1

2 MAIN GROUPS:

- Alimentary canal/ GI tract

- Accessory digestive organs

ORGANS OF ALIMENTARY CANAL:

1. Mouth/oral cavity
o Lips/labia
o Hard palate
o Soft palate
o Uvula
o Vestibule
o Tongue
2

2. Pharynx
- Subdivided into:
o Oropharynx
o Laryngopharynx
o Nasopharynx

3. Esophagus / Gullet
- Runs from the pharynx through the diaphragm to the stomach
- About 25cm (10 inches) long
- Essentially a passageway that conducts food to the stomach

4. Stomach
- C-shaped on the left side of abdominal cavity, nearly hidden by the liver and
diaphragm
- Cardiac region - surrounds the cardioesophageal sphincter through which
food enters the stomach from the esophagus
- Fundus – expanded part of the stomach lateral to the cardiac region
- Body- midportion
- Pylorus-is the funnel-shaped and continuous with the small intestine
through the pyloric sphincter/valve

- When it is full, it can hold about 4 liters/1 gallon of food

- The mucosa of the stomach is a simple columnar epithelium that produces
large amounts of mucus. This otherwise smooth lining is dotted with
millions of deep gastric pits, which lead into gastric glands that secrete the
solution called GASTRIC JUICE
- Some stomach cells produce INTRINSIC FACTOR, a substance needed for the
absorption of Vit. B12 from the small intestine
- The CHIEF CELLS produce protein-digesting enzymes, mostly PEPSINOGENS
- PARIETAL CELLS produce corrosive HYDROCHLORIC ACID which makes the
stomach contents acidic and activates the enzymes
- MUCUS NECK CELLS produce a sticky alkaline mucus which clings to the
stomach mucosa and protects the stomach wall itself from being damaged
by the acid and digested by the enzymes
- Most digestive activity occurs in the pyloric region of the stomach
3

- After food has been processed in the stomach, it resembles heavy cream
and is called CHYME

5. Small intestine
- Body’s major digestive/absorptive organ
- Muscular tube extending from the pyloric sphincter to the ileocecal valve
- Ave.length of 2-4m (6-13ft)
- 3 subdivisions:
o Duodenum – 25 cm (10 inches) long
o Jejunum – 2.5m (8 ft) long
o Ileum – 3.6m (12 ft) long
- Pyloric sphincter controls food movement into the small intestines and
prevents the small intestine from being overwhelmed
- Local collections of lymphatic tissue called Peyer’s patches found in the
submucosa increase toward the end of the small intestine. This reflects that
fact that the remaining (undigested) food residue in the intestine contains
huge numbers of becteria, which much be prevented from entering the
bloodstream

6. Large intestines
- About 1.5m (5 ft) long
- Its major functions are to dry out the indigestible food residue by absorbing
water, and to eliminate these residues from the body as feces
- Subdivisions:
o Cecum
o Appendix
o Colon
o Rectum
o Anal canal
- Goblet cells in mucosa produce mucus, the mucus acts as a lubricant to
ease the passage of feces to the end of digestive tract

ACCESSORY DIGESTIVE ORGANS:

1. Salivary glands
4

- Parotid glands lie anterior to the ears

- Submandibular and sublingual glands empty their secretions into the floor
of the mouth
- Saliva – a mixture of mucus and serous fluids
o Mucus moistens and helps to bind food together into a mass called
BOLUS
o The clear serous portion contain an enzyme, salivary amylase which
begins the process of starch digestion in the mouth
o Saliva also contain substances such as lysozyme and antibodies IgA
that inhibit becteria therefore it has a protective function
o Saliva dissolves food chemicals so they can be tasted

2. Teeth
- In the process, the teeth tear and grind the food, breaking it down into
smaller fragments
- The first set is the deciduous/milk teeth; a baby has a full set by the age 2
years (20 teeth)
- The second set of teeth, the deeper permanent teeth develop between the
ages of 6 and 12 years
- The 3rd molars also called wisdom teeth emerge later, between ages 17 and
25 (32)
- The chisel-shaped incisors are adapted for cutting
- The fang-like canines (eyeteeth) are for tearing or piercing
- Premolars and molars are best suited for grinding

3. Pancreas
- Soft, pink, triangular gland that extends across the abdomen from the
spleen to the duodenum
- The pancreatic enzymes are secreted into the duodenum in an alkaline
fluid, which neutralized the acidic chyme coming in from the stomach
- Also has an endocrine function, it produces the hormones insulin and
glucagon

4. Liver and gallbladder

5

LIVER
- The largest gland in the body; weighing 1200-1600g
- Liver overlies and almost completely covers the stomach; located in the
right upper abdominal quadrant, under the diaphragm
- Divide into 4 lobes: left, right, caudate, and quadrate; the lobes are further
subdivided into smaller units known as lobules
- The cell type of liver are hepatocytes (liver cells) and Kupffer cells
(phagocytic cells that engulf bacteria)

- Its digestive function is to produce bile

o Bile is continuously formed by hepatocytes (about 1L/day). It is
yellow-green, watery solution comprises water, electrolytes, lecithin,
fatty acids, cholesterol, bilirubin, and bile salts, bile pigments
o Bilirubin is pigment derived from the breakdown of hemoglobin.
Hepatocytes remove bilirubin from the blood and conjugate it with
glucoronic acid, which results in conjugated bilirubin being secreted
into bile
o Bile salts, which are synthesized by hepatocytes from cholesterol, are
required for emulsification of fats in the intestines. Bile salts are then
reabsorbed in the distal ileum and returned to the liver through the
portal vein to be used again
o Bile leaves the liver through the common hepatic duct and enters the
duodenum through the bile duct
- Blood supply to the liver is from the portal vein (75%), which drains the GI
tract and from the hepatic artery (25%)

- Only the bile salts and phospholipids aid in the digestive process
- Bile salts emulsify fats by physically breaking large fat globules into smaller
ones

GALLBLADDER – sac, stores bile

o When fatty food enters the duodenum, a hormonal stimulus prompts
the gallbladder to contract and spurt out stored bile
6

FUNCTIONS OF THE DIGESTIVE SYSTEM:

6 PROCESSES:

1. Ingestion
- Active, voluntary process called ingestion

2. Propulsion
- Peristalsis – involuntary and involves alternating waves of contraction and
relaxation of the muscles in the organ wall. The net effect is to squeeze the
food along the tract
- Segmentation- only moves the food back and forth across the internal wall,
serving to mix it with the digestive juices

3. Food breakdown: mechanical digestion

- Sequence of steps in which large food molecules are broken down to their
building blocks by enzymes
- The building blocks/units of carbohydrates are monosaccharides or simple
sugars
- Protein are digested to their building blocks, which are amino acids
- When lipid are digested, they yield 2 different types of building blocks –
fatty acids and alcohol called glycerol

4. Absorption
- Transport of digested end products from the lumen of the GI tract to the
blood or lymph
- The small intestine is the major absorptive site

5. Defecation
- Elimination of indigestible substances from the body via the anus in the
form of feces

Digestive activity is mostly controlled by reflexes via the parasympathetic

division of the autonomic nervous system
The sensors (mechanoreceptors, chemoreceptors) involved are located in the
walls of alimentary canal organs and respond to a number of stimuli, the most
important being:
7

- Stretch by food in its lumen

- pH of the contents
- presence of certain breakdown product of digestion

ACTIVITIES OCCURRING IN THE MOUTH, PHARYNX, AND ESOPHAGUS

- Food ingestion and breakdown
o 1st, food is physically broken down into smaller particles by chewing.
Then, as the food is mixed with saliva, salivary amylase begins the
chemical digestion of starch, breaking it down into maltose
- Food propulsion –swallowing and peristalsis
o Deglutition/swallowing is a process that involves the coordinated
activity of tongue, soft palate, pharynx and esophagus

2 MAJOR PHASES:
1. Voluntary buccal phase
o Occurs in the mouth, food is chewed and mixed-well with saliva
2. Involuntary pharyngeal-esopharyngeal phase
o Transports food through the pharynx and esophagus
o Parasympathetic (primarily the vagus nerve) controls this phase

- Once food reaches the end of the esophagus, it presses against the
cardioesophageal sphincter, causing it to open, and the food enters the
stomach

ACTIVITIES OF THE STOMACH

- Food breakdown
o The sight, smell, and taste of food stimulate parasympathetic nervous
system reflexes, which increase the secretion of gastric juice by the
stomach glands
o The presence of food and a falling pH in the stomach stimulate the
stomach cells to release the hormone gastrin
o Gastrin prods the stomach glands to produce more of the protein-
digesting enzymes (pepsinogens), mucus, and hydrochloric acid
o 2-3 liters of gastric juice are produced
8

o Hydrochloric acid makes the stomach contents very acid, however, as

long as enough mucus is made, the stomach is safe and will remain
unharmed
o The extremely acid environment that hydrochloric acid provides is
necessary, because it activates pepsinogen to pepsin, the active
protein-digesting enzyme
o Rennin-2nd protein-digesting enzyme produced by the stomach, works
primarily on milk protein and converts it to a substance that looks like
sour milk

