appearance Cobalamin deficiency

Leukoplakia Thickened white patches Premalignant lesion

Herpes simplex Benign vesicular lesion Herpes virus

Candidiasis White, curdlike lesions Candida albicans

surrounded by
erythematous mucosa
Glossitis Reddened, ulcerated, Exposure to
swollen tongue streptococci,
irritation, injury,
vitamin B
deficiencies, anemia

Acute marginal Friable, edematous, Irritation from ill-

gingivitis painful, bleeding gingivae fitting dentures or
orthodontic
appliances, calcium

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 deposits on teeth, food
impaction

Esophagus and
Stomach
Dysphagia Difficulty swallowing, Esophageal problems,
feeling of food sticking in cancer of esophagus
esophagus
Hematemesis Vomiting of blood Esophageal varices,
bleeding peptic ulcer
Pyrosis Heartburn, burning in Hiatal hernia,
epigastric or substernal esophagitis,
area incompetent lower
esophageal
sphincter

Dyspepsia Burning or indigestion Peptic ulcer disease,

gallbladder disease
Odynophagia Painful swallowing Cancer of esophagus,
esophagitis
Eructation Belching Gallbladder disease

Nausea and vomiting Feeling of impending GI infections, common

vomiting, expulsion of manifestation of many
gastric contents GI diseases; stress,
through mouth fear, and pathologic
conditions
Abdomen
Distention Excessive gas Obstruction, paralytic
accumulation, enlarged ileus
abdomen, generalized
tympany
Ascites fluid accumulation within Peritoneal
the abdominal cavity, inflammation, heart
eversion of umbilicus failure, metastatic
(usually) carcinoma, cirrhosis
Bruit Humming or swishing Partial arterial
sound heard through obstruction
stethoscope over vessel (narrowing of vessel),
turbulent flow
(aneurysm)
Hyperresonance Loud, tinkling rushes Intestinal obstruction
Borborygmi Waves of loud, gurgling Hyperactive bowel as
sounds result of eating
Absent bowel sounds No bowel sounds on Peritonitis, paralytic
auscultation ileus, obstruction
Absence of liver Tympany on percussion Air from viscus (e.g.,
dullness perforated ulcer)
Masses Lump on palpation Tumors, cysts

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 Rebound tenderness Sudden pain when fingers Peritoneal
withdrawn quickly inflammation,
appendicitis
Nodular liver Enlarged, hard liver with Cirrhosis, carcinoma
irregular edge or surface
Hepatomegaly Enlargement of liver, liver Metastatic carcinoma,
edge >1-2 cm below costal hepatitis, venous
margin congestion
Splenomegaly Enlarged spleen Chronic leukemia,
hemolytic states,
portal hypertension,
some infections
Hernia Bulge or nodule in Inguinal (in inguinal
abdomen, usually canal), femoral (in
appearing on straining femoral canal),
umbilical (herniation
of umbilicus), or
incisional (defect
in muscles after
surgery)
Rectum and Anus
Hemorrhoids Thrombosed veins in Portal hypertension,
rectum and anus (internal chronic constipation,
or external) prolonged sitting or
standing, pregnancy
Mass Firm, nodular edge Tumor, carcinoma
Pilonidal cyst Opening of sinus tract, Probably congenital
cyst in midline just above
coccyx
Fissure Ulceration in anal canal Straining, irritation
Melena Abnormal, black, tarry Cancer, bleeding in
stool containing digested upper GI tract from
blood ulcers, varices
Tenesmus Painful and ineffective Inflammatory/Irritable
straining at stool. Feeling bowel disease,
of incomplete evacuation diarrhea (food
poisoning)
Steatorrhea Fatty, frothy, foul-smelling Chronic pancreatitis,
stool biliary obstruction,
malabsorption
problems

DIAGNOSTIC AND LABORATORY STUDIES FOR GASTROINTESTINAL

DISEASES (Lewis, 2014)
Study Description and Purpose Nursing Responsibility/ies
a. Radiology

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 Upper Fluoroscopic x-ray study ▪ Explain procedure to
gastrointestin using contrast medium patient.
al (GI) series (patient drinks) ▪ Keep patient NPO/NBM 8-
or barium 12 hr prior to the procedure.
swallow Used to diagnose ▪ Instruct patient to avoid
structural abnormalities smoking after midnight before
of esophagus, study.
stomach, and
duodenum
After x-ray
▪ prevent contrast medium
impaction (pt. to take fluids,
laxatives)
▪ inform patient that stool
may be white up to 72 hr
after test.
Small bowel Contrast medium is ▪ Same as for upper GI.
series ingested and films taken
every 30 min until
medium reaches
terminal ileum.
Lower GI or Fluoroscopic x-ray Before procedure:
barium examination of colon ▪ Administer laxatives and
enema using contrast medium enemas until bowels are clear
administered rectally the evening before procedure.
(enema) ▪ Administer clear liquid diet
evening before procedure.
Double-contrast or air- ▪ Keep patient NPO for 8 hr
contrast barium before test.
enema is most preferred. ▪ Instruct patient about
(Air is infused after thick being given barium by enema.
barium flows through ▪ Explain that cramping and
transverse colon) urge to defecate may occur
during procedure

After procedure:
▪ Give fluids, laxatives, or
suppositories to assist in
expelling barium.
▪ Observe stool for passage of
contrast medium.
Cholangiogra Local anesthetic is ▪ Observe patient for signs of
phy administered and liver is hemorrhage, bile leakage, and
• entered with long needle infection.
Percutaneous (under fluoroscopy), bile ▪ Assess patient’s
Transhepatic duct is entered, bile medications for possible
Cholangiograp withdrawn, and contraindications,
hy (PTC) radiopaque contrast precautions, or complications
. medium injected. with use of contrast medium
.

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 Fluoroscopy - used to
determine filling of
hepatic and biliary
ducts.
IV antibiotics are given
for prophylaxis
• Surgical Performed during ▪ Explain to patient that
cholangiogra surgery on biliary anesthetic will be used.
m structures, such as ▪ Assess patient’s
gallbladder. medications for possible
contraindications,
Contrast medium is precautions, or complications
injected into common with use of contrast medium
bile duct.

• Magnetic Done to obtain images of ▪ Explain procedure to

resonance biliary and pancreatic patient.
cholangiopanc ducts using MRI ▪ Contraindicated in patient
reatography with metal implants (e.g.,
(MRCP) pacemaker) or in pregnant
women

Ultrasound Used to show the size

and configuration of
organ.
Noninvasive procedure
uses high-frequency
sound waves
(ultrasound waves),
which are passed into
body structures and
recorded as they are
reflected
(bounded).

•Abdominal Detects abdominal ▪ Instruct patient to be NPO

ultrasound masses (tumors, cysts), 8-12 hr before ultrasound.
biliary and liver disease, ▪ Air or gas can reduce
gallstones. quality of images.
A lubricant (K.Y. Jelly) ▪ Food intake can cause
is applied to the skin gallbladder contraction,
and a transducer is resulting in suboptimal study.
placed on the area.

•Endoscopic Small ultrasound ▪ Same as

ultrasound transducer is installed esophagogastroduodenoscopy
(EUS) on tip of endoscope. (EGD)
Detects and stages
esophageal, gastric,
rectal, biliary, and

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 pancreatic tumors and
abnormalities.
Fine-needle aspiration is
used to diagnose
dysplasia or cancer.

• FibroScan FibroScan uses an ▪ Patient lies in dorsal

or FibroTest ultrasound transducer decubitus position with the
to determine liver right arm in extreme
stiffness (fibrosis). Used abduction.
in patients with chronic ▪ A probe is positioned in an
hepatitis C and intercostal space between the
cirrhosis. ribs

Nuclear Shows size, shape, and ▪ Schedule no more than one

imaging position of organ to radionuclide test on the same
scans identify functional day.
(scintigraphy disorders and structural ▪ Explain that patient needs
) defects to lie flat during scanning.
Radionuclide
(radioactive isotope) is
injected IV, and a
scanning device picks
up radioactive emission
then recorded on paper.
Gastric Radionuclide study ▪ Same as above.
emptying (scintigraphy) is used to
studies assess ability of stomach
to empty solids.
Cooked egg containing
Tc-99m and toast are
eaten with water.
Images are obtained at
0, 1, 2, and 4 hr later.
Study is used in
patients with gastric
emptying disorders
caused by peptic ulcer,
ulcer surgery, diabetes,
gastric malignancies, or
functional disorders.

•Hepatobiliary Patient is given IV Same as above.

scintigraphy injection of Tc-99m and
(HIDA) positioned under camera
to record distribution of
tracer in liver, biliary
tree, gallbladder, and
proximal small intestine.

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 Used to identify
obstructions of bile
ducts (e.g., gallstones,
tumors), diseases of
gallbladder, and bile
leaks.

Computed Detects biliary tract, ▪ Explain procedure to

tomography liver, and pancreatic patient.
(CT) disorders. ▪ Determine sensitivity to
Use of oral and IV iodine or shellfish if contrast
contrast medium material used.
accentuates density
differences.

Magnetic Noninvasive procedure ▪ Explain procedure to

resonance using radiofrequency patient.
imaging waves and a magnetic ▪ Contraindicated in patient
(MRI) field to detect with metal implants (e.g.,
hepatobiliary disease, pacemaker) or one who is
hepatic lesions, and pregnant.
sources of GI bleeding TABLE 39-12 DIAGNOSTIC
and to stage colorectal
cancer.
IV contrast medium
(gadolinium) may be
used—cont’d

Esophagogas Visualizes directly Before procedure:

troduodenos mucosal lining of ▪ Keep patient NPO for 8 hr.
copy esophagus, stomach, ▪ Obtain signed consent
(EGD) and duodenum with ▪ Give preoperative
flexible endoscope. medication if ordered.
Can detect ▪ Explain procedure.
Inflammations,
ulcerations, tumors, After procedure:
varices, or Mallory-Weiss ▪ Keep patient NPO until gag
tears may be detected. reflex returns.
Biopsies may be taken ▪ Check temperature q15-
30min for 1-2 hr (sudden
temperature spike is sign of
perforation).

Colonoscopy Directly visualizes entire Before procedure:

colon up to ileocecal ▪ Explain procedure
valve with flexible ▪ Bowel preparation is done
fiberoptic scope to according to physician’s
diagnose or detect preference (ex. patients may
inflammatory bowel be kept on clear liquids 1-2
disease, polyps, tumors, days before procedure.

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 and diverticulosis and ▪ An enema is given the night
dilate strictures. before or one packet of Klean
Prep mixed with 1 liter of
Allows for biopsy and water to be drank every 15
removal of polyps mins. the night before
without laparotomy. colonoscopy and a second
packet morning of
colonoscopy.
—cont’d

After procedure:
▪ Patient may experience
abdominal
cramps caused by stimulation
of peristalsis because the
bowel is constantly inflated
with air during procedure.
▪ Observe for rectal bleeding
and manifestations of
perforation (e.g., malaise,
abdominal distention,
tenesmus).
▪ Check vital signs.
TABLE 39-12 DIAGNOSTIC
Sigmoidosco Visualizes rectum and ▪ Administer enemas evening
py sigmoid colon with before and morning of
lighted flexible procedure.
endoscope to detect ▪ Patient may have clear
tumors, polyps, liquids day before, or no
inflammatory and dietary restrictions may be
infectious diseases, necessary.
fissures, hemorrhoids. ▪ Explain to patient knee-
chest position (unless patient
is older or very ill), need to
take deep breaths during
insertion of scope, and
possible urge to defecate as
scope is passed.
▪ Encourage patient to relax
and let abdomen go limp.
▪ Observe for rectal bleeding
after polypectomy or biopsy.

Endoscopic Fiberoptic endoscope Before procedure:

retrograde (using fluoroscopy) is ▪ Explain procedure to
cholangiopan inserted via the mouth patient
creatography into descending ▪ Keep patient NPO 8 hr
(ERCP) duodenum, then before procedure.
common bile and

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 pancreatic ducts are ▪ Ensure consent form
cannulated. Contrast signed.
medium is injected into ▪ Administer sedation
ducts and allows for immediately before and
direct visualization of during procedure.
structures. Can also be
done to remove a After procedure:
gallstone from distal ▪ Check vital signs.
common bile duct, dilate ▪ Check for signs of
strictures, biopsy, perforation or infection.
diagnose pseudocysts. (pancreatitis is the most
. common complication).
▪ Check for return of gag
reflex
Endoscopic Combined use of ▪ Similar to EGD.
ultrasound endoscopy and
ultrasound using an
ultrasound transducer
attached to an
endoscope.
Enables visualization of
esophagus, stomach,
intestine, liver,
pancreas, and
gallstones.

Laparoscopy Peritoneal cavity and ▪ Obtain consent

(peritoneosc contents are visualized ▪ Keep patient NPO 8 hours
opy) with laparoscope. before study.
. Biopsy specimen may ▪ Administer preoperative
also be taken. sedative medication.
Double-puncture ▪ Ensure that bladder and
peritoneoscopy allows bowels are emptied.
better visualization of ▪ Observe for possible
abdominal cavity, complications of bleeding and
especially liver. bowel perforation after the
procedure

b. Blood
Studies
Amylase Measures secretion of ▪ Obtain blood sample
amylase by pancreas during acute attack of
which is important in pancreatitis.
diagnosing acute ▪ Explain procedure to
pancreatitis. patient

Level peaks in 24 hr and

then drops to normal in
48-72 hr.

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 Lipase Measures secretion of ▪ Explain procedure to
lipase by pancreas. patient.
Level stays elevated
longer than serum
amylase in acute
pancreatitis.
Reference interval: 31-
186 U/L (0.5-3.2
μkat/L).

Gastrin A hormone secreted by ▪ Explain procedure to

cells of the antrum of patient
the stomach, the
duodenum, and the
pancreatic islets of
Langerhans.
Reference interval: 25-
100 pg/mL when
fasting.

c. Liver Percutaneous procedure Before procedure:

Biopsy uses needle inserted ▪ Signed consent
between 6th and 7th or ▪ Check patient’s coagulation
8th and 9th intercostal status (prothrombin time,
spaces on the right side clotting or bleeding time).
to obtain specimen of ▪ Ensure that patient’s blood
hepatic tissue. is typed and crossmatched.
▪ Take vital signs as baseline
Often done using data.
ultrasound or CT ▪ Tell pt. to hold breath after
guidance. expiration when needle is
inserted.

After procedure:
▪ Check vital signs to detect
internal
Bleeding q15min × 2, q30min
× 4, q1hr × 4.
▪ Keep patient lying on right
side for minimum of 2 hr to
splint puncture site.
▪ Keep patient in bed in flat
position for 12-14 hr.
▪ Assess patient for
complications such as bile
peritonitis, shock,
pneumothorax.

d. Fecal
Tests ▪ Observe patient’s stools.

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 Fecal Form, consistency, and ▪ Collect stool specimens and
analysis color are noted. Check stools for blood.
Specimen examined for ▪ Keep diet free of red meat
mucus, blood, pus, for 24-48 hr before occult
parasites, and fat blood test.
content.
Test for occult blood
(guaiac test, Hemoccult,
Hemoccult II,
Hemoccult-SENSA,
Hematest)

Single DNA test (PreGen-

Plus) is a panel of DNA
markers used to detect
and monitor colorectal
cancer.

Stool culture Tests for the presence of ▪ Collect stool specimen

bacteria, including
Clostridium difficile.
e. Breath Gold standard test for H. Procedure:
Tests Pylori infection ▪ After the patient ingests a
. capsule of carbon labelled
urea, a breath sample is
obtained 10 to 20 minutes
later.
▪ H. pylori metabolises urea
rapidly, so the labelled carbon
is absorbed quickly; it can
then be measured as carbon
dioxide in the expired breath
to determine whether H.
pylori is present
▪ The patient is instructed to
avoid antibiotics or
loperamide for 1 month before
the test; sucralfate and
omeprazole for 1 week before
the test; and cimetidine,
famotidine, ranitidine and
nizatidine for 24 hours before
urea breath testing

NURSING DIAGNOSIS
(for a comprehensive nursing diagnosis, please refer to your NANDA)
PLANNING
Outcomes included:
a. Prevent complications
b. Pain relief

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 c. Attain adequate nutritional requirement
d. Decrease risk of aspiration
NURSING INTERVENTIONS
General Interventions
1. Patient Education
a. Oral Hygiene
b. Self-care/management
c. Explain any procedure/disease and management
d. Lifestyle modification
2. Provide psychological/emotional support to reduce anxiety
3. Prevent and monitor complications
4. Monitor hemodynamics/vital signs/dietary intake - monitor for signs of
dehydration
5. Collaborate with multidisciplinary team in the care of the patient
6. Perform peri-operative nursing care for patients with GI surgeries/
colostomy or ileostomy care

Surgical Procedures involved in GI Diseases

Procedure Description
AppendectomyUDY Removal of appendix
Cholecystectomy Removal of gallbladder
Choledochojejunostomy Opening between common bile duct and
jejunum
Choledocholithotomy Opening into common bile duct for removal of
stones
Colectomy Removal of colon
Colostomy Opening into colon
Esophagoenterostomy Removal of portion of esophagus with segment
of colon attached to remaining portion
Esophagogastrostomy Removal of esophagus and anastomosis of
remaining portion to stomach
Gastrectomy Removal of stomach
Gastrostom Opening into stomach
Glossectomy Removal of tongue
Hemiglossectomy Removal of half of tongue
Herniorrhaphy Removal of a hernia
lleostomy Opening into ileum
Mandibulectomy Removal of mandible
Pyloroplasty Enlargement and repair of pyloric sphincter
area
Vagotomy A Resection of branch of vagus nerve

RESPONSES TO ACUTE AND CHRONIC ALTERATIONS/PROBLEMS AND

ITS PATHOPHYSIOLOGIC BASIS IN NUTRITION AND GASTRO-
INTESTINAL

CHAPTER II.

A. Nutritional- Metabolic Patterns/ Responses to Altered Nutrition

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Contents
1. Disturbances in Ingestion
a. Gastroesophageal Reflux (GERD)
b. Hiatal Hernia
c. Achalasia
2. Disturbances in Digestion
a. Nausea and Vomiting
b. Gastrointestinal Bleeding
c. Gastritis
d. Peptic Ulcer Disease
3. Disturbance in Absorption and Elimination
a. Disorders of Intestinal Motility
b. Malabsorption Syndromes
c. Structural and Obstructive Bowel Disorders

Learning Outcomes:
At the end of module, the student will be able to:
a. Formulate a nursing care plan in the care of patients with
disturbances in ingestion, digestion, and absorption and elimination
b. Discuss the pathophysiology of gastrointestinal diseases

1. Disturbances in Ingestion
A. GASTROESOPHAGEAL REFLUX (GERD)
➢ Refers to symptoms or tissue damage due to retrograde (moving
backward) movement of gastric contents
➢ Considered as the most common gastrointestinal disorders with
increasing prevalence worldwide (El-Serag et al., 2014)
➢ Usually peaks at 30-60 years of age, affects both men and women
with men and older adults experiencing GERD- related
complications
➢ Most common cause of noncardiac chest pains (Akhtar, et al.,
2019)
Etiology & Pathophysiology:
- No single cause is known
- GERD occurs when the defenses of the esophagus are compromised
due to the reflux of acidic gastric contents (Gastric HCl acid and
pepsin secretions) into the esophagus leading to irritation and
inflammation of the esophagus (esophagitis)
- This gets worse by the presence of intestinal proteolytic enzymes (e.g.,
trypsin) and bile.
- The severity of inflammation depends on the amount and composition
of the gastric reflux and on the esophagus’s mucosal defense
mechanisms.
Factors
a. Incompetent LES (Lower Esophageal Sphincter)
➢ Normally, the LES functions as an anti-reflux barrier.
➢ An incompetent LES allows gastric contents to move from the
stomach to the esophagus when the person is supine or has an
increase in intraabdominal pressure.

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 Causes:
- foods (e.g. caffeine, chocolate, peppermint)
- drugs (e.g. anticholinergics)
b. Obesity - there is increased intraabdominal pressure
c. Cigarette and cigar smoking
d. Hiatal Hernia
e. TLESRs (transient lower esophageal sphincter relaxations)
➢ Occurs due to the relaxation of the lower esophageal sphincter
caused by gastric distention
➢ Can be triggered by increased gastric acid production, delayed
gastric emptying, distention, diminished esophageal clearance,
diet, medications

Risk factors and commonly associated conditions

Risk factors Commonly associated conditions

Obesity Barrett’s Esophagus
Pregnancy Peptic Ulcer Disease (PUD)
Hiatal Hernia Peptic Stricture (10% of patients with GERD)
Alcohol Use Erosive and Non-Erosive Esophagitis
Scleroderma Esophageal Adenocarcinoma
Tobacco Use Irritable Bowel syndrome
Extraesophageal Reflux, aspiration, chronic
cough, laryngitis, vocal cord granuloma, otitis
media
Halitosis
Hiatal Hernia (acid pocket)

Patients with severe GERD usually have hiatal hernia that can cause:

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 • Impaired gastric emptying
• Acid trapping in the hernial sac
• Increased retrograde acid flow rates
• Increased frequency of lower esophageal sphincter relaxations
• Reduced esophagogastric junction sphincter pressure
Clinical Manifestations:
Typical Symptoms
Most common: Less Common:
Heartburn – substernal burning Excessive saliva with stomach acid
sensation that may radiate to (Water brash)
the back and/or neck Burping
Regurgitation – feeling of Hiccups
retrograde movement of gastric Nausea
contents up the chest and often Vomiting
into the mouth Odynophagia (painful swallowing)
Dysphagia – difficulty swallowing – occurs in esophagitis
(reported in approx. 30% of Distal esophageal spasm
Hypertensive peristalsis
GERD patients)
(Jackhammer Esophagus)
Hypotensive peristalsis
(Scleroderma)

Atypical Symptoms
Chest pain – continuous for hours, may interrupt sleep, retrosternal
without lateral radiation and is usually associated with meals and
relieved by antacids
Chronic cough
Difficult to treat Asthma or wheezing
Laryngeal Symptoms (Sore throat, throat clearing, hoarseness)

Alarm Symptoms
Weight loss
Hematemesis and bleeding
Dysphagia
Vomiting
Early satiety
Choking/apnea (pediatric considerations)

Diagnostic Tests:
a. Upper GI endoscopy – most specific test for GERD
b. Barium swallow
c. 24-hour esophageal pH monitoring – determine degree of acid reflux
d. PPI trial (Proton Pump Inhibitors)
Examples: Omeprazole (Losec), Lanzoprazole, Pantoprazole
- 30-day PPI trial is one way of evaluating symptomatic responses
to treatment.
- Taken once daily 1 hour before breakfast is recommended,

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 - If a patient has GERD, symptoms improve in 7-14 days; if not,
additional diagnostic works such as an upper endoscopy is
recommended

BARRETT’S
ESOPHAGUS
A complication of
GERD
Occurs when the
lining of the
esophagus heals
abnormally and the
appearance
becomes salmon
pink color (normal -
white)
Symptoms:
• Heartburn
• Indigestion
• Dysphagia
• Nocturnal
regurgitation
(acidic)
• Hematemesis/mele
na
Diagnosis: Upper
Endoscopy or
Chromoendoscopy
(uses staining to
identify presence of
cancerous cells)

NURSING MANAGEMENT (GERD)

Assessment:
➢ Perform thorough history taking – important in correctly assessing
GERD and identify symptoms
Important information to note includes:
• History of heartburn that often occurs after meals and worsens with
stooping, bending, or lying down
• Time of symptom onset (usually worse at night)
• Presence of extraesophageal symptoms (sore throat, bronchospasm,
chronic coughing, difficult-to treat asthma, wheezing, and/or lung
damage
• Presence of atypical symptoms (epigastric fullness/pressure/pain,
nausea, dyspepsia, bloating, bitter belching, sour stomach sensation,
chest pain, and/or lump in throat

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 • Consumption of food/drinks associated with GERD that can lower
esophageal sphincter pressure (large meals, food with high fat/sugar
contents, chocolates, caffeine, coffee, onions, carbonated drinks,
alcohol)
• Citrus products - mucosal irritants (tomato-based, spicy foods)
• Progression, pattern, severity of symptoms
• Complaints of regurgitation or sour taste in mouth (water brash)
• Medications that can decrease LES tone such as: Calcium Channel
Blockers, hormones, beta adrenergic agents, barbiturates, nitrates
• Mealtime routine
• Presence of alarm symptoms
Physical assessment:
• Presence of halitosis (bad breath)
• Stigmata of chronic systemic disease
• Epigastric tenderness
• Presence of epigastric mass
• Obesity – can contribute to symptoms (Calculate BMI)
*Undetected GERD can lead to Barrett’s Esophagus which may progress to
adenocarcinoma
Nursing interventions
a. Lifestyle modifications
• Diet: low-fat diet; avoid caffeine, tobacco, beer, milk, foods containing
peppermint or spearmint, and carbonated beverages
• Instruct patient to avoid eating or drinking 2 hours before bedtime
• Maintain normal body weight
b. Raising the head of the bed to at least 30 degree angle when lying down
c. Avoid tight fitting clothes
d. Drug therapy
• PPIs (omeprazole) and H2 receptor blockers (ranitidine)
• Aimed at controlling symptoms, suppressing acid secretion and
preventing complications
* Surgical interventions may be done if medical management is not effective
Fundoplication – wrapping of a portion of the gastric fundus around
the sphincter of the esophagus

B. HIATAL HERNIA
▪ Also termed as diaphragmatic hernia or esophageal hernia
▪ Occurs when a weakened muscle in the upper part of the stomach
bulges through the large muscle or an opening in the diaphragm.
▪ The diaphragm has a small opening called the hiatus where the
esophagus passes before connecting to the stomach
▪ The most common abnormality found on x-ray examination of the
upper GI tract and are common in older women and obese people
Classifications:
1. Sliding hernia:
▪ The most common type which usually occurs when the patient is in
supine position, and the hernia goes back into the abdominal cavity
when the patient is in standing position.
2. Paraesophageal, or rolling hernia

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 ▪ Occurs when the fundus and the greater curvature of the stomach
roll up through the diaphragm, forming a pocket alongside the
esophagus.
▪ Acute paraesophageal hernia is a medical emergency.
Factors causing hiatal hernia:
▪ structural changes caused by ageing leading to a weakened muscle in
the diaphragm
▪ persistent and intense pressure around the muscles of the abdomen
during coughing, vomiting, straining when passing stool, exercising,
lifting heavy objects, obesity, tumor
▪ Trauma or certain types of surgery that can lead to injury to the area
▪ Congenital unusually large hiatus

Clinical Manifestations and

Complications
➢ Small hiatal hernias may
not show symptoms
▪ Heartburn
▪ Regurgitation of food or
liquids into the mouth
▪ Backflow of stomach acid
into the esophagus (acid
reflux)
▪ Difficulty swallowing
▪ Chest or abdominal pain
▪ SOB
▪ Vomiting of blood or
passing of black stools
which could be indicative
of GI bleeding

Complications:
▪ Esophagitis
▪ hemorrhage from erosion
▪ stenosis (narrowing of the esophagus)
▪ ulcerations of the herniated portion of the stomach
▪ strangulation of the hernia
▪ regurgitation with tracheal aspiration.