- Food propulsion
o The pylorus of the stomach, which holds about 30ml of chyme, acts
like a meter that allows only liquids and very small particles to pass
through the pyloric sphincter
o Because the pyloric sphincter barely opens, each contraction of the
stomach spits or squirts 3ml or less of chyme into the small intestine
o Generally, it takes about 4hours for the stomach to empty completely
after eating a well-balanced meal, and 6 hours or more if the meal
has a high fat content

ACTIVITIES OF THE SMALL INTESTINE

- Food breakdown and absorption
o The process of chemical digestion is accelerated as the food now
takes a wild 3-6 hour journey through the looping coils and twists of
the small intestine
o The microvilli of small intestine bear few important enzymes. The
brush border enzymes that break down double sugars into simple
sugars and complete protein digestion

o Pancreatic juice contains enzymes that

 Along with brush border, complete the digestion of starch
(pancreatic amylase)
 Carry out about half of protein digestion (via the action of
trypsin, chymotrypsin, carboxypeptidase)
 Are totally responsible for fat digestion since the pancreas is
the only source of lipases
 Digest nucleic acids (nucleases)
9

o Pancreatic juice contains a rich supply of bicarbonate, which makes it

very basic (pH 8). When pancreatic juice reaches the small intestine,
it neutralizes the acid chyme from the stomach and provides the
proper environment for activation and activity of intestinal and
pancreatic digestive enzymes

o 2 hormones – influence the release of pancreatic juice and bile

 Secretin –causes the liver to increase its output of bile
 Cholecystokinin (CCK) – causes the gallbladder to contract and
release stored bile into the bile duct so that bile and pancreatic
juice enter the small intestine

o BILE – is not an enzyme, instead, it acts like a detergent to emulsify or

mechanically breakdown large fat globules into thousands of tiny
ones, providing a much greater surface area for the pancreatic lipases
to work on
 Bile is also necessary for absorption of fats and fat soluble
vitamins from the intestinal tract

o Most substances are absorbed through the intestinal cell plasma

membrane by the process of active transport

- Food propulsion
o Peristalsis

ACTIVITIES OF THE LARGE INTESTINE

- Food breakdown and absorption
o The residue still has 12-24h more to spend in the colon
o The resident bacteria that live within its lumen metabolize some of
the remaining nutrients, releasing gases (methane and hydrogen
sulfide) that contribute to the odor of feces
o About 500ml of gas (flatus) is produced each day, much more when
certain carbohydrate-rich foods are eaten
o Bacteria residing in the large intestine also make some vitamins (Vit
K, and B vitamin)
10

o Absorption is limited to the absorption of these vitamins, some ions,

and most of the remaining water
o Feces-more or less solid product delivered to the rectum, contain
undigested food residues, mucus, millions of bacteria, and just
enough water to allow their smooth passage

- Propulsion of residue and defecation

o Peristalsis and mass movements are 2 major types of propulsive
movements in the large intestine
o Mass movements – are slow, long-moving but powerful contractile
waves that move over large areas of the colon 3-4× a day and force
the contents toward the rectum. Typically, they occur during or just
after eating, when food begins to fill the stomach and small intestine
o Bulk/fiber in the diet increases the strength of colon contractions and
softens the stool, allowing the colon to act as a well-oiled machine
o The rectum is generally empty, but when feces are forced into it by
mass movements and its walls are stretched, the defecation reflex is
initiated
o Defecation reflex is a spinal (sacral region) reflex that causes the walls
of the sigmoid colon and the rectum to contract and the anal
sphincter to relax

METABOLISM
- a broad term referring to all chemical reactions that are necessary to
maintain life
- CATABOLISM – involves the breakdown of complex structures into simpler
forms, example, the breakdown of carbohydrates to produce ATP
- ANABOLISM – simpler molecules combine to build more complex
structures, example, amino acids bond to form proteins

- CARBOHYDRATE METABOLISM
o The cells of the body use of carbohydrates as their preferred fuel to
produce cellular energy (ATP)
o Glucose/blood sugar is the major breakdown product of carbohydrate
digestion
11

o Glucose is also the major fuel used for making ATP in most body cells
o Because glucose is the major fuel for making ATP, homeostasis of
blood glucose levels is critically important
o Pyruvic acid – product of carbohydrate

- FAT METABOLISM
o For fat products to be used for ATP synthesis, they must first be
broken down to acetic acid; within the mitochondria, the acetic acid
is oxidized and carbon dioxide, water and ATP are formed
o When there is not enough glucose to fuel the needs of the cells for
energy, larger amounts of fats are used to produce ATP. Under such
conditions, fat oxidation is fast but incomplete, and some of the
intermediate products such as acetoacetic acid and acetone begin to
accumulate in the blood. These cause the blood to become acidic and
the breath takes on a fruity odor as acetone diffuses from the lungs
o Ketosis is a common consequence of “no-carbohydrate” diets,
uncontrolled DM, and starvation in which the body is forced to rely
almost totally on fats to fuel its energy needs

- PROTEIN METABOLISM
o Ingested proteins are broken down to amino acids
o Cells cannot build their protein unless all the needed amino acids,
which number around 20 are present. Since 8 of these amino acids
cannot be made by the cells, they are available to the cells only
through the diet. Such amino acids are called essential amino acids
o Amino acids are used to make ATP only when proteins are
overabundant and or when carbohydrates and fats are not available
o When it is necessary to oxidize amino acids for energy, their amine
groups are removed as ammonia. The ammonia that is released is
toxic to body cells, especially nerve cells. The liver comes to the
rescue by combining the ammonia with carbon dioxide to form urea
which is then flushed from the body in urine

CENTRAL ROLE OF THE LIVER IN METABOLISM:

- Manufacture of bile
12

- The liver’s phagocytic cells remove and destroy bacteria that have managed
to get through the walls of the digestive tract and into the blood

- GLUCOSE METABOLISM:
o After a meal, glucose is taken up from the portal venous blood by the
liver and converted into glycogen, which is stored in the hepatocytes
o Glycogen is converted back to glucose and released as needed into
the bloodstream to maintain normal levels of blood glucose
o Additional glucose can be synthesized by the liver through a process
called gluconeogenesis. For this process, the liver uses amino acids
from protein breakdown or lactate produced by exercising muscles
 General metabolic functions:
 Glycogenesis – glycogen formation
 Glycogenolysis – glycogen splitting
 Glyconeogenesis – formation of new sugar from non-
carbohydrate substances such as fats and proteins

- AMMONIA CONVERSION:
o Use of amino acids from protein for gluconeogenesis results in the
formation of ammonia as a byproduct. The liver converts this
metabolically generated ammonia into urea
o Ammonia produced by bacteria in the intestine is also removed from
portal blood for urea synthesis. In this way, the liver converts
ammonia, a potential toxin, into urea, a compound that can be
excreted in the urine

- FAT METABOLISM
o Fatty acids can be broken down for the production of ketone bodies
(acetoacetic acid, beta-hydroxybutyric acid, and acetone)
o Ketone bodies are small compounds that can enter the bloodstream
and provide a source of energy for muscles and other tissues.
Breakdown of fatty acids into ketone bodies occurs primarily when
the availability of glucose for metabolism is limited as during
starvation or in uncontrolled diabetes
13

o Fatty acids and their metabolic products are also used for the
synthesis of cholesterol, lecithin, lipoproteins, and other complex
lipids
o Under some conditions, lipids accumulate in the hepatocytes,
resulting in the abnormal condition called fatty liver

- VITAMIN AND IRON STORAGE

o Vitamins A, B and D and several of the B-complex vitamins are stored
in large amounts in the liver
o Iron and copper are also stored in the liver
o Because the liver is rich in these substances, liver extracts have been
used for therapy for a wide range of nutritional disorders

- DRUG METABOLISM
o One of the important pathways for meds metabolism involves
conjugation (binding) of the meds with a variety of compounds, such
as glucuronic/acetic acid, to form more soluble substances
o The conjugated products may be excreted in the feces/urine, similar
to bilirubin excretion

- CHOLESTEROL METABOLISM AND TRANSPORT

o Cholesterol is the structural basis of steroid hormones and vitamin D
and is a major building block of plasma membrane
o 15% of blood cholesterol comes from the diet, the other 85% is made
by the liver
o Cholesterol is lost from the body when it is broken down and
secreted in bile salts, which eventually leave the body in feces
o Since fatty acids, fats and cholesterol are insoluble in water, they
cannot circulate freely in the bloodstream. Instead they are
transported bound to a small-lipid-protein complexes called
lipoproteins
o LDLs transport cholesterol and other lipids to body cells. If large
amount of LDLs are circulating, the chance that fatty substances will
be deposited on the arterial walls, initiating atherosclerosis
 LDL’s tagged as “bad lipoproteins”
14

 The lipoproteins that transport cholesterol from the tissue cells

(or arteries) to the liver for disposal in bile are HDL
 HDLs are considered “good” because the cholesterol is
destined to be broken down and eliminated from the body

METABOLIC RATE AND BODY HEAT PRODUCTION

- The energy value of foods is measured in a unit called kilocalorie (kcal)
- In general, carbohydrates and proteins each yield 4kcal/gram and fats yield
9 kcal/gram when they are broken down for energy production

- (BMR) BASAL METABOLIC RATE

o Is the amount of heat produced by the body per unit of time when it
is under basal conditions - that is, at rest
o It reflects the energy supply a person’s body needs just to perform
essential life activities such a breathing, maintaining the heartbeat,
and kidney function

- (TMR) TOTAL METABOLIC RATE

o Total amount of kilocalories the body must consume to fuel all
ongoing activities. Muscular work is the major body activity that
increases TMR

- BODY TEMPERATURE REGULATION

o Foods are burned to produce ATP
o Most of the energy released as foods are oxidized escapes as heat
o The heat released warms the tissues and the blood which circulates
to all body tissues, keeping them at homeostatic temperature which
allows metabolism to occur frequently
o Heat-promoting mechanisms
 Vasoconstriction
 Shivering
o Heat-loss mechanisms
 Radiation
 Evaporation
15

PHYSICAL EXAMINATION OF DIGESTIVE SYSTEM:

1. Anthropometric measures
- Provide an assessment of body mass or body compartments
- Height, weight, frame size, body mass index, mid-arm muscle
circumference, and waist-to-hip proportions

A. Height and weight:

o Use a telescoping ruler and balance scale to measure height and
weight. If patient cannot bear weight, use a calibrated swing/
wheelchair scale
o Describe clothing and other accessories (light clothing, shoes with or
without heels, orthopedic casts, braces) worn by the patient
o If the patient cannot stand, use an arm span measurement to
approximate height. To do so, extend the patient’s arms laterally and
measure from the tip of the middle finger on one hand to the tip of
the middle finger on the other hand
o Compare the patient’s current weight to her reported usual weight,
unintentional weight changes of less than 90% or more than 100% of
the patient’s usual weight are considered significant
o To calculate the difference as a percentage of usual weight, divide the
patient’s current weight by the usual weight and multiply by 100

%usual weight=current weight/usual weight × 100

B. Ideal body weight and frame size

o Calculate body frame size by measuring the patient’s wrist
circumference and dividing it into the height
o Traditional method is to use a formula based on height, weight, and
body frame size

C. Body mass index (BMI)

o To calculate BMI, divide the patient’s weight in Kg by the height in
meters squared

D. Circumferential measurement
o Assess muscle mass and body fat proportions and distribution
16

2. Mouth
- Assessment of oral cavity includes inspection and palpation
- Good illumination is essential
- Penlight and tongue blade may also be used

A. Inspection
o Begin assessment of the patient’s mouth by inspecting the lips for
symmetry
o Put on clean gloves and ask patient to remove any dentures
o Note symmetry of facial movements
o Ask patient to open mouth wide and inspect structures inside
o Inspect tongue for symmetry, color and moisture; then ask patient to
stick out his tongue, move it from side to side, upward, downward

B. Palpation
o Palpate the lips, gingivae, and buccal mucosa
o Check for loose teeth, masses, swellings, or areas of tenderness
o If you find lesions, note the location size, color, consistency, and
presence or absence of tenderness
o Gently grasp the tongue with cotton gauze and extend and lift while
inspecting and palpating the underside of the tongue and floor of the
mouth
o Many precancerous oral lesions are pain-free and asymptomatic
o Release the tongue and depress it with a tongue blade; ask the
patient to say “ahhh”. Note symmetry and movement of the uvula
and soft palate
o Give patient a sip of water and observe for symptoms of difficulty in
swallowing/dysphagia

3. Abdomen
- ask the patient to void before the exam, because a full bladder can interfere
with abdominal assessment
- place patient in a supine position with arms at sides
- place small pillow under the patient’s knees to relax abdominal muscles
17

A. Inspection
o Stand at the patient’s right side and begin inspecting the abdomen by
noting condition of skin and abdominal contour
o Skin should be smooth and intact, with varying amounts of hair
o The contour should be flat, concave, or rounded, depending on the
client’s body type
o Inspect abdomen for rashes, discoloration, scars, petechiae, striae,
and dilated veins
o Scars on the abdomen should correlate with the patient’s history of
past surgical procedures and striae should correlate with reported
changes in weight
o Umbilicus should be concave, located at midline, and the same color
as the abdominal skin, with no evidence of drainage
o Next, sit at eye level to the client’s abdomen and observe for
peristaltic movements or abdominal pulsation. Normally, peristaltic
movements are not visible but may be observed in a very thin patient

B. Auscultation
o Using the diaphragm of the stethoscope, press lightly, beginning in
the right lower quadrant at the area of the ileocecal valve
o Continue in a clockwise fashion
o As air and fluid move through the GI tract, soft clicks and gurgles can
be heard every 5 to 15 seconds
o Normal bowel sounds can occur irregularly at a rate of 5-35/min
o Loud, high pitched bowel sounds (borborygmi) represent
hyperactivity of the GI tract; borborygmi may be present in patients
who are hungry/ who have gastroenteritis/ they may be present in
early intestinal obstruction
o To determine the absence of bowel sounds, listen for a total of 5 min
or at least 1 min per quadrant
o The terms NORMAL (sounds heard about every 5-20 seconds),
HYPOACTIVE ( 1 or 2 sounds in 2 minutes), HYPERACTIVE ( 5 to 6
sounds heard in less than 30 seconds), or absent (no sounds in 3-5
minutes)

C. Percussion
18

o Determine the size and location of abdominal organs and to detect

fluid, air or masses
o Normally, percussion sounds over the abdomen are high-pitched,
loud or “musical” (tympanic) over gas and dull (thud-like) over fluid
or solid changes

D. Palpation
o Start with light palpation, depressing the abdomen 1-2cm (.5-.75 inch
lightly; 1 or 1.5 – 2 inches deeply)
o Light palpation is for identifying areas of tenderness or swelling
o Deep palpation to identify masses in 4 quadrants to elicit rebound
tenderness, the nurse exerts pressure over the area and then
releases it quickly, it is important to note any pain experienced on
withdrawal of the pressure

- The final part of the examination is inspection of the anal and perianal area
- A digital rectal examination can be performed to note any areas of
tenderness of mass

DIAGNOSTIC TESTS:

1. BLOOD TESTS – are ordered initially

o CBC
o CEA – carcinoembryonic antigen
o Liver function tests
o Serum cholesterol
o Triglycerides

2. STOOL TESTS
o Inspecting the specimen for consistency and color and testing for
occult blood (hematest)

3. BREATH TESTS
o Hydrogen breath test evaluate carbohydrate absorption; also used to
aid in the diagnosis of bacterial overgrowth in the intestine and short
bowel syndrome
19

o Urea breath test- detect in the absence of H. Pylori

4. ABDOMINAL ULTRASONOGRAPHY
o Generally used to indicate the size and configuration of abdominal
structures
o Useful in detection of cholelithiasis, cholecystitis, and appendicitis
o Patient fast for 8-12hours before the test to decrease the amount of
gas in the bowel; patient should eat a fat-free meal the evening
before the test

5. DNA TESTING
o Prevent / minimize disease by intervening before its onset, and to
improve therapy
o Persons at risk for colon cancer often are targeted for DNA testing

6. IMAGING STUDIES
A. UPPER GASTROINTESTINAL TRACT STUDY / BARIUM SWALLOW
- Radiopaque liquid (barium sulfate) which is tasteless, odorless, non-
granular and completely insoluble (non-absorbable) powder in the form of
thick/thin aqueous suspension for the purpose of studying the upper GI
tract
- Detect anatomic / functional derangement of upper GI or sphincters
- Multiple x-ray films are obtained during the procedure

- Nursing management:
o Low residue for several days before the test
o Nothing by mouth after midnight before the test
o Laxative to clean out intestinal tract
o Discourage patient from smoking in the morning before the exam
because smoking stimulate gastric motility
o Withhold all medications

B. LOWER GASTROINTESTINAL TRACT STUDY / BARIUM ENEMA

- Barium is instilled rectally
20

- Detect the presence of polyps, tumors and other lesions of the large
intestine and to demonstrate any abnormal anatomy / malfunction of the
bowel
- The patient may feel some cramping / discomfort with this process
- Nursing management:
o Laxative
o Low-residue diet 1-2 days before the test

C. COMPUTED TOMOGRAPHY
- Detecting and localizing many inflammatory conditions of the colon such as
appendicitis, diverticulitis, regional enteritis, and ulcerative colitis
- Diseases of the liver, spleen, kidney, pancreas and pelvic organs

- Nursing management:
o Patient should not eat/drink for 6-8 hours before the test
o If barium studies are performed, it is important to schedule them
after CT scanning, so as not to interfere with imaging