Diagnostic Studies
a. Esophagram (barium swallow) - may show the protrusion of gastric
mucosa through the esophageal hiatus
b. X-ray of upper digestive system
c. Upper endoscopic visualization of the lower esophagus – gives
information on the degree of mucosal inflammation or other
abnormalities.
d. Esophageal manometry – measures the coordination and force exerted
by the muscles of the esophagus

NURSING AND COLLABORATIVE MANAGEMENT

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Conservative
a. Teach the patient to reduce intraabdominal pressure by eliminating
constricting garments and avoiding lifting and straining.
b. Eat small frequent meals during the day instead of three large ones
c. Avoid foods that trigger heartburn (fatty or fried foods, tomato sauce,
alcohol, chocolate, mint, garlic, onion, and caffeine.
d. Avoid lying down after a meal or eating late in a day
e. Eat at least two to three hours after bedtime
f. Maintain a healthy weight
g. Stop smoking elevate head of the bed approx. 6 inches
Drug Therapy
a. Antacids to neutralize stomach acids (Gaviscon, Kremil-S)
b. H-2 receptor blockers to reduce acid production (ranitidine, cimetidine)
c. Proton Pump Inhibitors (PPI) that block acid production and heal the
esophagus (lansoprazole, omeprazole)- stronger that H2 receptor blockers
Surgical treatment:
Goals:
▪ reduce the hernia
▪ provide an acceptable LES pressure
▪ prevent movement of the gastroesophageal junction
a. herniotomy (excision of the hernia sac)
b. herniorrhaphy (closure of the hiatal defect) to prevent reflux
c. gastropexy (attachment of the stomach subdiaphragmatically to
prevent reherniation)
Antireflux surgeries for hiatal hernia are laparoscopically performed

C. ACHALASIA
▪ Means “failure to relax”
▪ A rare, chronic disease affecting the esophagus wherein the lower
esophageal sphincter (LES) is unable to open and let food pass into
the stomach
Pathophysiology
▪ There is absence of peristalsis in the lower 2/3 of the smooth muscles
of the esophagus
▪ The pressure on the LES produce incomplete relaxation during
swallowing that can result to obstruction of the esophagus at or near
the diaphragm occurs due to accumulation of food or fluid in the
lower esophagus
▪ This can lead to a hypertensive esophageal sphincter
Clinical Manifestations:
▪ Dysphagia (most common)
▪ Regurgitation (nocturnal)
▪ Chest pain (substernal -same with angina)
▪ Heartburn
▪ Weight loss
▪ Halitosis
▪ Inability to eructate (belch)
Diagnostic Studies:
a. Barium Swallow (esophagram) – shows bird-beak appearance
b. Prolonged esophageal pH monitoring – to rule out GERD

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 c. Esophagogastroduodenoscopy (EGD)- to rule out Ca of the GEJ
(gastroesophageal junction)

MANAGEMENT:
Goal of treatment:
▪ relieve dysphagia and regurgitation
▪ improve esophageal emptying by disrupting the LES
▪ prevent development of megaesophagus (enlargement of the lower
esophagus).
Surgical options:
a. Endoscopic pneumatic dilation is done first - LES muscle is disrupted
from within using balloons of progressively larger diameter (3.0, 3.5,
and 4.0 cm)
b. Heller myotomy - LES is surgically disrupted (myotomy) with
antireflux surgery performed at the same time.
Drug therapy:
a. Smooth muscle relaxants such as nitrates (isosorbide dinitrate
[Isordil]) and calcium channel blockers (e.g., nifedipine [Procardia])
taken sublingually 30 to 45 minutes before meals to improve
dysphagia
b. botulinum toxin injection endoscopically into the LES may short-term
relief of symptoms and improves esophageal emptying.
Symptomatic treatment:
▪ eating a semisoft diet
▪ eating slowly and drinking fluid with meals
▪ sleeping with the head elevated.

2. Disturbances in Digestion
A. NAUSEA AND VOMITING

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 ▪ the most common manifestations of gastrointestinal (GI) diseases and
are usually closely related and treated as one problem.
Nausea
▪ a feeling of discomfort in the epigastrium with a conscious desire to
vomit.
Vomiting
▪ the forceful ejection of partially digested food and secretions (emesis)
from the upper GI tract.
▪ a complex act that requires the coordinated/simultaneous activities
of several structures:
- closure of the glottis
- deep inspiration with contraction of the diaphragm in the
inspiratory position
- closure of the pylorus
- relaxation of the stomach and lower esophageal sphincter
(LES),
- and contraction of the abdominal muscles with increasing
intraabdominal pressure that force the stomach contents up
through the esophagus, into the pharynx, and out of the
mouth.
Regurgitation
▪ an effortless process in which partially digested food slowly comes up
from the stomach without prior retching or vomiting.

Projectile vomiting
▪ a forceful expulsion of stomach contents without nausea and is
characteristic of CNS (brain and spinal cord) tumors/injury
Etiology and Pathophysiology
• Nausea and vomiting occur in a wide variety of GI disorders and in
conditions that are unrelated to GI disease. These include:
- pregnancy
- infection
- central nervous system (CNS) disorders (e.g., meningitis, tumor)
- cardiovascular problems (e.g., myocardial infarction, heart
failure)
- metabolic disorders (e.g., diabetes mellitus, Addison’s disease,
renal failure)
- postoperatively after general anesthesia
- side effects of drugs (e.g., chemotherapy, opioids, digitalis)
- psychologic factors (e.g., stress, fear)
- conditions in which the GI tract becomes overly irritated,
excited, or distended.
• A vomiting center in the brainstem coordinates the multiple
components involved in vomiting.
- This center receives input from various stimuli.
- Neural impulses reach the vomiting center via afferent pathways
through branches of the autonomic nervous system.
- Receptors for these afferent fibers are located in the GI tract,
kidneys, heart, and uterus.

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 - When stimulated, these receptors relay information to the
vomiting center, which then initiates the vomiting reflex
• The chemoreceptor trigger zone (CTZ) located in the brainstem
responds to chemical stimuli of drugs, toxins, and labyrinthine
stimulation (e.g., motion sickness).
• Once stimulated, the CTZ transmits impulses directly to the vomiting
center.
• This action activates the autonomic nervous system, resulting in both
parasympathetic and sympathetic stimulation.
• Sympathetic activation produces tachycardia, tachypnea, and
diaphoresis.
• Parasympathetic stimulation causes relaxation of the LES, an increase
in gastric motility, and a pronounced increase in salivation.

Clinical Manifestations
Nausea is a subjective complaint.
▪ Anorexia (lack of appetite) usually accompanies nausea
▪ Dehydration if vomiting persists - loss of water and essential
electrolytes (e.g., potassium, sodium, chloride, hydrogen) can lead to
severe electrolyte imbalances, loss of extracellular fluid volume,
decreased plasma volume, and eventually circulatory failure.
▪ Weight loss
▪ Metabolic alkalosis due to loss of gastric hydrochloric (HCl) acid.
▪ pulmonary aspiration in older or unconscious patients or in patients
with impaired gag reflex. (To prevent aspiration in these patients,
position them in semi-Fowler’s or side-lying position)

NURSING AND COLLABORATIVE MANAGEMENT

▪ Assess the patient for precipitating factors
▪ It is important to describe the contents of the emesis and differentiate
between vomiting, regurgitation, and projectile vomiting.

Characteristics of emesis GI disorder

▪ partially digested food several ▪ gastric outlet obstruction or
hours after a meal delayed
▪ gastric emptying.
▪ presence of fecal odor and bile ▪ intestinal obstruction below the
after prolonged vomiting level of the pylorus
▪ Bile ▪ obstruction below the ampulla of
Vater.
▪ “coffee ground” appearance ▪ gastric bleeding, where blood
changes to dark brown as a
result of its interaction with HCl
acid.
▪ Bright red blood ▪ active bleeding could be due to
(Mallory-Weiss tear -disruption of
the mucosal lining near the
esophagogastric junction due to
severe retching and vomiting,
esophageal varices, gastric

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 or duodenal ulcer, or neoplasm.

Drug Therapy.
▪ Most antiemetic drugs act in the CNS by blocking the neurochemicals
that trigger nausea and vomiting.
▪ Administering antiemetics and antinausea drugs depends on the
cause of the problem as it can mask the underlying disease which can
delay diagnosis and treatment.
DRUG ALERT:
Promethazine Injection:
▪ should NOT be administered into an artery or under the skin due to
the risk of developing severe tissue injury leading to gangrene.
▪ If administered IV, it can leak to the surrounding tissue causing
serious damage
▪ Deep muscle injection is the preferred route
Metoclopramide (Reglan)
▪ Prolonged use can cause tardive dyskinesia - a neurologic condition
characterized by involuntary and repetitive movements of the body
(e.g., extremity movements, lip smacking) even after discontinuing the
drug.

B. GASTROINTESTINAL BLEEDING
▪ Characterized as bleeding from the gastrointestinal system
Etiology and Pathophysiology
▪ The severity of bleeding depends on the origin (venous, capillary, or
arterial).
▪ Bleeding from artery - profuse, blood is bright red (indicating blood is
not contact with gastric HCl acid secretion)
- “coffee-ground” vomitus - indicates that the blood has been in the
stomach for some time.
▪ Severe upper GI hemorrhage - loss of more than 1500 mL of blood or
25% of intravascular blood volume.
Melena (black, tarry stools) – indicates slow bleeding from an upper GI
source.
▪ The longer the passage of blood through the intestines, the darker the
stool color because of the breakdown of hemoglobin and the release of
iron.
Hematochezia -passage of fresh blood in feces which indicates bleeding from
lower GI

Types and manifestations of GI bleeding

Type Manifestations
Obvious bleeding Hematemesis
▪ Bloody vomitus appearing as fresh, bright red
blood or “coffee-ground” appearance (dark,
grainy digested blood).
Melena
▪ Black, tarry stools (often foul smelling) caused
by digestion of blood in the GI tract. Black
appearance is from the presence of iron.

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 Hematochezia
Occult bleeding Small amounts of blood in gastric secretions,
vomitus, or stools not apparent by appearance.
Detectable by Guaiac test

Causes of bleeding
Drug Induced
• Corticosteroids
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Salicylates
Esophagus
• Esophageal varices
• Esophagitis
• Mallory-Weiss tear
Stomach and Duodenum
• Stomach cancer
• Hemorrhagic gastritis
• Peptic ulcer disease
• Polyps
• Stress-related mucosal disease
Systemic Diseases
• Blood dyscrasias (e.g., leukemia, aplastic anemia)
• Renal failure

Origin of bleeding-21 COMMON CAUSES OF UPPEGASTROINTESTINANG

a. Esophageal Origin.
▪ Bleeding from the esophagus is most likely due to chronic esophagitis,
Mallory-Weiss tear, or esophageal varices.
Chronic esophagitis – may be due to GERD, the ingestion of drugs that
irritate the mucosa, alcohol, and cigarette smoking.
Esophageal varices – due to cirrhosis of the liver.
b. Stomach and Duodenal Origin.
▪ Bleeding peptic ulcers account for 40% of the cases of upper GI
bleeding.
▪ Drugs are the most common cause
- Aspirin, NSAIDs, and corticosteroids can cause irritation and
disruption of the gastroduodenal mucosa.
- Most OTC preparations contain aspirin.

▪ Stress-related mucosal disease (SRMD)

- also known as physiologic stress ulcers
- occurs in patients who have had severe burns or trauma or
major surgery.
- There is diffuse superficial mucosal injury or discrete deeper
ulcers in the fundus and body portions of the stomach
- Patients with coagulopathy and those who experience
respiratory failure resulting in mechanical ventilation for more
than 48 hours are at highest risk.