D. MRI
- Supplement ultrasound and CT scanning
- Useful in evaluating abdominal soft tissues as well as blood vessels,
abscesses, fistulas, neoplasms and other sources of bleeding
- Contraindicated for patients with permanent pacemakers, artificial heart
valves and defribrillators, implanted insulin pumps, implanted
transcutaneous electrical nerve stimulation (TENS) because the magnetic
field could cause malfunction
- MRI is also contraindicated for patients with internal metal devices or
intraocular metallic fragments

- Nursing management:
o Patient should not eat or drink for 6-8 hours before the test
o Remove all jewelry and other metals
o Entire procedure takes 30-90minutes
21

o Warn patient that the close-fitting scanners may induce feeling of

claustrophobia and that the machine will make a knocking sound
during the procedure

E. SCINTIGRAPHY
- Extraction of blood and mixed with iodine
- Reveal displaced anatomic structures, changes in organ size and presence of
neoplasms / other focal lesions such as cysts / abscesses
- Abnormal concentrations of blood cells are then detected at 24-48H
intervals

F. GASTROINTESTINAL MOTILITY STUDIES

- Assess gastric emptying and colonic transit time
- Helpful for evaluating any functional cause of gastric emptying
- Patient is given a capsule containing 20 radionuclide markers and
instructions to follow a regular diet and normal daily activities
- Abdominal x-rays are taken every 24H until all markers are passed
- This process usually takes 4-5 days but in the presence of severe
constipation may take as long as 10 days

7. ENDOSCOPIC PROCEDURES

A. UPPER GASTROINTESTINAL FIBROSCOPY /

ESOPHAGOGASTRODUODENOSCOPY (EGD)
- Direct visualization of the esophageal, gastric, and duodenal mucosa
through a lighted endoscope (gastroscope)
- Patient may experience nausea, gagging or choking
- Use of topical anesthetics and moderate separation makes it important to
monitor and maintain oral airway during and after the procedure
- Finger / ear oximeter to monitor oxygen saturation
- Mouthguard to keep from biting the scope

- Nursing management:
o Check consent
o NPO for 6-12H before the exam
22

o Spray/gargle with a local anesthetic and administer midazolam IV

(provides moderate sedation and relieves anxiety)
o Atropine to reduce secretions
o Glucagon, if needed and prescribed, to relax smooth muscle
o Position patient on left side to facilitate saliva drainage and provide
easy access for the endoscope
o After the procedure, nurse instructs the patient not to eat or drink
until the gag reflex returns (in1-2hrs) to prevent aspiration of
food/fluids
o Sim’s position until patient is awake and then place the patient in
semi-fowlers until ready for discharge
o Assess signs of perforation: pain, bleeding, unusual difficulty
swallowing and elevated temperature
o Nurse monitors the pulse and blood pressure for changes that can
occur with sedation
o After the patient’s gag reflex has returned, offer lozenges, saline
gargle, and oral analgesics to relieve minor throat discomfort
o Bed rest until fully alert
o Instruct patient not to drive for 10-12H if sedation is used

B. ANOSCOPY, PROCTOSCOPY, AND SIGMOIDOSCOPY

- Directly viewing the lower portion of the colon to evaluate rectal bleeding,
acute / chronic diarrhea, change in bowel patterns and to observe for
ulceration, fissures, abscesses, tumors, polyps, and other pathologic process
- Anoscope is a rigid scope for examining the anus and lower rectum
- Proctoscopes and sigmoidoscopes are rigid scopes used to inspect the
rectum and sigmoid colon
- For rigid scope procedures, the patient assumes the knee-chest position
- During the exam, it is important to keep the patient informed about the
progress of the examination and to explain that the pressure exerted by the
instrument will create the urge to have a bowel movement
- For flexible scope procedures, the patient assumes a comfortable position
on the left side with the right leg bent and placed anteriorly
- Biopsies and polypectomies can be performed during this procedure

- Nursing management:
23

o Warm tap water / fleet enema until returns are clear

o Dietary restrictions usually are not necessary
o Sedation usually not required
o Monitor vital signs, skin color and temperature, pain tolerance, and
vagal response
o Monitor patient for rectal bleeding and signs of intestinal perforation
(fever, rectal drainage, abdominal distention and pain)
o Patient can resume regular activities and dietary practices after the
test

C. FIBEROPTIC COLONOSCOPY
- Direct visual inspection of the colon to the cecum
- Frequently used for cancer screening and for surveillance in patients with
previous colon cancer or polyps
- Tissue biopsies can be obtained and polyps can be removed and evaluated
- Also evaluate patients with diarrhea of unknown cause, occult bleeding or
anemia
- Colonoscopy is performed while the patient is lying on the left side with the
legs drawn up toward the chest
- Takes about 1h
- Nursing management:
o Enemas for optimal visualization
o Limit intake of liquids for 24-72h before the exam
o Informed consent before the test
o NPO after midnight before the test

D. SMALL-BOWEL ENDOSCOPY
- Allow direct inspection of the wall of the small intestine

E. ENDOSCOPY THROUGH OSTOMY

- Visualizing a segment of the small/large intestine
- Indicated to evaluate an anastomosis, to screen for recurrent disease, or to
visualize and treat bleeding in a segment of the bowel
24

F. MANOMETRY AND ELECTROPHYSIOLOGIC STUDIES

- ESOPHAGEAL MANOMETRY
o Is used to detect motility disorders of the esophagus and lower
esophageal sphincter
o Measures changes in intraluminal pressures and coordination of
muscle activity in the GI tract
- GASTRODUODENAL, SMALL-INTESTINE, AND COLONIC MANOMETRY
o Are used to evaluate delayed gastric emptying and gastric and
intestinal motility disorders
- ANORECTAL MANOMETRY
o Measures the resting tone of internal anal sphincter and
contractibility of the external anal sphincter
- RECTAL SENSORY FUNCTION TEST
o Is used to evaluate rectal sensory function and neuropathy
- ELECTROGASTROGRAPHY
o Assess gastric motility disturbances, electrodes are placed over the
abdomen, and gastric electrical activity is recorded for up to 24h
o Useful in detecting motor / nerve dysfunction in the stomach

G. DEFECOGRAPHY
- Measures anorectal function
- Very thick barium paste is instilled into the rectum, and then fluoroscopy is
performed to assess the function of the rectum and anal sphincter while
the patient attempts to expel the barium
- Requires no preparation

H. LAPAROSCOPY (PERITONEOSCOPY)
- Performed through a small incision in the abdominal wall; allow direct
visualization of organs and structures within the abdomen

8. GASTRIC ANALYSIS
- Measure secretions of HCl and pepsin in the stomach
- Gastric analysis consist of :
o Basal cell secretion
o Gastric acid stimulation test
25

ASSESSMENT OF THE LIVER:

1. Health history
- Cardinal signs and symptoms indicating altered hepatic, biliary, and
pancreatic function include:
o Jaundice
o Changes in urine and stool color
o Vague to severe abdominal pain especially after eating high fatty
foods
o Abdominal tenderness and distention
- Explore patient’s health history for risk factors:
o Alcohol consumption
o Diet high in fat
o Infectious agents
o Malnutrition

2. Physical examination
- Inspection
o Inspect abdomen for contour, pigmentation, and color, scars and
striae
o Assess for any visible masses, peristalsis and pulsations
- Palpation
o Palpate the liver to assess for consistency and firmness, pain, shape
and nodules
o Lightly palpate all 4 quadrants for masses, pain, and any
abnormalities and then follow with deep palpation
- Percussion
o Percuss all 4 quadrants in a systematic manner
o Assess liver size by percussing the upper and lower liver borders
o Record the level at which the lower border descends below the right
costal margin
- Auscultation
o Auscultate bowel sounds in all 4 quadrants
o Auscultate for any abnormal bruits
26

LABORATORY AND DIAGNOSTIC STUDIES:

1. LIVER FUNCTION TESTS – identify the degree of liver failure and include:
o Alkaline phosphate level
 A sensitive measure of biliary tract obstruction

o Serum glutamic-pyruvic transaminase (SGPT) which is now more

commonly known as alanine aminotransferase (ALT)
 Increase primarily in liver disorders, and may be used to
monitor the course of hepatitis/cirrhosis/the effects of
treatment that may be toxic to the liver

o Serum glutamic-oxaloacetic transaminase (SGOT) which is now

known as aspartate amino-transferase (AST)
 AST is present in tissues that have high metabolic activity; thus,
the level may be increased if there is damage to or death of
tissues of organs such as the heart, liver, skeletal muscle, and
kidneys. Levels of AST may be increased in cirrhosis, hepatitis
and liver cancer

o Lactate dehydrogenase (LDH), gamma glutamyl transferase (GGT)/G-

glutamyl transpeptidase (GGTP)
 Elevated in alcohol abuse
 Marker for biliary cholestasis

o Serum proteins
 Proteins are manufactured by the liver. Their levels may be
affected in a variety of liver impairments
 Albumin
 Cirrhosis
 Chronic hepatitis
 Edema, ascites
 Globulin
 Cirrhosis
 Liver disease
 Chronic obstructive jaundice
 Viral hepatitis
27

o Direct and indirect bilirubin

 Measure the ability of the liver to conjugate and excrete
bilirubin
 Associated with jaundice clinically

o Serum ammonia
 Ammonia rises in liver failure

o Clotting factors
 Prothrombin time may be prolonged in liver disease. It will not
return to normal with vitamin K in severe liver cell damage

o Serum lipids
 Cholesterol levels are elevated in biliary obstruction and
decreased in parenchymal liver disease

o Liver biopsy
 Sampling of liver tissue by needle aspiration for histologic
analysis, can establish a diagnosis of specific liver disease

o CT scan
 Can detect neoplasms, cysts, abscesses, and hematomas

o Angiography
 Visualize hepatic circulation/masses

o Splenoportography
 Determine adequacy of portal blood flow

o Liver scan
 Demonstrate liver size and shape

DISORDERS OF THE MOUTH

1. STOMATITIS
28

- Inflammation of the oral cavity

CAUSES:
- May be of infectious origin or a manifestation of a systemic condition
- May be caused by mechanical trauma such as injury or chemical trauma
Jagged teeth, cheek-biting, and mouth breathing also may result in
mechanical trauma
- Foods and drinks and sensitivity to mouthwashes or toothpaste may
produce chemical trauma
- Inflammatory sloughing of tissue allows organisms to multiply; thus
stomatitis may lead to infection by viruses, bacteria, yeasts, or fungus

CLASSIFICATION:

- PRIMARY
o Aphthous stomatitis
o Herpes simples type 1
o Vincent’s angina
- SECONDARY
o Results when a client’s lowered resistance allows an opportunistic
infection to develop
o Can be caused by a local / systemic disorder
o Allergies
o Bone marrow disorders
o Nutritional disorders
o Immunodeficiency disorders
o Chemotherapy, radiation therapy, or immunosuppressive therapy

A. APHTHOUS STOMATITIS
29

-
- Commonly known as canker sores
- Recurrent, small, and ulcerated
- Develop in soft tissues of the mouth, lips, tongue, and insides of the cheeks
- May be related to emotional stress, trauma, vitamin deficiencies, and viral
infections
- Prevention is almost impossible because the exact cause is unknown
- Lesions are not infectious but are simply inflammatory
- Heal within 1-3 weeks without treatment
- Assessment reveals a well-circumscribed erythematous macule that
undergoes necrosis, creating a well-defined pseudomembranous ulcer with
an erythematous border

- MANAGEMENT:
o Topical application of amelxanox (aphthasol)
o Topical / systemic steroids shorten healing time
o Teach clients prone to allergic reactions to avoid tomatoes, chocolate,
eggs, shellfish, milk products, nuts, and citrus fruits
30

B. HERPEX SIMPLEX STOMATITIS

- A form of inflammation and ulceration caused by the herpes simples virus
(HSV)

- Primary HS, when the client is first infected with the HSV, lesions appear in
the oral cavity
- Vesicles appear throughout the oral cavity, rupture to form ulcerated areas
that resemble canker sores and heal within several weeks
- Client’s tongue has a characteristic heavy white coating
- Client may have manifestations of generalized infection

- Secondary herpes – recurrent infection that appears dormant after the

primary herpes infection
- Secondary herpes takes the form of herpes labialis (fever blister, cold sore)
- Any infection, especially upper respiratory infection, fever, stress, or even
sunlight, can reactivate the virus
- Assessment reveals clear, vesicular lesions, most often appearing at the
mucocutaneous junction of the lips and face
- Lesions are contagious, last about 1 week, and heal without scarring
31

- Later in the course of infection, the tongue may appear coated and the
client may complain of a foul breath odor

- MANAGEMENT:
o General pain is treated with analgesics; local ointments and
anesthetics may soothe lesions
o IV acyclovir (Zovirax) for immunocompromised patients; oral acyclovir
or topical penciclovir (Zovirax) for patients with competent immune
systems
o Antimicrobial treatment does not affect the ulcer unless it is
secondarily infected

C. VINCENT’S ANGINA / TRENCH MOUTH / NECROTIZING ULCERATIVE

GINGIVITIS
32

- Acute bacterial infection of the gingival caused by resident flora in the

mouth, fusiform bacteria, and spirochetes

- Precipitating factors:
o Poor oral hygiene
o Increased age
o Local tissue damage
o Debilitating diseases such as infectious mononucleosis, non-specific
viral infections, bacterial infections, blood dyscrasias, and DM

- Disease is of sudden onset, causes erythema and ulceration of the gingivae,

and affects the entire oropharynx
- Assessment reveals ulcers covered with a pseudomembrane
- Elevated WBC count
- Client may complain of foul taste, pain , choking sensation, fever, thick
secretions, anorexia, lymphadenopathy

- MANAGEMENT:
o Removing devitalized tissue and correcting the underlying cause with
rest
33

o Improve oral hygiene

o Bland diet and vitamins
o Pain medications and saline, peroxide, or half-saline half-peroxide
mouthwashes promote comfort

D. CANDIDIASIS (THRUSH / MONILIASIS)

- Caused by the organism Candida Albicans, a yeast-like fungus that is part of

the normal flora of the oral cavity
- Commonly seen in immunosuppressed clients, such as those receiving
chemotherapy / those with HIV infection
- Also increase in clients with DM and those who are pregnant, under stress,
receiving high-dose or long-term antibiotic therapy, or receiving long-term
tube feeding

- CLINICAL MANIFESTATIONS:
o White patches on the tongue, palate and buccal mucosa
o Often referred to as “milk curds” because of their appearance
o Clients describe the lesions as dry and hot

- MANAGEMENT:
o Topical antifungal agents to alleviate the infection and provide pain
relief
34

o Analgesics such as acetaminophen or aspirin to promote pain relief

o Mouthwashes of warm saline or water or half warm saline/water or
half hydrogen peroxide as part of oral hygiene regimen
o Do not eat or drink 30 minutes after giving the medication; remove
dentures at bedtime

NURSING MANAGEMENT:
- Assessment:
o Whether the client has pain, tenderness or bleeding in any part of
the oral cavity or has had any febrile episodes. Ask about a history of
previous infection elsewhere in the body and the use of any
medications, especially antibiotics
o Ask patient about a history of therapy with radiation / chemotherapy
because both can affect the oral mucosa
o To perform oral assessment, have a tongue blade and good lighting
and wear gloves
o Note any areas of inflammation, vesicular eruptions, ulcers, white
patches or erythema of the gingivae

- ACUTE PAIN RELATED TO ALTERED ORAL MUCOUS MEMBRANE AND

ULCERATION
o Minimize pain
 Assess for oral pain using a pain-scale
 Administer analgesic, such as aspirin / acetaminophen as
ordered
 Topical agents and mouth rinses often provide pain relief
 Antifungal agents to rinse with and swallow are used to
alleviate infection
 Client should avoid spicy foods, citrus juices, and hot liquids
o Provide oral care
 Mouthwashes – warm saline / half-strength hydrogen peroxide
 Gauze pads may replace toothbrushes
 Oral rinses may be needed to clean the area of debris and
promote healing
o Promote self care
35

 Give patient oral and written instructions regarding dental

hygiene regimen, diet, medications, and manifestations of
complications

- IMBALANCED NUTRITION: LESS THAN BODY REQUIRMENTS

o Assess food intake as well as the patient’s ability to chew and
swallow. Weigh daily. Provide assistive devices such as straws /
feeding syringes
o Encourage high-calorie, high protein diet considering food
preferences. Offer soft, lukewarm or cool foods / liquids. Providing
frequency in small amounts. Obtain nutritional consultation

- IMPAIRED ORAL MUCOUS MEMBRANE

o Assess and document oral mucous membrane and character of any
lesions every 4-8 h
o Assist with thorough mouth care after meals, at bedtime, and every
2-4h while awake. If unable to tolerate a toothbrush, offer
sponge/gauze toothettes. Avoid using alcohol-based mouthwashes
o Assess knowledge and teach about condition, mouth care and
treatments. Instruct to avoid alcohol, tobacco, and spicy and irritating
foods

DISORDERS OF THE ESOPHAGUS

1. ESOPHAGITIS
- Occasionally, the cardioesophageal sphincter fails to close tightly and gastric
juice backs up into the esophagus, which has little mucus protection. This
results in a characteristic pain known as heartburn which uncorrected leads
to inflammation of the esophagus

- A common cause is hiatal hernia, a structural abnormality in which the

superior part of the stomach protrudes slightly above the diaphragm. Since
the diaphragm no longer reinforces the cardioesophageal sphincter which is
a weak sphincter, gastric juice flow into the unprotected esophagus
36