Diagnostic Studies

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a. Endoscopy
▪ primary tool for diagnosing the source (e.g. esophageal or gastric
varices, gastritis) of upper GI bleeding
b. Angiography
▪ used in diagnosing upper GI bleeding when endoscopy cannot be done
or when bleeding persists after endoscopic therapy
▪ an invasive procedure requiring preparation and setup time and may
not be appropriate for a high-risk, unstable patient.
Procedure:
- a catheter is placed into the left gastric or superior mesenteric
artery and advanced until the site of bleeding is discovered.
Laboratory studies
a. CBC – serves as a baseline for further treatment
b. blood urea nitrogen (BUN)- elevated when there is marked hemorrhage,
but also in renal hypoperfusion or renal disease
c. serum electrolytes
d. prothrombin time
e. partial thromboplastin time
f. liver enzymes
g. arterial blood gases (ABGs)
h. type and crossmatch for possible blood transfusions
i. All vomitus and stools should be tested for gross and occult blood

COLLABORATIVE MANAGEMENT
a. Emergency Assessment and Management.
➢ focus is on early identification of signs and symptoms of shock
(tachycardia, weak pulse, hypotension, cool extremities, prolonged
capillary refill, and apprehension.
➢ Monitor vital signs every 15 to 30 minutes
➢ Assess for gut perforation and peritonitis (tense, rigid, board-like
abdomen)
➢ Do a thorough abdominal examination, and note the presence or
absence of bowel sounds.
➢ Start IV lines, preferably two, with a 16- or 18-gauge needle are placed
for fluid and blood replacement.
Initial fluid is usually an isotonic crystalloid solution (e.g., lactated
Ringer’s solution), followed by packed RBC if bleeding is not
profuse
For severe hemorrhage - Whole blood, packed RBCs, and fresh
frozen plasma may be given When upper GI bleeding is less
profuse, infusion of isotonic
➢ Administer supplemental oxygen.
➢ Insert and indwelling urinary catheter to measure hourly urine output
(measures vital organ perfusion)
➢ A central venous pressure (CVP) line may be inserted for fluid volume
status assessment.
➢ If the patient has a history of valvular heart disease, coronary artery
disease, or heart failure, a pulmonary artery catheter may be
necessary to monitor the patient.

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b. Endoscopic Therapy
➢ Endoscopy performed within the first 24 hours of bleeding is
important for diagnosis and to determine if surgical or radiologic
intervention is to be done
➢ The goal of endoscopic hemostasis is to coagulate or thrombose the
bleeding vessel.

Types used:
1) thermal (heat) probe* - a heating element is directly applied to the
bleeding site to clot the blood
2) multipolar and bipolar electrocoagulation probe*
3) argon plasma coagulation (APC)- produces coagulation by delivering
polar current to tissue
*most commonly used

DRUGS used for GI bleeding 42-22 DRUG THERAPY

Drug Source of Mechanism of Action
GI Bleeding
vasopressin Esophageal Causes vasoconstriction.
(Pitressin) varices ↓ Pressure in the portal
circulation
and stops bleeding

octreotide Upper GI Somatostatin analog that

(Sandostatin) bleeding, ↓ blood
esophageal flow to GI tract
varices ↓ HCl acid secretion by ↓
release

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 of gastrin

epinephrine Bleeding from Injection therapy often

ulceration combined
Injection during endoscopy with other therapies (e.g.,
produces hemostasis laser)
Causes tissue edema and
pressure
on the source of bleeding
*Other drugs used to treat GI bleeding are antacids, H2-receptor blockers,
and protein pump inhibitors
c. Surgical Therapy
▪ Performed when bleeding continues regardless of the therapy provided
and when the site of the bleeding has been identified.
▪ Surgical therapy may be necessary when the patient continues to
bleed after rapid transfusion of up to 2000 mL of whole blood or
remains in shock after 24 hours.
▪ The site of the hemorrhage determines the choice of operation
▪ For variceal bleeding, other strategies include variceal ligation,
injection sclerotherapy, and balloon tamponade
d. Drug Therapy
▪ In active bleeding, high dose PPI therapy given IV bolus and
subsequent infusion is usually given before performing endoscopy to
decrease bleeding
▪ Injection therapy with epinephrine (1:10,000 dilution) during
endoscopy is effective for acute hemostasis
- Epinephrine produces tissue edema which then puts pressure
on the source of bleeding
▪ Somatostatin or its long-acting analog octreotide (Sandostatin) may be
administered when endoscopy is not available during an acute stage
to reduce blood flow to the GI organs and acid secretion.
- an initial bolus of somatostatin is given then used for 3 to 7
days
- octreotide is given for 3 days after the start of bleeding.

NURSING MANAGEMENT
Assessment
a. Assess patient’s level of consciousness, vital signs (every 15-30 minutes),
skin color, and capillary refill.
b. Check the abdomen for distention, guarding, and peristalsis. Immediate
determination
c. Assess for signs and symptoms of shock - low BP; rapid, weak pulse;
increased thirst; cold, clammy skin; and restlessness. Monitor the
patient’s
Answer these questions:
▪ Is there a history of previous bleeding episodes?
▪ Has the patient received blood transfusions in the past, and were
there any transfusion reactions?

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 ▪ Are there any other illnesses (e.g., liver disease, cirrhosis) or
medications that may contribute to bleeding or interfere with
treatment?
▪ Does the patient have a religious preference that prohibits the use of
blood or blood products?
Nursing diagnoses
▪ Decreased cardiac output related to loss of blood
▪ Deficient fluid volume related to acute loss of blood and gastric
secretions
▪ Ineffective peripheral tissue perfusion related to loss of circulatory
volume
▪ Anxiety related to upper GI bleeding, hospitalization, uncertain
outcome, source of bleeding
Planning
The overall goals:
1) have no further GI bleeding
2) have the cause of the bleeding identified and treated
3) experience a return to a normal hemodynamic state
4) experience minimal or non-symptoms of pain or anxiety.

NURSING INTERVENTIONS;
1. Health promotion/education
a. Instruct patient to avoid gastric irritants such as alcohol and
smoking, and to take only prescribed medications.
- OTC drugs - may contain ingredients (e.g., aspirin) that increase
the risk of bleeding.
b. Instruct the patient how to test vomitus or stools for occult blood.
- report positive results to the health care provider.
c. Instruct patient who are taking aspirin, corticosteroids, or NSAIDs
about the potential for GI bleeding
- Taking these drugs with meals or snacks; or with PPI or H2
receptor blocker lessens their direct irritation.
d. Emphasize the importance of treating an upper respiratory tract
infection promptly
- Severe fragile varices may lead to severe bleeding
e. Instruct patients with blood dyscrasias (e.g., aplastic anemia) or liver
dysfunction or those who are taking cancer chemotherapy drugs that
they are at risk due to a decrease in clotting factors and platelets that
may lead to bleeding.
2. Acute intervention.
a. Allay anxiety by talking calmly to patient
b. Use caution when administering sedatives for restlessness because it
is one of the warning signs of shock and may be masked by the drugs.
c. Once an infusion has been started, maintain the IV line for fluid or
blood replacement.
d. Record accurate intake and output to assess hydration status
- Hourly urine output monitoring
- Record CVP readings 1-2 hourly
e. Hemodynamic monitoring to assess signs of fluid overload

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 - Auscultate breath sounds and closely observe the respiratory
effort
- Keep the head of the bed elevated to provide comfort and
prevent aspiration
- Perform ECG monitoring
f. Closely monitor vital signs
g. NG tube management – proper position and note for blood in the
aspirate
- Perform gastric lavage when advised and if competent -
approximately 50 to 100 mL of fluid is instilled at a time into
the stomach
3. Ambulatory and home care
a. Teach the patient and the caregiver in preventing future bleeding
episodes and the importance of adhering to treatment
EVALUATION
The expected outcomes are that the patient with upper GI bleeding
will:
▪ Have no upper GI bleeding
▪ Maintain normal fluid volume
▪ Experience a return to a normal hemodynamic state
▪ Understand potential etiologic factors and make appropriate
lifestyle modifications

c) GASTRITIS
▪ an inflammation of the gastric mucosa that is commonly affecting the
stomach.

Etiology and Pathophysiology

▪ it occurs due to a breakdown in the normal gastric mucosal barrier
which normally protects the stomach tissue from the corrosive action
of HCl acid and pepsin.
▪ When this barrier is impaired, HCl acid and pepsin can diffuse back
into the mucosa causing tissue edema, disruption of capillary walls
with loss of plasma into the gastric lumen, and possible hemorrhage.

Risk Factors.
a. Drug-Related Gastritis.
▪ NSAIDs prevent the synthesis of prostaglandins that protect the
gastric mucosa making it more prone to injury
▪ NSAIDs include aspirin, piroxicam (Feldene), naproxen (Naprosyn),
sulindac (Clinoril), indomethacin (Indocin), diclofenac (Voltaren), and
ibuprofen (Advil).
Risk factors for NSAID-induced gastritis
Female
over age 60
having a history of ulcer disease
taking anticoagulants, other NSAIDs (including low-dose aspirin), or
other ulcerogenic drugs (including corticosteroids)
having a chronic debilitating disorder such as cardiovascular disease

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b. Diet.
▪ alcoholic drinking binge – can lead to acute damage to the gastric
mucosa ranging from localized injury of superficial epithelial cells to
destruction of the mucosa with mucosal congestion, edema, and
hemorrhage.
▪ Eating large quantities of spicy, irritating foods
c. Metabolic conditions
▪ renal failure
Helicobacter pylori.
▪ an important cause of chronic
gastritis common in
underdeveloped countries and in
people of low socioeconomic
status.
▪ Infection likely occurs during
childhood with transmission from
family members to the child,
possibly through a fecal-oral or
oral-oral route

Causes of Gastritis 42-12 CAUSES OF GASTRITIS

Drugs Pathophysiologic
• Aspirin Conditions
• Corticosteroids • Burns
• Nonsteroidal antiinflammatory • Large hiatal hernia
drugs (NSAIDs) • Physiologic stress
Diet • Reflux of bile and pancreatic
• Alcohol secretions
• Spicy, irritating food • Renal failure (uremia)
Microorganisms • Sepsis
• Helicobacter pylori • Shock
• Salmonella organisms Other Factors
• Staphylococcus organisms • Endoscopic procedures
Environmental Factors • Nasogastric tube
• Radiation • Psychologic stress
• Smoking

d. Other Risk Factors.

▪ Bacterial, viral, and fungal infections, including Mycobacterium
species, cytomegalovirus (CMV), and syphilis
▪ surgical procedures (e.g., gastroduodenostomy, gastrojejunostomy)
which can lead to reflux of bile salts from the duodenum into the
stomach
▪ Prolonged vomiting causing reflux of bile salts
▪ Intense emotional responses and CNS lesions causing hypersecretion
of Hcl Acid leading to inflammation of the mucosal lining
Autoimmune Gastritis.
▪ Also called Autoimmune metaplastic atrophic gastritis or autoimmune
atrophic gastritis
▪ mostly affects women of northern European descent

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 ▪ A genetic condition of immune response causing loss of parietal cells
leading to low chloride levels, inadequate production of intrinsic
factor, cobalamin (vitamin B12) malabsorption, and pernicious
anemia.
▪ High risk of developing stomach cancer
Clinical Manifestations
▪ Anorexia
▪ nausea and vomiting
▪ epigastric tenderness
▪ a feeling of fullness.
▪ Hemorrhage associated with alcohol abuse
▪ Acute gastritis can last from few hours to a few days, with expected
complete healing of the mucosa
Diagnostic Studies
Mostly depend on the patient’s history of drug and alcohol use.
a. Endoscopic examination with biopsy
b. Determine presence of H. Pylori infection (Breath, urine, serum, stool,
and gastric tissue)
c. complete blood count (CBC) to rule out anemia
d. Stools test for occult blood.
e. Serum tests for antibodies to parietal cells and intrinsic factor
f. Tissue biopsy to rule out gastric carcinoma

NURSING AND COLLABORATIVE MANAGEMENT

ACUTE GASTRITIS
▪ Prevention is important
▪ If there is vomiting, provide rest, NPO status, and IV fluids may be
prescribed.
▪ If severe, insert NG tube:
- to monitor for bleeding
- to lavage the precipitating agent from the stomach
- to keep the stomach empty and free of noxious stimuli.
- Clear liquids are resumed when symptoms have subsided, with
gradual reintroduction of solids.
▪ If hemorrhage is considered likely, frequently check vital signs and
test the vomitus for blood. (Check nursing management for GI
bleeding)
▪ Administer drug therapy to reduce irritation of the gastric mucosa and
provide symptomatic relief (H2-receptor blockers or PPIs) with

CHRONIC GASTRITIS
▪ Aim is to evaluate and eliminate the specific cause (e.g., cessation of
alcohol intake, abstinence from drugs, H. pylori eradication)
▪ antibiotic combinations are used to eradicate H. pylori
▪ cobalamin for pernicious anemia (administered orally, nasally, or by
injections)
▪ lifestyle modifications (nonirritating diet in small frequent feeds/day,
smoking cessation, no alcohol)

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Treatment Duration Eradication Rate
Triple-Drug Therapy 7-14 days 70%-85%
proton pump inhibitor (PPI)*
amoxicillin 1 g BD
clarithromycin 500 mg BD
Quadruple Therapy 10-14 days
PPI*
Bismuth 120-300 mg/300 QID
Tetracycline 500 mg QID
metronidazole (Flagyl) 250-500
mg QID

* standard dose (Omeprazole 20 mg, Lansoprazole 30 mg)