- Conservative treatment involves restricting food intake after the evening

meal, taking antacids, and sleeping with head elevated

2. ESOPHAGEAL DIVERTICULA

- Is a sac-like outpouching in one or more layers of the esophagus

- Occur in one of the three areas of esophagus
o Pharyngoesophageal / upper part of the esophagus
o Midesophageal area
o Epiphrenic / lower area of esophagus
- Most common type of diverticulum is Zenker’s Diverticulum /
Pharyngoesophageal Pulsion diverticulum or a pharyngeal pouch → most
commonly found in the upper esophagus; occur 3× more often in men

- 2 categories of diverticula:
o Traction diverticulum – the esophageal mucosa has pulled outward
from the esophagus
 Commonly found in the middle esophagus
o Pulsion diverticulum - esophageal mucosa has pushed outward
through a defect in the esophageal musculature
 Commonly found in the upper esophagus
37

ETIOLOGY RISK FACTORS:

- Congenital defect
- Esophageal trauma
- Scar tissue
- Inflammation

CLINICAL MANIFESTATIONS:
- Initially, difficulty swallowing
- Eructation/belching
- Regurgitation of undigested food
- Halitosis
- Sour taste in the mouth
- Gurgling noises after eating
- Coughing may occur because of irritation of the trachea from regurgitated
food
- Dysphagia and chest pain
- Dysphagia is the most common complaint of patients with intramural
diverticulosis

ASSESSMENT AND DIAGNOSTIC FINDINGS:

- Barium swallow
o Determine the exact nature and location of diverticulum
- Manometric studies
o Rule out motor disorder
- Esophagoscopy
o Usually contraindicated because of the danger of perforation of the
diverticulum

MEDICAL MANAGEMENT:
- Dietary management and positioning
- Small, frequent meals of semi-soft foods often facilitate passage of food
- Note which foods ease or worsen the manifestations
38

- Raise the head of bed for 24h after meals

- Sleeping with head of bed elevated prevent nocturnal reflux
- Avoid constrictive clothes and vigorous exercise after eating

SURGICAL MANAGEMENT:
- When manifestations become severe, surgery is indicated
- Cervical approach is used for Zenker’s diverticulum
- Thoracic approach for diverticula located lower in esophagus
- Diverticulum is excised and the esophageal mucosa is reanastomosed

NURSING MANAGEMENT:
- RISK FOR INJURY RELATED to SURGICAL PROCEDURE AND PRESENCE OF
CHEST TUBES
o Provide teaching
 Discuss the normal preoperative routines. Explain that the
client will be taking nothing by mouth after surgery and that an
NGT will be present until healing occurs
o Maintain the NG tube
 Give the client written and verbal instructions about tube
feedings, diet and positioning
o Promote comfort
 Assess patient’s pain, and administer and evaluate prescribed
analgesics
 After surgery, head of bed should be elevated 30 degrees to
reduce edema around neck and upper chest

- IMBALANCED NUTRITION, LESS THAN BODY REQUIREMENTS, RELATED TO

DIFFICULTY SWALLOWING
o Encourage patient to eat slowly and to chew all food thoroughly so
that it can pass easily into the stomach
o Small, frequent feedings of non-irritating foods to promote digestion
and to prevent tissue irritation
o Liquid swallowed with food helps the food pass through the
esophagus
39

o Food should be prepared in an appealing manner to help stimulate

appetite
o Irritants such as tobacco and alcohol should be avoided
o Baseline weight is obtained and daily weights are recorded

- RISK FOR ASPIRATION RELATED TO DIFFICULTY SWALLOWING

o Decreasing risk of aspiration:
 Semi-fowler’s position to decrease the risk of aspiration
 Use of oral suction

- ACUTE PAIN
o Relieving pain:
 Small, frequent feedings to prevent food overload and gastric
reflux
 Avoid activities that increase pain
 Remain upright for 1-4 hours after each meal to prevent reflux
 Head of bed should be elevated
 Eating before bedtime is discouraged
 Advise patient that excessive use of OTC antacids can cause
rebound acidity

- DEFICIENT KNOWLEDGE ABOUT THE ESOPHAGEAL DISORDER, DIAGNOSTIC

STUDIES, MEDICAL MANAGEMENT, SURGICAL INTERVENTION AND
REHABILITATION
o Providing patient education
 Reassuring the patient and discussing the procedure and their
purposes
 Patient is given sufficient information to participate in care and
diagnostic tests

DISORDERS OF THE STOMACH AND DUODENUM

1. GASTRITIS
40

- Inflammation of the gastric mucosa / stomach lining that causes a

breakdown of the normal gastric protective barrier / gastric mucosal
barriers with subsequent diffusion of hydrochloric acid into the gastric
lumen
- Highest in the 5th and 6th decade of life
- Men are more frequently affected; greater in clients who are heavily
drinkers and smokers
- May be acute, lasting several hours to a few days, or chronic, resulting from
repeated exposure to irritating agents/recurring episodes of acute gastritis

ACUTE GASTRITIS
- May be seen with nausea and vomiting, epigastric discomfort, bleeding,
malaise and anorexia
- Usually stem from ingestion of a corrosive, erosive, or infectious substances

- ETIOLOGY AND RISK FACTORS

o Common causes are:
 Aspirin and NSAIDS, digitalis, chemotherapeutic drugs,
steroids, acute alcoholism and food poisoning (typically caused
by staphylococcus organisms)
 Food substances including excessive amounts of tea, coffee,
mustard, paprika, cloves, and pepper can precipitate acute
gastritis
 Foods with a rough texture / those eaten at an extremely
high temperature can also damage the stomach mucosa
 Ingestion of corrosive agents, such as lye/drain cleaner,
also causes acute gastritis
 Disorders linked with acute gastritis include uremia, shock, CNS
lesions, hepatic cirrhosis, portal hypertension, and prolonged
emotional tension

 Erosive gastritis / stress-induced gastritis

 Severe form of acute gastritis
41

 Occurs as a complication of other life-threatening

conditions such as shock, severe trauma, major surgery,
sepsis, burns, or head injury

 Erosions which follow a major burn are called CURLING’S

ULCER. When stress ulcers occur following head injury /
CNS surgery, they are referred to as CUSHING’s ULCER

PATHOPHYSIOLOGY:
- The mucosal lining of the stomach normally is protected from the digestive
substances. It secrete – HCL acid and pepsin. By the gastric mucosal barrier,
which include:
o An impermeable hydrophobic lipid layer that covers gastric epithelial
cells. This lipid layer prevents diffusion of water soluble molecules
except aspirin and alcohol
o Bicarbonate ions (HCO3 )– secreted in to hydrochloric acid secretion
by the parietal cells of the stomach. When HCO3 secretion equal to
hydrogen ion secretion, the gastric mucosa remains intact.
Prostaglandins, chemical messengers involved in inflammation
response, support bicarbonate production and blood flow to the
gastric mucosa
o Mucus gel, protects the surface of the stomach lining from the
damaging effects of pepsin and traps bicarbonate to neutralize HCL
acid. It also acts as a lubricant preventing mechanical damage to the
stomach lining
o If the barrier is penetrated, gastritis occurs, with resultant injury to
the mucosa. When HCL acid comes into contact with the mucosa,
injury to small vessels occurs with edema, hemorrhage, and possible
ulcer formation

CLINICAL MANIFESTATIONS:
- Epigastric discomfort
- Abdominal tenderness
- Cramping
- Belching
- Reflux
42

- Severe nausea and vomiting

- Sometimes hematemesis or melena; sometimes GI bleeding is the only
manifestation
- Anorexia
- Hiccupping
- When contaminated food is the cause of gastritis, the patient usually
develops diarrhea within 5h of ingestion of the offending substance
- Erosive gastritis is typically not associated with pain. The initial symptom is
often painless gastric bleeding, 2 or more days after the initial stressor
- Corrosive gastritis can cause severe bleeding, signs of shock and acute
peritonitis if perforation occurs

CHRONIC GASTRITIS
PATHOPHYSIOLOGY:
- Results from repeated exposure to irritating agents / recurring episodes of
acute gastritis
- Begins with superficial inflammation and gradually leads to atrophy of
gastric tissues
- The initial stage is characterized by superficial changes in the gastric mucosa
and a decrease in mucus
- The inflammatory process involves deep portions of the mucosa, which
thins and atrophies

3 different forms:
1. Superficial gastritis
– causes a reddened, edematous mucosa with small erosions and
hemorrhages
2. Atrophic gastritis
– occurs in all layers of the stomach, develops frequently in association
with gastric ulcer and gastric cancer and is invariably present in pernicious
anemia
- It is characterized by a decreased number of parietal and chief cells
3. Hypertrophic gastritis
- Produces a dull and nodular mucosa with irregular, thickened or nodular
rugae; hemorrhages occur frequently
43

Other classifications:

TYPE A GASTRITIS / AUTOIMMUNE GASTRITIS

- Less common
- The body produces antibodies to parietal cells and to intrinsic factors. These
antibodies destroy gastric mucosal cells resulting in tissue atrophy and loss
of hydrochloric acid and pepsin secretion. Because intrinsic factor is
required for the absorption of vitamin B12, this immune response also
results in pernicious anemia

TYPE B GASTRITIS
- More common form
- Its incidence increases with age, reaching nearly 100% in people over age of
70
- Caused by chronic infection by HELICOBACTER PYLORI which causes
inflammation of the gastric mucosa
- Outermost layer of gastric mucosa thins and atrophies, providing a less
effective barrier against the autodigestive properties for HCL acid and
pepsin
- The mucosa usually heals without scarring, but ulcer formation and
bleeding can occur. The atrophic changes eventually result in a minimal
amount of acid being secreted into the stomach (achlorhydria), which is a
major risk factor for the development of gastric cancer

CLINICAL MANIFESTATIONS:
- Vague gastric distress
- Epigastric heaviness after meals / ulcerlike symptoms
- Anorexia
- A feeling of fullness
- Dyspepsia
- Belching
- Nausea and vomiting
- Intolerance of spicy / fatty foods
- Fatigue and other symptoms of anemia
44

- If intrinsic factors is lacking, paresthesias and other neurologic

manifestations of vitamin B12 deficiency

DIAGNOSTIC FINDINGS:
1. Gastric analysis
o Assess HCL acid secretion

2. Hgb, Hct, and RBC indices

a. Evaluated for evidence of anemia

3. Serum vitamin B12 levels

a. Are measured to evaluate for possible pernicious anemia

4. Upper endoscopy
a. Done to inspect the gastric mucosa for changes, identify areas of
bleeding, and obtain tissue for biopsy

5. Upper GI radiologic studies

6. Serologic testing for antibodies against H. Pylori, I minute ultra rapid

urease test

7. Breath test

MEDICAL MANAGEMENT:
Acute gastritis:
- Refraining from alcohol and food until symptoms subside
- Initially foods and fluids are withheld until nausea and vomiting subsides (6-
12hours)
- Once the client tolerates food, the diet includes decaffeinated tea, gelatin,
toast, and simple bland foods
- Patient should Avoid spicy foods, caffeine and large, heavy meals

MEDICATIONS:
a. Phenothiazine for frequent vomiting
45

b. If ingestion of NSAIDs is a problem, a prostaglandin E1, (PGE1)

analog may be prescribed to protect the stomach mucosa and
inhibit gastric acid secretion
c. If gastritis is caused by ingestion of strong acids / alkalis,
treatment consists of diluting and neutralizing the offending
agent. To neutralize acids, common antacids (aluminum
hydroxide) are used; to neutralize an alkali, diluted lemon juice or
diluted vinegar is used
d. Therapy is supportive and may include NG intubation, analgesic
agents, sedatives, antacids, and IV fluids
e. If corrosion is extensive / severe, emetics and lavage are avoided
because of the danger of perforation and damage to the
esophagus
f. In extreme cases, emergency surgery may be required to remove
gangrenous / perforated tissues

Chronic gastritis:
- Modifying diet, promoting rest
- Reducing stress
- H. Pylori may be treated with antibiotics (tetracycline, amoxicillin, combined
with clarithromycin, metronidazole and omeprazole
- Proton pump inhibitor (lanzoprazole, omeprazole)
- Bismuth salts (pepto-bismol)
- Corticosteroids to induce parietal cell regeneration
- IM injections of Vit B12 if patient has pernicious anemia
- Gastric lavage
o Dilution and removal of corrosive substances

NURSING MANAGEMENT:
1. Assessment
a. Health history
 Client’s diet, patterns of eating, use of prescription and OTC
medications
 Lifestyle, including alcohol consumption and cigarette smoking
 Diet history plus a 72-h dietary recall
46

2. Reduce pain
- Teaching patient about the causes of pain and foods that may worsen the
disease
- Help the patient assess factors that increase manifestations, such as
stress/fatigue, taking certain medications on an empty stomach, ingestion
of foods and beverages, alcohol consumption and smoking. Encourage the
patient to avoid these agents
- Aluminum hydroxide with magnesium trisilicate (Gaviscon), produces a
soothing foam; is the best antacid for gastritis
- H2-receptor antagonists, proton pump inhibitors, anti-secretory agents and
drugs that enhance mucosal defenses also provide pain relief

3. Promote self-care
- Instruct the patient with chronic gastritis to see the health care provider at
regular intervals. This is particularly important if the diagnosis is H. Pylori
infection and atrophic gastritis because they are closely related to gastric
cancer
- Teach patient to use medications correctly, to maintain adequate nutrition
and to control risk that contribute to gastritis

4. Monitor and maintain fluid and electrolyte balances

5. Control nausea and vomiting
- NPO until able to tolerate foods, then bland diet

6. Administer meds as ordered

- Antiemetics, antacids, sedatives

7. Maintain patency of NGT

8. Provide patient teaching, and discharge planning concerning avoidance of
foods/meds such as coffee, spicy foods, alcohol, salicylates, ibuprofen,
steroids

9. Reducing anxiety
- Offer supportive therapy if patient has ingested acids/alkalis
- Use a calm approach to assess the patient and to answer all questions as
completely as possible
47

- It is important to explain all procedures and treatments according to the

patient’s level of understanding

10. Promoting optimal nutrition

- The patient should take no foods / fluids by mouth – possibly for days –
until the acute symptoms subside to allow gastric mucosa to heal
- After the symptoms subside, the nurse can offer the patient ice chips
followed by clear liquids
- Introducing solid food as soon as possible will provide oral nutrition,
decrease the need for IV therapy, and minimize irritation to the gastric
mucosa
- Discourage intake of caffeinated beverages, because caffeine is a CNS
stimulant that increases gastric activity and pepsin secretion
- Discourage alcohol use
- Discourage cigarette smoking because nicotine reduces the secretion of
pancreatic bicarbonate and thus inhibits the neutralization of gastric acid in
the duodenum. Refer patient for alcohol counseling and smoking cessation
programs

11. Promoting fluid balance

- Daily fluid I and O are monitored to detect early signs of dehydration
- If food and fluids are withheld, IV fluids (3L/day) usually are prescribed and
a record of fluid intake and caloric value (1L of 5% dextrose in water = 170
calories of carbohydrates)
- Electrolyte values (sodium, potassium, chloride) are assessed every 24h to
detect imbalance
- Be alert for any indicators of hemorrhage which include hematemesis,
tachycardia, hypotension. Notify physician

2. PEPTIC ULCER DISEASES

- An excavation, a break in the mucous lining of the GI tract
- Peptic ulcer is frequently referred to as a gastric, duodenal, or esophageal
ulcer depending on its location
- Erosion of a circumscribed area of mucous membrane is the cause
48

- Peptic ulcers are more likely to be in the duodenum than in the stomach
- Chronic gastric ulcers tend to occur in the lesser curvature of the stomach,
near the pylorus

TYPES:
A. DUODENAL ULCERS
- Most common
- Usually develop between ages 30 and 55 and are more common in men
- These ulcers are usually characterized by high gastric acid secretion
- Some are associated with normal gastric secretion associated with rapid
emptying of the stomach
- Hypersecretion of acid is attributed to a greater mass of parietal cells.
Stimuli for acid secretion include protein-rich meals, alcohol consumption,
calcium and vagal stimulation.
49

- The combined effect of hypersecretion of acid and rapid emptying of food

from the stomach reduces the buffering effect of food and results in a large
acid load in the duodenum
- Within the duodenum, inhibitory mechanisms and pancreatic secretion may
be insufficient to control the acid load

B. GASTRIC ULCERS
- Form within 1inch ( 2.5 cm) of the pylorus of the stomach in an area where
gastritis is common
- Probably caused by a break in the mucosal barrier
- An incompetent pylorus may decrease production of mucus, the usual
gastric defense. The reflux of the bile acids through an incompetent pylorus
into the stomach may break the mucosal barrier
- Decreased blood flow to the gastric mucosa may also alter the defensive
barrier and may make the duodenum more susceptible to gastric acid and
pepsin

C. STRESS-INDUCED AND DRUG-INDUCED ULCERS

- Stress ulcers / stress-erosive gastritis can occur after an acute medical crisis
- May occur in patients who are exposed to stressful conditions
- Major assaults that give rise to gastroduodenal ulcerations include:
o Severe trauma / major illness
o Severe burns (curling’s ulcer)
o Head injury / intracranial disease (cushing’s ulcers)
o Ingestion of a drug (aspirin, NSAIDs, steroids, and alcohol)
o Shock
o Sepsis

D. ESOPHAGEAL ULCERS
- Occurs as a result of the backward flow of hydrochloric acid from the
stomach into the esophagus (GERD)
50

ETIOLOGY AND RISK FACTORS:

- 90% of all peptic ulcer has been attributed to H. Pylori
- Excessive secretion of HCL in the stomach may contribute to the formation
of gastric ulcers
- Stress may be associated with increased gastric secretions
- Ingestion of milk and caffeinated beverages, smoking, and alcohol increase
HCL secretions
- Familial tendency may be a significant predisposing factor. People with
blood type O are more susceptible to peptic ulcers than those with blood
type A, B, or AB
- Zollinger – Ellison Syndrome (ZES) consist of severe peptic ulcers, extreme
gastric hyperacidity, and gastrin-secreting benign/malignant tumors of the
pancreas
- Long term use of steroids, severe burns, and chronic renal failure