D. PEPTIC ULCER DISEASE

▪ an excavation in the mucosal wall of the stomach, in the pylorus
(opening between stomach and duodenum), in the duodenum or in the
esophagus (Farell, 2016)
▪ A peptic ulcer is frequently referred to as a gastric (near the pylorus),
duodenal or esophageal ulcer (due to GERD), depending on its
location, or as peptic ulcer disease.
▪ The main cause is erosion of a circumscribed area of mucous
membrane that may extend to the deep muscle layers to the
peritoneum.
▪ Most commonly occur in the duodenum
Etiology and Pathophysiology
▪ Peptic ulcers develop only in an acid environment although an excess
of HCl acid may not be necessary for ulcer development.
▪ When the stomach acid level is neutralized by food or antacids or acid,
secretion is blocked by drugs, the pH is increased to 3.5 or more
resulting in little or no proteolytic for pepsin
▪ The diffusion of HCl acid into the mucous membrane of the stomach
cause cellular destruction and inflammation and histamine is released

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 resulting in vasodilation and increased capillary permeability and
more secretion of acid and pepsin.
Common causes:
1. Helicobacter pylori
• a gram- negative bacillus that is found within the gastric epithelial
cells
• accounts for 90% of duodenal ulcers and 70-90% of gastric ulcers
• usually acquired during childhood in which the bacteria in the
stomach can survive for long by colonizing the gastric epithelial
cells within the mucosal layer.
• The bacteria secretes urease which is responsible in breaking
down urea into ammonia and protects the organism by
neutralizing the acid gastric environment
• Not every person infected with H. pylori develop ulcers. In one
scenario,
2. NSAID-associated PUD
• Ulcerogenic drugs, such as aspirin and NSAIDs, prevent synthesis
of prostaglandins, increase gastric acid secretion, and reduce the
integrity of the mucosal barrier by decreasing mucosal blood flow.
3. Other medications
• Patients on corticosteroids, anticoagulants, and selective serotonin
reuptake inhibitors (e.g., fluoxetine [Prozac]) increase risk of ulcer
development.
• Corticosteroids affect mucosal cell renewal and decrease its
protective effects.
4. Lifestyle Factors.
• Alcohol stimulates acid secretion which irritates the gastric
mucosa.
• Coffee (caffeinated and decaffeinated) is a strong stimulant of
gastric acid secretion.
• Psychologic distress, including stress and depression, can
negatively influence the healing of ulcers
• Smoking also delays ulcer healing
Classifications:
According to degree and duration:
1) Acute- associated with superficial erosion and minimal inflammation
short duration and resolves quickly when the cause is identified and
removed
2) Chronic - long duration, eroding through the muscular wall with the
formation of fibrous tissue, continuously for many months or intermittently
throughout the person’s lifetime. more common than acute erosions.

According to location:
1) Gastric Ulcer
• Most commonly found in the antrum of the stomach but are less
common than duodenal ulcers
• Can result in obstruction
• Factors include H. Pylori, medications, smoking and bile reflux

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Clinical Manifestations
▪ Usually occurs 1-2 hours after meals
▪ Burning or gaseous pain which could be exacerbated by food

2) Duodenal Ulcer.
• accounts for about 80% of all peptic ulcers.
• incidence is between 35 and 45 years of age.
• Factors include H. Pylori infection, alcohol, smoking stimulates acid
secretion)
• located in the mid-epigastric region beneath the xiphoid process
• Silent peptic ulcers are more likely to occur in older adults and those
taking NSAIDs
Risk groups:
a. COPD
b. Cirrhosis of the liver
c. chronic pancreatitis
d. hyperparathyroidism
e. chronic kidney disease
f. Zollinger-Ellison syndrome (a rare condition characterized by severe
peptic ulceration and HCl acid hypersecretion).
Clinical Manifestations (occurs 2-5 hours after meals)
▪ “burning” or “cramp like” pain
▪ Occasionally back pain.
▪ Can be intermittent
Complications of PUD (considered an emergency)
1) Hemorrhage
▪ Most common complication
2) Perforation and Penetration (both need surgical intervention)
Penetration
▪ is erosion of the ulcer through the gastric serosa into adjacent
structures such as the pancreas, biliary tract or gastrohepatic
omentum.
▪ Characterized by back and epigastric pain not relieved by
medications that were effective in the past
Perforation is the erosion of the ulcer through the gastric serosa into the
peritoneal cavity without warning.
Characteristics of Perforation:
▪ sudden, severe abdominal pain which can radiate to the back and is
not relieved by food or antacids
▪ rigid and board-like abdomen
▪ shallow and rapid respirations
▪ hypotension and tachycardia, weak pulse (indicate shock)
▪ absent bowel sounds
▪ nausea and vomiting
* If not treated, bacterial peritonitis may occur
3) Gastric Outlet Obstruction.
▪ Obstruction occurs in the distal stomach and duodenum caused by
edema, inflammation, or pylorospasm and fibrous scar tissue
formation.

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 ▪ Characterized by nausea and vomiting, constipation, epigastric
fullness, anorexia and, later, weight loss
Diagnostic Studies
1. Endoscopy
2. Biopsy of the antral mucosa and testing for urease or rapid urease
testing) - considered the gold standard for in diagnosing H. pylori
infection.
3. Stool testing
4. Urea breath test to determine active infection.
▪ Urea is a by-product of the metabolism of H. pylori bacteria.
5. A barium contrast study – to check for obstruction or ulceration in the
stomach
6. Laboratory tests - CBC, liver enzyme studies, serum amylase
determination (to determine pancreatic function when duodenal ulcer
penetration of the pancreas is suspected)
Collaborative Care
▪ Goal of treatment is to decrease gastric acidity and improve the
defense of the gastric mucosa
a. Drug therapy
• Histamine (H2)- Receptor Blockers – Famotidine, Ranitidine,
Cimetidine
• Proton Pump Inhibitors – Omeprazole, Lanzoprazole,
- more effective than H2-Receptor Blockers
- combined with antibiotic therapy for 7-14 days to treat
ulcers caused by H. Pylori
• Antibiotic Therapy – combined with a PPI
• Antacids – aluminum hydroxide or magnesium hydroxide
- Increase gastric pH by neutralizing HCL acid
- (Read about Antacids)
• Sucralfate – for short term treatment of ulcers
- Given 30 minutes before and after an antacid
• Other drugs – antidepressants (Doxepin), Anticholinergic drugs
(used occasionally) – be aware of side effects
b. Other therapies: (for complications)
• Treat perforation
• Insert NG tube, CVP line
• IV fluids, Blood if Hb is low
• Perform ECG, Insert urinary catheter
c. Surgical management
• recommended for patients with intractable ulcers (those who fail to
heal after 12 to 16 weeks of medical treatment), life-threatening
hemorrhage, perforation or obstruction, and for those not
responding to medications

List of surgical procedures for PUD (adapted from Farell, 2016)

Surgical procedure Description Comments

Vagotomy Severing of the vagus May be performed to
nerve. Decreases reduce gastric acid

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 gastric acid by diminishing secretion. A drainage
cholinergic stimulation to type of procedure (see
the parietal cells, making pyloroplasty) is usually
them less responsive to performed to assist with
gastrin. May be done via gastric emptying
open surgical approach, (because there is
laparoscopy or total denervation of the
thoracoscopy stomach). Some
patients experience
problems with feelings
of fullness, dumping
syndrome, diarrhoea
and gastritis

Truncal vagotomy Severs the right and left This type of vagotomy is
vagus nerves as they enter most commonly used to
the stomach at the distal decrease acid secretions
part of the esophagus. and reduce gastric and
intestinal motility.
Recurrence rate of ulcer
is 10% - 15%.

Selective vagotomy Severs vagal innervation to

the stomach but maintains
innervation to the rest of
the abdominal organs.

Proximal (parietal cell) Denervates acid-secreting No dumping syndrome.

gastric vagotomy parietal cells but preserves No need for drainage
without drainage vagal innervation to the procedure. Recurrence
gastric antrum and rate of ulcer is 10% -
pylorus. 15%.

Pyloroplasty A surgical procedure in Usually accompanies

which a longitudinal truncal and
incision is made into the selective vagotomies,
pylorus and transversely which produce delayed
sutured closed to enlarge gastric emptying due to
the outlet and relax decreased innervation.
the muscle
Antrectomy Removal of the lower May be performed in
Billroth I portion of the antrum of together with a truncal
(Gastroduodenostomy) the stomach (which vagotomy. The
contains the cells that patient may have
secrete gastrin) as well as problems with feelings
a small portion of the of fullness, dumping
duodenum and pylorus. syndrome and diarrhea.
The remaining segment is Recurrence rate of ulcer
anastomosed to the is 1%.
duodenum (Billroth I) or to
the jejunum (Billroth II

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Subtotal gastrectomy Removal of distal 2/3 of Dumping syndrome,
with Billroth I or II stomach and anastomosis anemia, malabsorption,
Anastomosis with duodenum or weight loss. Recurrence
jejunum. Removes gastrin- rate of ulcer is 10%- 15
producing cells in the
antrum and part of the
parietal cells.

NURSING MANAGEMENT
Assessment
▪ Health history including lifestyle habits – smoking, alcohol intake,
▪ Ask patient to describe pain – pain is usually burning and gnawing;
occurs 2 hours after a meal and frequently awakens the patient
between midnight and 3 am.
▪ Health history - Is patient taking antacids? NSAIDs?
▪ History of vomiting – note vomitus characteristics. Is it bright red?
coffee ground -like or is there undigested food from previous meals?
▪ Note presence of bloody or tarry black stools

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 ▪ Ask patient about their usual food intake for a 72-hour period and to
describe food habits including speed of eating, regularity of meals,
preference for spicy foods, use of seasonings, use of caffeinated
beverages and decaffeinated
▪ Assess stress/ anxiety level/ coping mechanisms
▪ Assess vital signs
Nursing diagnoses
▪ Nursing diagnoses related to PUD may include, but are not limited to,
the following:
➢ Acute pain related to increased gastric secretions
➢ Ineffective self–health management related to lack of knowledge of
long-term management of PUD
➢ Nausea related to acute exacerbation of disease process
Planning
Goals include:
1. Adhere to the prescribed therapeutic regimen
2. experience a reduction in or absence of discomfort
3. exhibit no signs of GI complications
4. have complete healing of the peptic ulcer
5. make appropriate lifestyle changes to prevent recurrence.
Nursing implementation
Health Education.
▪ Advise patients to take drugs for ulcer with food.
▪ Encourage patients to report symptoms of gastric irritation to health
care providers
Interventions
a. NPO for a few days to prevent worsening of N & V and pain (during acute
phase)
- Insert NG tube connected to intermittent suction and have IV fluid
replacement
b. Regular mouth care to soothe dry mouth.
c. Cleansing and lubrication of the nares facilitate breathing and decrease
soreness.
d. Analysis of gastric contents may include pH testing and analysis for
blood, bile, or other substances.
e. Pain relief – administer prescribed medications
f. Physical and emotional rest
g. Reduce stress and provide rest
h. Encourage lifestyle modification – avoid smoking and alcohol
i. Maintain optimal nutritional status –
1. Encourage intake of dry foods with a low carbohydrate content and
moderate protein and fat content
2. Resting after each meal helps in preventing dumping syndrome
3. During hypoglycemia, take sugary foods immediately but limit the
amount of sugar taken with meals
4. Eat small, frequent feedings
5. avoid foods that trigger symptoms (caffeine, hot and spicy foods,
carbonated drinks) assess for weight loss or malnutrition Instruct
patient to limit drinking fluids with meals
j. Monitor and manage potential complications

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Hemorrhage
➢ Asses for signs of hemorrhage
➢ same management with GI bleeding management
Perforation
➢ if perforation is suspected, notify surgeon immediately
➢ monitor vital signs every 15-30 minutes
➢ keep NPO stat
➢ administer IVF
➢ administer antibiotics as prescribed
➢ prepare patient for surgery if necessary
Gastric Outlet Obstruction.
➢ Regular NG aspiration and irrigation with normal saline solution (NSS)
➢ Administer IVF with electrolytes as prescribed
➢ Record accurate intake and output including gastric aspirates
➢ Prepare patient for surgery if necessary
Evaluation
The patient with PUD will:
➢ Have controlled pain without analgesics
➢ Verbalize understanding of the disease and its management
➢ Commit to adherence to self-care and management
➢ Have no complications

NURSING MANAGEMENT (for patients undergoing PUD surgery)

PREOPERATIVE MANAGEMENT
▪ Perform the usual preoperative nursing care for surgical patients
including expectations, comfort measures, pain relief, coughing and
breathing exercises, NG tube, IVF, urinary catheter.

POSTOPERATIVE MANAGEMENT
1. Care for a patient with an NG tube
➢ Assess gastric aspirate for color, amount, and odor
- Aspirate is usually bright red initially, then gradually darkens
within the first 24 hours, yellow-green 36-48 hours
Postoperative Complications.
• Post-op bleeding
• Dumping syndrome – after surgery the stomach no longer has
control over the amount of gastric chyme entering the small intestine.
• Postprandial hypoglycemia – low blood sugar after a meal
• Bile reflux gastritis – gastric surgery can lead to bile reflux in the
stomach that can damage the gastric mucosa, cause chronic gastritis
and recurrence of PUD

OBESITY
➢ a metabolic disease characterized by fat that accumulates to the
extent that health is impaired (American Society for Metabolic
and Bariatric Surgery [ASMBS], 2012).
➢ BMI exceeds 30kg/m2
Morbid obesity
▪ A term applied to people who are more than two times their ideal body
weight or whose BMI exceeds 40 kg/m2

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 ▪ They are at higher risk of health complications like diabetes, heart
disease, stroke, hypertension, gallbladder disease, osteoarthritis, sleep
apnea and other breathing problems, and some forms of cancer
(uterine, breast, colorectal, kidney and gallbladder)
▪ They usually have a low self-esteem and impaired body image.
Medical management
a. Lifestyle modification
▪ Involves weight loss diet together with behavioral modification and
exercise.
▪ Collaboration with a dietitian is highly recommended
b. Pharmacological management
▪ Orlistat - reduces kilojoule intake by binding to gastric and pancreatic
lipase to prevent digestion of fats. Vitamin is recommended when
taking this drug
▪ Phentermine - affects the appetite centre in the brain making the
person less hungry
▪ Antidepressant – for those who are depressed as study shows
depression can cause weight gain as the person tend to eat more
c. Surgical management
Bariatric surgery
▪ Done for morbid obesity if other nonsurgical attempts at weight
control have failed.
▪ Average loss after surgery is 60%
▪ Gastric restriction procedures are usually performed laparoscopically
to reduce gastric capacity and done for patients if BMI is > 40 kg/m2
or 35 kg/m2
▪ It involves massive counseling, education and evaluation by a
multidisciplinary team, including social workers, dieticians, a nurse
counsellor, a psychologist or psychiatrist and a surgeon
Most common surgeries
a. Roux-e n - Y gastric bypass

▪ A gastric surgery
wherein a small pouch
from the stomach is
created and attached to
the small intestine

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b. Sleeve gastrectomy

▪ The stomach is incised vertically

and up to 85% of the stomach is
surgically removed, leaving a
'sleeve'-shaped tube that retains
intact nervous innervation and
does not obstruct or decrease
the size of the gastric outlet.

Criteria for Bariatric Selection (Farell, 2016)

▪ Weight greater than 45 kg above the ideal body weight for sex and
height
▪ BMI >40 by itself or >35 if there is an associated obesity illness,
such as diabetes or sleep apnea
▪ Reasonable attempts at other weight-loss techniques
▪ Age 18 to 65 years
▪ Obesity-related health problems
▪ No psychiatric or drug dependency problems
▪ A capacity to understand the risks and commitment associated with
the surgery
Adapted from Obesity Surgery Society of Australia & New Zealand. (2015a)
Obesity- Are You A Candidate? Available December 20 1 5 at: www.ossanz.com .au/obesity _ candidate.htm

r bariatric surgery
3. Disturbances in absorption and elimination
A. DISORDERS OF INTESTINAL MOTILITY

a) DIARRHEA
▪ Characterized by increased frequency in passing stool (3 or more in a
day), increased amount (more than 200g/day) and altered consistency
(loose or liquid stools).
Etiology and Pathophysiology
▪ Acute diarrhea is usually due to ingestion of infectious organisms
▪ Infectious organisms attack the intestines in different ways
▪ Some organisms (e.g., Rotavirus A, Norovirus, G. lamblia) alter
secretion and/or absorption of the enterocytes of the small
intestine without causing inflammation.
▪ Other organisms (e.g., Clostridium difficile) impair absorption by
destroying cells, cause inflammation in the colon, and produce toxins
that also cause damage.

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Most common causes
a. Bacterial and Viral infections
- Viral infections can be deadly, but they are usually short lived
(48 hours) and mild – treatment is not often sought
- e.g. Norwalk virus, Norovirus
Bacterial infections
➢ Escherichia coli- most common cause of bloody diarrhea which
is transmitted by improperly cooked contaminated beef or
chicken or fruits and veggies contaminated with manure.
➢ Giardia Lamblia – most common intestinal parasite in the U.S.
b. Medications - thyroid hormone replacement, stool softeners and
laxatives, prokinetic agents, antibiotics, antiarrhythmics,
antihypertensives, chemotherapy, magnesium-based antacids
➢ These medications alters stomach acid that kills ingested
pathogens, thus the patient becomes more susceptible to
pathogens
➢ Clostridium difficile – most common antibiotic-associated
diarrhea
➢ Probiotics (Saccharomyces boulardii and Lactobacillus), may be
helpful in preventing antibiotic-induced diarrhea
c. Metabolic and endocrine disorders – DM, Addison’s disease,
thyrotoxicosis
d. Immunocompromised (HIV- AIDS)
e. Nutritional and maladaptive disorders – Celiac Disease
f. Anal sphincter defect
g. Zollinger-Ellison syndrome
h. Paralytic ileus
i. intestinal obstruction.
Pathophysiology:
Types of Diarrhea
a) Secretary diarrhea - usually high-volume diarrhea and is due to
increased production and secretion of water and electrolytes by the
intestinal mucosa into the intestinal lumen.
b) Osmotic diarrhea - water is pulled into the intestines by the osmotic
pressure of unabsorbed particles, slowing the reabsorption of water.
➢ causes include lactase deficiency, pancreatic dysfunction or
intestinal hemorrhage
c) Malabsorptive diarrhea combines mechanical and biochemical
actions, inhibiting effective absorption of nutrients manifested by
markers of malnutrition that include hypoalbuminemia. Low serum
albumin levels lead to intestinal mucosa swelling and liquid stool.
Exudative diarrhea is caused by changes in mucosal integrity,
epithelial loss or tissue destruction by radiation or chemotherapy
(Blaser et al., 2015).

Clinical Manifestations
▪ increased frequency and fluid content of stools
▪ abdominal cramps
▪ distension
▪ intestinal rumbling (i.e. borborygmus)

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 ▪ anorexia
▪ thirst
▪ Painful spasmodic contractions of the anus and ineffectual straining
(i.e. tenesmus) may occur with defecation.
▪ Infections that attack the upper GI tract (e.g., Norovirus, G. lamblia)
usually produce large-volume, watery stools; cramping; and
periumbilical pain, have either a low-grade or no fever and often
experience nausea and vomiting
▪ Severe diarrhea can result in life-threatening dehydration, electrolyte
disturbances (e.g., hypokalemia), and acid-base imbalances (metabolic
acidosis) C. difficile infection which can lead to fulminant colitis and
intestinal perforation.
▪ Infections of the colon and distal small bowel (e.g., Shigella,
Salmonella, C. difficile) produce fever and small frequent bloody
diarrhea
Characteristics:
a) Watery stools – associated with small bowel disease
b) loose, semisolid stools – usually associated with disorders of the colon
c) Voluminous, greasy stools – indicative of intestinal malabsorption
d) Presence of mucus and pus - suggests inflammatory enteritis or colitis
(amoebiasis)
e) Oil droplets on the toilet water – diagnostic of pancreatic in sufficiency
f) Nocturnal diarrhea - manifestation of diabetic neuropathy
g) Unexplained diarrhea – consider Clostridium difficile infection in
patients who recently took antibiotics (Blaser et al., 2015)
Diagnostic Studies
▪ Stool Analysis including C & S
➢ Stools are examined for blood, mucus, white blood cells (WBCs),
and parasites, and cultures are performed to identify infectious
organisms.
▪ full blood cell count – elevated WBC, decreased Fe and Folate
(anemia); Increased hematocrit, blood urea nitrogen (BUN), and
creatinine levels in chronic diarrhea are signs of fluid deficiency
▪ chemical profile
▪ urinalysis
▪ routine stool examination and stool examinations
▪ Endoscopy or barium enema may assist in identifying the cause.
Complications
▪ Arise due to fluid and electrolytes loss
a) Hypokalemia - decreased potassium levels cause cardiac arrhythmias
(i.e. atrial and ventricular tachycardia, ventricular fibrillation and
premature ventricular contractions) that can lead to death.
b) Irritant dermatitis
Clostridium difficile Infection.
▪ a particularly hazardous health care–associated infection.
▪ Its spores can survive for up to 70 days on objects, including
commodes, telephones, thermometers, bedside tables, and floors
▪ C. difficile can be transmitted from patient to patient by health care
workers who do not adhere to infection control precautions.
Treatment:

*For IFSU USE ONLY

 Metronidazole (Flagyl) IV – first line drug
Vancomycin for severe cases

NURSING AND COLLABORATIVE MANAGEMENT (acute infectious

diarrhea)
Assessment
a. thorough history and physical examination
- describe pattern and associated symptoms (duration, frequency,
character, and consistency of stool, and other symptoms such
as pain and vomiting.
b. Ask about medical conditions and current medications that might
cause diarrhea
c. Ask any travel history
d. Food preparation practices, food intolerance and changes in diet
e. Assess for fever and signs of dehydration (dry skin, low grade fever,
orthostatic changes to pulse and blood pressure, decreased and
concentrated urine)
f. Assess abdomen for distention, pain, and guarding
g. Inspect the perineal skin for signs of redness and breakdown from the
diarrhea.
Nursing diagnoses
May include:
▪ Diarrhea related to acute infectious process
▪ Deficient fluid volume related to excessive fluid loss and decreased
fluid intake
Planning
Goals: the patient with diarrhea will have
1. no transmission of the microorganism causing the infectious diarrhea
2. cessation of diarrhea and resumption of normal bowel patterns
3. normal fluid, electrolyte, and acid base balance
4. normal nutritional status
5. no perianal skin breakdown.
Nursing implementation
a) Observe strict infection control measures
➢ Wash your hands before and after contact with each patient and when
handling body fluids of any kind.
➢ Flush vomitus and stool in the toilet
➢ Teach the patient and caregiver to wash contaminated clothing
immediately with soap and water and other hygiene and infection
control precautions
➢ Discuss proper food handling, cooking, and storage with the patient
and the caregiver.
➢ Provide private rooms for patients with C. difficile infection as spores
are difficult to kill – make sure that visitors and health care providers
wear gloves and gowns and practice isolation precautions
b) Drug therapy
➢ Administer parenteral fluids, electrolytes, vitamins, and nutrition if
losses are severe.
➢ Antidiarrheal agents may be given to coat and protect mucous
membranes, absorb irritating substances, prevent intestinal transit,

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 decrease intestinal secretions, or decrease central nervous system
stimulation of the GI tract
- Given only for a short period of time and contraindicated in the
treatment of some infectious diarrheas due to prolonged
exposure to the organism
- used cautiously in inflammatory bowel disease (IBD) due to the
danger of toxic megacolon (colonic dilation greater than 5 cm).

b) FECAL INCONTINENCE
▪ Involuntary passage of stool from the rectum
Etiology and Pathophysiology
▪ It occurs from conditions that interrupt or disrupt the structure or
function of the anorectal unit
Causes
▪ trauma (e.g. after surgical procedures involving the rectum)
▪ neurological disorder (e.g. stroke, multiple sclerosis, diabetic
neuropathy, dementia)
▪ inflammation
▪ infection
▪ radiation treatment
▪ fecal impaction
▪ pelvic floor relaxation
▪ laxative abuse
▪ medications
▪ advancing age (i.e. weakness or loss of anal or rectal muscle tone)
Diagnostic Studies and Collaborative Care
a) rectal examination – to detect internal prolapse, rectocele,
hemorrhoids, fecal impaction, and masses.
b) Abdo Xray or CT scan if impaction is higher
c) Anorectal manometry or ultrasonography
d) Sigmoidoscopy/colonoscopy – to detect inflammation, tumors,
fissures, and other pathologic conditions.
e) Barium enema
Clinical manifestations
▪ Minor soiling
▪ Urgency and loss of control
▪ Complete incontinence
▪ Poor control of flatus, diarrhea or constipation

NURSING AND COLLABORATIVE MANAGEMENT

a) Diagnosis and effective management of fecal incontinence require a
thorough health history and physical examination
- number of incontinent episodes per week, stool consistency, volume,
and the degree that incontinence interferes with work and social
activities.
b) Rectal examination
c) Manual evacuation if there is fecal impaction
d) Initiate bowel training program to resume bowel regularity
e) Diet modification

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 - Intake of foods that cause diarrhea and rectal irritation (coffee, dried
fruit, onions, mushrooms, green vegetables, fruit with peels, spicy
foods, and foods with monosodium glutamate) may need to be reduced
or eliminated.
f) Surgical procedures include surgical reconstruction, sphincter repair or
fecal diversion
g) Drugs - An antidiarrheal agent (loperamide [Imodium]) may be used to
slow intestinal transit.
h) Kegel exercises to strengthen and coordinate the pelvic floor muscles to
improve continence
i) Biofeedback therapy is advised to improve awareness of rectal sensation,
coordinate internal and external anal sphincters, and increase the
strength of external sphincter contraction.
NURSING MANAGEMENT
Assessment
a. Be sensitive to the patient’s feelings when talking about incontinence as
this can be embarrassing.
b. Ask about bowel patterns before the incontinence developed bowel
c. Assess whether the patient has defecation urgency and sensation of
passing flatus and leaking stool
d. Check the perineal area for irritation or breakdown
incontinence-associated dermatitis (IAD)
▪ Occurs in patient who are incontinent of feces due to chemical
irritants in feces
▪ characterized by erythema and skin denudement (erosion) of
the perianal or genital areas, buttocks, or upper thighs
e. Ask about daily activities (mealtimes and work), diet, and family and
social activities.
The Bristol Stool Chart helps in assessing stool

Nursing diagnoses (include but not limited to)

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 ▪ Bowel incontinence related to inability to control bowel function
▪ Self-care deficit (toileting) related to inability to manage bowel
evacuation voluntarily
▪ Risk for situational low self-esteem related to inability to control bowel
movements
▪ Risk for impaired skin integrity related to incontinence of stool
Planning
Overall goals: pt will have
1. predictable bowel elimination
2. maintain perianal skin integrity
3. participate in work and social activities
4. prevent self-esteem problems related to bowel control.

Nursing implementation
a) Plan a bowel program based on the patient’s bowel pattern to assist
the patient in achieving fecal continence or manage elimination
problems
b) Provide assistance to bedpan, commode, to the toilet to help establish
regular defecation
c) Administer laxative to stimulate anal reflex – discontinue when
regular bowel schedule is achieved (administered 15-30 minutes
before normal evacuation time but check first for stool in the rectum
before inserting suppository)
d) Encourage patient to increase fiber in the diet and avoid caffeine
e) Check for skin integrity due to incontinence – continence brief and
pads may be used
f) Provide psychological support as this can be embarrassing for the
patient and family
g) Assist in bowel management system devices (external pouches)

c) CONSTIPATION
▪ characterized by absent or infrequent stools and hard, dry stools that
are difficult to expel
Etiology and Pathophysiology
▪ Constipation occurs with diseases that decrease GI transit and alter
neurologic function such as diabetes mellitus, Parkinson’s disease,
and multiple sclerosis.
Common causes
▪ insufficient intake of dietary fiber or fluids
▪ decreasing physical activity
▪ ignoring the defecation urge – muscles and mucosa of the rectum
becomes insensitive to fecal presence
▪ drugs, especially opioids, cause constipation.
▪ Emotions including anxiety, depression, and stress, affect the GI tract
which can cause constipation.
Cathartic colon syndrome
➢ a condition wherein the colon becomes dilated and atonic (lack of
muscle tone).
➢ This can be caused by laxative overuse until the person is unable to
defecate without laxatives

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Clinical Manifestations
▪ Stools are absent or hard, dry, and difficult to pass.
▪ Abdominal distention
▪ Bloating
▪ increased flatulence
▪ increased rectal pressure
Hemorrhoids - most common complication of chronic constipation caused by
venous engorgement due to repeated Valsalva maneuvers and venous
compression from hard impacted stool.
Valsalva maneuver
▪ these are frequent straining especially when defecating
▪ risky in patients with heart failure, cerebral edema, hypertension, and
coronary artery disease.
▪ During straining, there is increase in both intraabdominal and
intrathoracic pressures causing decrease in venous return to the
heart →heart rate ↓ (bradycardia) temporarily, → the cardiac output ↓,
and a transient drop in arterial pressure occurs
▪ When the patient relaxes, thoracic pressure falls, resulting in a
sudden flow of blood into the heart, increased heart rate (tachycardia),
and an immediate rise in arterial pressure which could be fatal for the
patient
Diagnostic Studies and Collaborative Care
a. Perform a thorough history and physical examination
b. Abdominal x-rays, barium enema,
c. colonoscopy, sigmoidoscopy, and anorectal manometry
Prevention
▪ increase fiber in diet,
▪ increase fluid intake
▪ exercise
Collaborative Management
a. Laxatives and enemas for acute constipation
▪ Stool softeners include Bisacodyl tablets and suppositories, milk of
magnesia, and lactulose but not used for long as they may cause
dependence
▪ Enemas that can be given but with caution and not for long periods
include:
➢ Soapsuds enemas - produce inflammation of colon mucosa
➢ tap water – may lead to water intoxication
➢ sodium phosphate (e.g., Fleet) enemas - cause electrolyte
imbalances in patients with cardiac and renal problems.
▪ Biofeedback therapy may benefit patients who are constipated as a
result of anismus (uncoordinated contraction of the anal sphincter
during straining)
▪ In a patient with unrelenting constipation, a subtotal colectomy with
ileorectal anastomosis may be performed.
b. Nutritional Therapy
▪ increase intake of dietary fiber and fluids (2L/day)
NURSING MANAGEMENT
Assessment
Nursing diagnosis

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 Example
▪ Constipation related to inadequate intake of dietary fiber and fluid and
decreased physical activity
Planning
Goals:
a) increase dietary intake of fiber and fluids
b) increase physical activity
c) pass soft, formed stools
d) not have any complications, such as bleeding hemorrhoids.

Nursing implementation
▪ Nursing management should be based on the patient’s symptoms and
assessment
a) Teach the patient about the importance of diet (high fiber, increased fluid
intake) and exercise in the prevention of constipation.
b) Advise the patient to establish a regular time to defecate and not to
suppress the urge to defecate.
c) Discourage the use of laxatives and enemas to achieve fecal elimination.
d) Instruct patient on proper defecation technique – knees higher than the
hips. For a patient in bed using the bedpan, elevate the head of the bed
as high as tolerated and allowed.
e) Encourage to exercise abdominal muscles, do sit-ups and straight-leg
raises

B. MALABSORPTION SYNDROMES
Malabsorption
▪ the inability of the digestive system to absorb one or more of the major
vitamins (especially vitamin B), minerals (iron, calcium) and nutrients
(carbohydrates, fats and proteins)- (Farell, 2016)
▪ most common causes of malabsorption are diseases of the digestive system
Etiology & Pathophysiology
Causes
Categories of diseases causing malabsorption
a) Mucosal (transport) disorders - coeliac sprue, Crohn's disease, radiation
enteritis
b) Infectious diseases - small bowel bacterial overgrowth, tropical sprue,
Whipple's disease
c) Luminal problems - bile acid deficiency, Zollinger-Ellison syndrome,
pancreatic insufficiency
d) Postoperative malabsorption - after gastric or intestinal resection
e) Disorders that cause malabsorption of specific nutrients - disaccharidase
deficiency leading to lactose intolerance

Clinical manifestations
• The hallmarks include diarrhea or frequent, loose, bulky, foul-
smelling stools that have increased fat content and are often greyish
• abdominal distension
• pain
• increased flatus
• weakness

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 • weight loss
• decreased sense of wellbeing.
Main complications:
Malnutrition
• Patients with a malabsorption syndrome, if untreated, become weak
and emaciated due to starvation and dehydration
• Manifestations include: weight loss and other signs of vitamin and
mineral deficiency (e.g. easy bruising, osteoporosis, anemia).

Avitaminosis
▪ Failure to absorb the fat-soluble vitamins A, D and K
Assessment and diagnostic findings
• Stool studies for quantitative and qualitative fat analysis
• Lactose tolerance tests
• D-xylose absorption tests
• Schilling tests
• Endoscopy with biopsy of the mucosa - best diagnostic tool.
• Ultrasound studies, CT scans and x-ray findings can reveal pancreatic
or intestinal tumors that may be the cause
• Full blood count to detect anemia.
Medical management
▪ Intervention is aimed at
▪ Antibiotics (e.g. tetracycline, ampicillin) are sometimes needed in the
treatment of tropical sprue and bacterial overgrowth syndromes.
▪ Anti-diarrheal agents (e.g. propantheline) may be used to relieve
intestinal spasms.
▪ Parenteral fluids may be necessary to treat dehydration

C. STRUCTURAL AND OBSTRUCTIVE BOWEL DISORDERS

a) INTESTINAL OBSTRUCTION
➢ occurs when intestinal contents are unable to pass through the GI
tract due to an obstruction in the small intestine or colon which
may be partial or complete, simple or strangulated.
➢ A simple obstruction has an intact blood supply, and a
strangulated one does not.
➢ Most obstructions occur in the small intestine
➢ Cancers (lung, breast, melanoma) can spread to the abdomen and
cause bowel obstruction
➢ Medical management includes surgical treatment of intestinal
obstruction which depends mainly on the cause of the obstruction,
the duration of the obstruction and the condition of the intestine.

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Types of intestinal obstruction
a. Mechanical Obstruction
➢ An obstruction in the lumen
of the intestine due to
pressure from the intestinal
walls
➢ Ex. polypoid tumors and
neoplasms, stenosis,
strictures, adhesions,
abscesses

Pseudo-obstruction

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 ▪ is a mechanical obstruction of the intestine without demonstration of
obstruction by radiologic methods.
▪ Collagen vascular diseases and neurologic and endocrine disorders
may cause pseudo-obstruction, but many times the cause is
unknown.
b. Functional Obstruction
The intestinal musculature is unable to propel the contents along
the bowel which could be due to vascular, endocrine or
neuromuscular disorders
It can be temporary blockage and the result of the manipulation of
the bowel during surgery.
Ex. amyloidosis, muscular dystrophy, endocrine disorders
(diabetes) or neurological disorders (Parkinson's disease).

Paralytic (adynamic) ileus

▪ lack of intestinal peristalsis and bowel sounds which occurs usually
after any abdominal surgery
Causes may include adhesions, peritonitis, inflammatory
responses (e.g., acute pancreatitis, acute appendicitis), electrolyte
abnormalities (especially hypokalemia), and thoracic or lumbar
spinal fractures
Diagnostic Studies
▪ Perform a thorough history and physical examination.
▪ CT scans and abdominal x-rays
▪ Sigmoidoscopy or colonoscopy
▪ CBC and blood chemistries
- Increased WBC → may indicate strangulation or perforation.
- Elevated hematocrit values → hemoconcentration.
- Low hemoglobin and hematocrit → bleeding from a neoplasm or
strangulation with necrosis.
- Metabolic alkalosis can develop due to vomiting.

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 Small bowel obstruction
▪ The most common
cause of small bowel
obstruction is
adhesion, followed by
hernias and neoplasms

Pathophysiology
▪ Intestinal contents, fluid and gas accumulate above the intestinal
obstruction.
▪ Accumulated fluid decrease the absorption of fluids and stimulate
more gastric secretion causing abdominal distension
▪ This causes pressure within the intestinal lumen resulting in a
decreased venous and arteriolar capillary pressure → edema,
congestion, necrosis and eventual rupture or perforation of the
intestinal wall, leading to peritonitis.
▪ Metabolic acidosis may occur as result of vomiting due to abdominal
distention.
▪ Vomiting can lead to a loss of hydrogen ions and potassium from the
stomach, resulting in decreased chlorides and potassium in the blood
and to metabolic alkalosis.

Clinical manifestations
a. Initial symptom is cramping, wave-like and colicky pain
b. Patient may pass blood and mucus, but no fecal matter or flatus.
c. In complete obstruction, the peristaltic waves initially become
extremely vigorous and eventually assume a reverse direction, with
the intestinal contents propelled towards the mouth instead of
towards the rectum.
d. If obstruction is in the ileum, fecal vomiting occurs.
e. signs of dehydration become evident: intense thirst, drowsiness,
generalized malaise, aching and a parched tongue and mucous
membranes
f. abdomen becomes distended - the lower the obstruction is in the GI
tract, the more marked the abdominal distension.
g. If the obstruction continues uncorrected, hypovolemic shock occurs
from dehydration and loss of plasma volume.

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 h. Diagnostic findings include:
Abdo x-ray shows abnormal quantities of gas, fluid or both in the
bowel, often showing air-fluid levels.
Laboratory studies (i.e. electrolyte studies and CBC) indicate
dehydration, loss of plasma volume and possible infection.
Medical intervention:
▪ Bowel decompression through NGT
▪ Surgical intervention if strangulation is present – prior to surgery, IV
therapy is administered for fluid and electrolyte replacement (water,
sodium, chloride and potassium)
▪ In obstruction caused by hernia and adhesions, surgical procedure
involves repair of the hernia or dividing the adhesion to which the
intestine is attached.
▪ In other cases, the portion of affected bowel may be removed and an
anastomosis performed.

Nursing management
▪ maintain the function of the nasogastric tube,
▪ assess and measure the nasogastric output
▪ assess for fluid and electrolyte imbalance
▪ monitor nutritional status and assessing improvement (e.g. return of
normal bowel sounds, decreased abdominal distension, subjective
improvement in abdominal pain and tenderness, passage of flatus or
stool).

Large bowel obstruction

(Image from: Cleveland Clinic)

Pathophysiology
▪ Obstruction in the large bowel may lead to severe distension and
perforation and even necrosis (tissue death) and strangulation if blood
supply to the colon is cut off

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 ▪ Adenocarcinoid tumors account for the majority of large bowel
obstructions.
Clinical Manifestations
▪ Constipation
▪ Anemia (if blood loss in stool continues)
▪ weakness, weight loss and anorexia.
▪ Distended abdomen, large bowel loops become visibly outlined
through the abdominal wall
▪ crampy lower abdominal pain
▪ fecal vomiting develops.
▪ Symptoms of shock may occur
Medical management
➢ Colonoscopy - may be done to untwist and decompress the bowel
➢ Cecostomy (surgical opening done into the caecum) - for patients who
are poor candidates for surgery and who need relief from the
obstruction.
➢ Insertion of rectal tube - to decompress an area that is lower in the
bowel.
➢ Surgery - surgical resection to remove the obstructing lesion.
Colostomy
▪ Surgical opening in the colon to remove obstructing lesion which can
be temporary or permanent
Ileoanal anastomosis
▪ Maybe done to remove the entire large colon
▪ The ileum and anus are anastomosed (joined together)

Specific nursing interventions

▪ provide emotional support and comfort

▪ administers IV fluids and electrolytes as prescribed
▪ prepare patient for surgery, if indicated including providing
preoperative education
▪ Provide post-op care
Collaborative Care
▪ many bowel obstructions resolve with conservative treatment
▪ Emergency surgery is done for strangulated bowel
Initial treatment of bowel obstruction as a result of adhesions:
➢ put patient on NPO
➢ insert an NG tube for decompression
➢ provide IV fluid therapy with NSS or Lactated Ringer’s solution
➢ Corticosteroids that have antiemetic properties

NURSING MANAGEMENT (intestinal obstruction)

Assessment
a) Detailed assessment and physical examination
➢ location, duration, intensity, and frequency of abdominal pain and
presence of abdominal tenderness or rigidity is present.
b) Assess bowel function, including the passage of flatus.
c) Perform IAPP process of abdominal assessment

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d) Maintain strict intake and output record, including emesis and tube
drainage.
e) Note laboratory results
Nursing diagnoses
▪ Acute pain related to abdominal distention and increased peristalsis
▪ Deficient fluid volume related to a decrease in intestinal fluid
absorption, third space fluid shifts into the bowel lumen and
peritoneal cavity, NG suction, and vomiting
Planning
Goals:
▪ relief of the obstruction and return to normal bowel function
▪ minimal to no discomfort
▪ normal fluid and electrolyte and acid-base status.
Nursing implementation (see specific interventions for small and large
bowels obstruction)

b) COLORECTAL CA (discussed in Ca Nursing)

▪ Treatment of choice for colon and rectal cancer is surgery either
through key hole (laparoscopic) or open surgery
Colectomy
▪ Most common type of surgery for colon cancer which is done
depending on the what part of the colon to be removed
▪ The surgeon cuts the bowels on both sides and joins the ends of
the both bowels back together (anastomosis)
▪ Lymph nodes near the colon and a bit of normal bowel is also
removed
▪ Sometimes a colostomy is done where one end of the bowel is
brought through an opening on the abdomen and stitched onto the
skin

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c) OSTOMY SURGERY
Ostomy
▪ surgical procedure that allows intestinal contents to pass from the
bowel through an opening (stoma) in the skin on the abdomen.
▪ Ostomies are described according to location and type
Stoma
▪ created when normal elimination is not possible and the intestine is
brought through the abdominal wall and sutured to the skin
▪ The intestinal contents then empty through the hole on the surface of
the abdomen instead of through the anus.
▪ A collection bag is attached to the stoma
Ileostomy – involves the ileum
- Output is watery and usually drains continuously

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A. Site of stoma B. Normal color of stoma

Colostomy – involves the colon; can be sigmoid or transverse colostomy

depending on the site
- Output for sigmoid colostomy is similar to normal formed stool,
and patients can empty regularly

Ostomies may be:

a. Temporary
➢ Examples for a temporary ostomy - a draining fistula to prevent stool
from reaching the diseased area, trauma to the intestines (e.g.,
gunshot wounds, stabbing)

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b. Permanent
➢ Ex: Cancer of the rectum
Major types of ostomies
a) End Stoma.
➢ surgically constructed by dividing the bowel and bringing out the
proximal end as a single stoma. The distal portion of the GI tract is
surgically removed, or the distal segment is oversewn and left in the
abdominal cavity with its mesentery intact and an end colostomy or
ileostomy is constructed.
Hartmann’s pouch
▪ term used when the distal bowel is oversewn rather than removed
and there is possibility of the bowel to be re-anastomosed (connected)
and the stoma closed.
b) Loop Stoma
➢ This is constructed by bringing a loop of bowel to the abdominal
surface and then opening the anterior wall of the bowel to provide
fecal diversion.
➢ This results in one stoma with a proximal opening for feces and a
distal opening for mucus drainage (from the distal colon).
➢ An intact posterior wall separates the two openings. The loop of bowel
is frequently held in place with a plastic rod for 7 to 10 days after
surgery to prevent it from slipping back into the abdominal cavity
➢ A loop stoma is usually temporary
c) Double-Barreled Stoma
➢ When the bowel is divided, both the proximal and distal ends are
brought through the abdominal wall as two separate stomas
➢ The proximal one is the functioning stoma. The distal, nonfunctioning
stoma is referred to as the mucus fistula.
➢ This is usually temporary

NURSING MANAGEMENT for ostomy surgery

Management is geared towards:
1) emotional support due to a radical change in body image
2) patient and caregiver teaching on stoma care
PREOPERATIVE CARE
1) Provide patient psychological and emotional support in preparation for
the ostomy
2) Assist in the selection of a flat site on the abdomen that allows secure
attachment of the collection bag
3) Explain procedure to patient and family
4) Perform pre-op routine care.
POSTOPERATIVE CARE
1) Assess the stoma – stoma should be dark pink to red
- A dusky blue stoma is indicative of ischemia
- Brown-black is a sign of necrosis
- Assess and document stoma color every 4 hours and ensure that
there is no excessive bleeding.
- Advise patient that the stoma is mildly to moderately swollen the first
2 to 3 weeks after surgery

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2) Provide an appropriate pouching system to protect the skin and have a n
effective collection drainage
- a charcoal filter helps control odor
3) Assess skin for any irritation and excoriation
4) Provide continuous teaching on stoma care- refer to stoma nurse
5) Advise patient to have a well-balanced diet and adequate fluid intake.

d) DIVERTICULOSIS AND DIVERTICULITIS

Diverticula
▪ dilatations or outpouchings of the mucosal sac of the colon
Diverticulitis - is characterized by inflammation of the diverticula and
increased luminal pressures resulting in the erosion of the bowel wall, and
eventually perforation into the peritoneum
Diverticulosis – multiple non-inflamed diverticula
Diverticular disease can be asymptomatic, uncomplicated
diverticulosis to diverticulitis with complications such as perforation,
abscess, fistula, and bleeding.

(Image from Harvard Health -Harvard University)

Etiology and Pathophysiology
▪ Diverticula may occur anywhere in the GI tract but are most
commonly found in the left (descending, sigmoid) colon.
▪ The etiology of diverticulosis of the sigmoid colon is thought to be
associated with high luminal pressures from a deficiency in dietary
fiber intake.
▪ Uncommon in vegetarians as they consume more fiber in the diet
Clinical Manifestations and Complications (diverticular disease)
The majority of patients have no symptoms
▪ abdominal pain
▪ bloating
▪ flatulence
▪ changes in bowel habits
▪ bleeding diverticula in more serious situations
Complications
▪ Diverticulitis
- Symptoms include: acute pain in the left lower quadrant

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 (location of sigmoid colon), a palpable abdominal mass, and
systemic symptoms of infection (fever, increased C-reactive protein,
and leukocytosis with a shift to the left).
▪ Bleeding
▪ Peritonitis
Diagnostic Tests
a. sigmoidoscopy
b. colonoscopy.
c. Diagnosis of diverticulitis is based on the history and physical
examination
d. CT scan with oral contrast.

NURSING AND COLLABORATIVE MANAGEMENT

a. Encourage patient to take red meat, a high-fiber diet, mainly from
fruits and vegetables, and decreased fat intake
b. Advise weight loss if overweight
c. Increase physical activity
d. Advise patient to avoid factors that triggers the disease (straining at
stool, vomiting, bending, lifting, and wearing tight restrictive clothing)
that can increase intra-abdominal pressure
e. If hospitalized, the patient is kept on NPO status in an acute attack
and when it subsides, give oral fluids first and then semisolids
f. Provide bed rest until allowed
g. Administer IV fluids and antibiotics as prescribed
h. Observe for signs of abscess, bleeding, and peritonitis
i. monitor WBC count.
j. Provide perioperative care if for surgery – resection of the colon or a
temporary colostomy

Types of bowel surgeries

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e) POLYPS OF THE COLON AND RECTUM
Polyp
▪ A mass of tissue that protrudes into the lumen of the bowel and can
occur anywhere in the intestinal tract and rectum.
Classifications
a. neoplastic (i.e. adenomas and carcinomas) – common in men
b. non-neoplastic (i.e. mucosal and hyperplastic).
- Usually benign epithelial growths that are common in Western
countries They occur
Clinical manifestations
a. rectal bleeding – most common
b. Lower abdominal pain
c. weight loss may occur
d. symptoms of obstruction may be present in large polyps
Diagnostic tests
▪ Patient history
▪ digital rectal examination
▪ barium enema studies
▪ sigmoidoscopy or colonoscopy.
Surgical procedure:
▪ After a polyp is identified, it should be removed by colonoscopy with
the use of special equipment (i.e. hot biopsy forceps and snares)
▪ laparoscopy or colonoscopic excision with laparoscopic visualisation if
the polyp is not endoscopically resectable.
The major complications of perforation and bleeding may occur with
polypectomy (removal of polyps)

f) DISEASES OF THE ANORECTUM

Anorectal abscess
➢ Occurs due to an obstruction of an anal gland, resulting in retrograde
infection.

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 ➢ People with Crohn's disease or immunosuppressive conditions such
as AIDS are more at risk of these infections.
➢ These abscesses result in fistulas.
Characteristics:
▪ contains a quantity of foul-smelling pus and is painful.
▪ Presence of swelling, redness and tenderness for superficial abscess
▪ A deeper abscess may result in toxic symptoms, lower abdominal
pain and fever.
Treatment:
▪ Palliative therapy include sitz baths and analgesics
▪ Surgical treatment to incise and drain the abscess is the treatment of
choice.
Anal fistula
▪ a tiny, tubular, fibrous tract that extends into the anal canal from an
opening located beside the anus and are usually the result of an
infection

Treatment
▪ antibiotics or anti-inflammatory- type agents (e.g. azathioprine,
infliximab, cyclosporin)
▪ A fistulectomy (i.e. excision of the fistulous tract) is the surgical
procedure of choice.
Anal fissure
▪ It is a longitudinal tear or ulceration in the lining of the anal canal as
a result of trauma from passing a large, firm stool or from persistent
tightening of the anal canal because of stress and anxiety.
▪ Other factors include childbirth, trauma and overuse of laxatives.
▪ Can be healed conservatively with stool softeners, emollient
suppositories, sitz baths, increased water intake
▪ Procedure include anal dilatation under anesthetic or combining
suppository and anesthetic with corticosteroid
Characteristics:
▪ Extremely painful defecation, burning and bleeding measures
Hemorrhoids
➢ dilated portions of veins in the anal canal.
➢ Shearing of the mucosa during defecation results in the sliding of the
structures in the wall of the anal canal, including the hemorrhoidal
and vascular tissues.
➢ Pregnancy can cause hemorrhoids due to Increased pressure in
hemorrhoidal tissue
➢ They cause itching and pain and are the most common cause of bright
red bleeding during defecation
Classifications
a) Internal Hemorrhoids
▪ Those above the internal sphincter
▪ Not usually painful until they bleed or prolapse
b) External sphincter
▪ those appearing outside the external sphincter

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 ▪ they are characterized by severe pain from the inflammation and
oedema due to thrombosis that can lead to ischemia of the area and
eventual necrosis.
Management
▪ manage symptoms by avoiding excessive straining during defecation,
eat high- residue diet, increased fluid intake
▪ apply warm compresses, sitz baths, analgesic ointments and
suppositories, astringents (e.g. witch hazel) and bed rest to allow
engorgement to subside.
Non-surgical treatments
a. lnfrared photocoagulation
b. bipolar diathermy
c. laser therapy
d. Injecting sclerosing solutions for small, bleeding hemorrhoids.
e. rubber-band ligation procedure - hemorrhoid is visualized through the
anoscope and its proximal portion above the mucocutaneous lines is
suctioned into the band application. A small rubber band is then
slipped over the hemorrhoid. Tissue distal to the rubber band
becomes necrotic after several days and sloughs off.
It can be painful to others and complications that may arise are
secondary hemorrhage and perianal infection
f. Cryosurgical hemorrhoidectomy - involves freezing the hemorrhoid for
a sufficient time to cause necrosis
Not commonly used as discharge is very foul smelling and there is
prolonged wound healing
Hemorrhoidectomy
▪ A surgical excision of the hemorrhoid that involves removing all the
redundant tissue
Pilonidal sinus or cyst
▪ Occurs due to local trauma caused by the penetration of hairs into the
epithelium and subcutaneous tissue and are usually found in the
intergluteal cleft on the posterior surface of the lower sacrum
▪ Hair frequently is seen protruding from these openings, and this gives
the cyst its name, pilonidal (i.e. a nest of hair)
▪ Perspiration and friction easily irritate this area.
▪ Treatment with antibiotics or surgery is indicated (excision of pilonidal
sinus)

References:
Hammer, G., McPhee, S., (2014). Pathophysiology of Disease: An
Introduction to Clinical Medicine, 7th Edition, Mcgraw Hill
Harding M. et al. (2022). Lewis’s Medical-Surgical Nursing: Assessment and
Management of Clinical Problems, 12th Edition, Mosby & Elsevier
Inc., USA
Herdman, T. et al., (2021). NANDA International Nursing Daignoses,
Definitions and Classification 2021-2023, 12th Edition, Thieme
Publishing
Hinkle, J., et al (2022). Brunner & Suddarth’s Textbook of Medical-Surgical
Nursing, 15th Edition, Philadelphia, Wolters Kluwer Health

*For IFSU USE ONLY

 Prepared by: Marichu N. Guyguyon

*For IFSU USE ONLY