PATHOPHYSIOLOGY:
- Peptic ulcers occur mainly in the gastroduodenal mucosa because this
tissue cannot withstand the digestive action of gastric acid (HCL) and
pepsin. The erosion is caused by the increased concentration or activity of
acid-pepsin or by decreased resistance of the mucosa. A damaged mucosa
cannot secrete enough mucus to act as a barrier against HCL. The use of
NSAIDs inhibits the secretion of mucus that protects the mucosa

- Patients with duodenal ulcer disease secrete more acid than normal,
whereas patients with gastric ulcer tend to secrete normal or decreased
levels of acid

- In the formation of gastric ulcer, the mucosal barrier may be interrupted by

the chronic presence of injurious substances as:
o Aspirin
o NSAIDs
o Cortisone
o Alcohol
o Adrenocorticotrophic hormone (ACTH)
o Caffeine
o Phenylbutazone
51

o Chemotherapeutic agents
- These substances may stimulate acid production, cause local mucosal
damage, and suppress mucus secretion. These substances strip away
surface mucus and cause degeneration of epithelial cell membranes and
massive diffusion of acid back into the gastric epithelial wall

- For duodenal peptic ulcers: activity of the vagus nerve is increased in

people with duodenal ulcers, particularly during a fasting state and at night.
The vagus nerve stimulates the pyloric antrum cells to release gastrin,
which travels via the bloodstream and acts on the gastric parietal cells to
stimulate the release of HCL acid

- Another factor in PUD is emotional stress, which can increase gastric

secretion, blood supply, and gastric motility by thalamic stimulation of the
vagal nerves. Hormonal influence takes place via the hypothalamus through
the pituitary adrenal route. In patients with stress reactions, the SNS causes
the blood vessels in the duodenum to constrict which makes the mucosa
more vulnerable to trauma from gastric acid and pepsin secretion. On
activation of the adrenal cortex, mucus production decreases and gastric
secretion increases. Together these factors result in increased vulnerability
to ulceration

- Zollinger – Ellison Syndrome is characterized by abnormal secretion gastrin

by a rare islet cell tumor in the pancreas. Pathophysiologic changes
associated with this syndrome include hypergastrinemia and diarrhea
secondary to fat malabsorption resulting from decreased duodenum-
inactivating pancreatic lipase or acid-induced injury of the villi. In addition
to increased gastric secretion, hyperplasia of the gastric mucosa is induced
by the trophic effects of gastrin. Treatment of ZES is aimed at suppression of
acid secretion

- Critically ill patients are susceptible to stress ulcers. Gastric mucosal

changes caused by stress develop within 72h in 78% of clients with greater
than 35% burns on their body. Stress ulcers manifest with superficial gastric
erosions, often accompanied by painless massive gastric hemorrhage. The
patient characteriscally has multiple lesions, usually small and superficial,
52

that do not extend through the muscularis mucosae. These lesions may
appear to ooze blood. The mechanism causing stress ulceration is unknown
but it probably involves ischemia. Ischemia can produce erosive gastritis
and ulcerations. Increased hydrogen ion back-diffusion and decreased
mucosal perfusion may also contribute to stress ulcer formation. Low
gastric pH is necessary for development of stress ulcers

CLINICAL MANIFESTATIONS:
1. PAIN
- Aching, burning, cramp-like, gnawing pain
- Dull, gnawing pain or a burning sensation in the midepigastrium or in the
back. Pain occurs when the increased acid content of the stomach and
duodenum erodes the lesion and stimulates the exposed nerve endings.
Another theory suggests that contact of the lesion with acid stimulates a
local reflex mechanism that initiates contraction of adjacent smooth muscle
- Gastric ulcer pain often occurs in the upper epigastrium, with localization to
the left of the midline, whereas duodenal pain is in the right epigastrium
- With gastric ulcers, food may cause the pain and vomiting may relieve it.
Patients with duodenal ulcers have pain with an empty stomach, and
discomfort may be relieved by ingestion of food/antacids because food
neutralizes the acid, or by taking an alkali; however, once the stomach has
emptied or the alkali’s effect has decreased, the pain returns. Sharply
localized tenderness can be elicited by applying gentle pressure to the
epigastrium or slightly to the right of the midline

2. NAUSEA AND VOMITING

- Patients with a duodenal ulcer usually have a normal appetite unless
pyloric obstruction is present
- Vomiting occurs more often with gastric ulcer. It also occurs more
frequently when the ulcer is in the pylorus or antrum of the stomach.
Vomiting results from gastric stasis of pyloric obstruction, and the patient
typically vomits undigested food. Severe retching and vomiting may suggest
an esophageal tear. Vomiting may or may not be preceeded by nausea;
usually it follows a bout of severe pain and bloating which is relieved by
ejection of the gastric contents
53

3. BLEEDING
- Occur as massive hemorrhage or may be occult, with slow oozing and
occurs often when an ulcer erodes through a blood vessel
- A CBC with decreased Hgb values may indicate bleeding

DIAGNOSTIC FINDINGS:
- Diagnosis of ulcer is confirmed on the basis of manifestations

- UPPER GI SERIES
o Using barium as a contrast medium can detect 80-90% of peptic
ulcers
o Commonly the diagnostic procedure chosen first: less costly and less
invasive
o Small/very superficial ulcers may be missed

- GASTROSCOPY
o Visualizes esophageal, gastric and duodenal mucosa and direct
inspection of ulcers. Tissue also can be obtained for biopsy
- SEROLOGIC TESTING AND UREA BREATH TEST
o Detect IgG antibodies
o Urease produced by H. Pylori bacteria converts urea to ammonia and
which can be measured as patient exhales

- GASTRIC ANALYSIS
o Evaluate gastric acid secretion
o Done if ZES is suspected

MEDICAL MANAGEMENT:
- Primary objective of intervention for peptic ulcer is to provide stomach rest.
Approaches include neutralizing/buffering HCL acid, inhibiting acid
secretions, decreasing activity of pepsin and HCL acid and eradicating H.
Pylori from the GI tract. Specific measures include medications, physical and
emotional rest, dietary management, and stress reduction

A. PHARMACOLOGIC THERAPY:
54

- Antibiotics, proton pump inhibitors and bismuth salts suppress H. Pylori

- Clarithromycin + metronidazole + omeprazole / ranitidine
- Histamine 2 (H2) receptor antagonists and proton pump-inhibitors are used
to treat NSAID-induced and other ulcers not associated with H. Pylori
- Rest, sedative, and tranquilizers may add to the patient’s comfort
- H2 receptor antagonists for patients with ZES
- Octreotide (sandostatin) suppresses gastrin levels
- Patients at risk for stress ulcers may be treated prophylactically with IV H2
receptor antagonists and cytoprotective agents (misoprostol sucralfate)
- Frequent gastric aspiration is performed to allow monitoring of gastric
secretion pH
- Anticholinergics
- Antacids
- Pepsin inhibitor

B. STRESS REDUCTION AND REST:

- Reducing environmental stress requires physical and psychological
modifications on the patient’s part as well as the aid and cooperation of
family members and s.o.
- The patient may benefit from regular rest periods during the day at least
during the acute phase of the disease
- Biofeedback, hypnosis, or behavior modification

C. SMOKING MODIFICATION:
- Smoking decreases the secretion of bicarbonate from the pancreas into the
duodenum, resulting in increased acidity of the duodenum, therefore
patient is strongly encouraged to stop smoking. Smoking cessation support
groups and other smoking cessation approaches are helpful

D. DIETARY MODIFICATION:
- Avoiding extremes of temperature and overstimulation from consumption
of meat extracts, alcohol, coffee, and other caffeinated beverages, and diets
rich in milk and cream
- Neutralize acid by eating 3 regular meals a day
55

- Small, frequent feedings are not necessary as long as an antacid / histamine

blocker is taken
- Patient eats foods that can be tolerated and avoids those that produce pain

E. PREVENT AND TREAT COMPLICATIONS

- Hemorrhage
o Assess bleeding
 Hemorrhage tend to occur more often with gastric ulcers
 Onset of hemorrhage may be associated with fatigue, nervous
tension, upper respiratory tract infection, dietary indiscretion,
alcoholism, irritating drugs
 With mild bleeding (<500ml), the patient may experience only
slight weakness and diaphoresis. Severe loss of more than 1L of
blood/ 24h may cause manifestations of shock
o Prevent shock
 Patient who should be fasting, receives IV fluids until the
bleeding subsides
 NGT inserted to assess the rate of bleeding, prevent gastric
dilation, and administer room temperature saline to remove
blood from the stomach
 Gastric cooling may also be promoted by cool saline lavage
which has vasoconstrictive effect
o Replace fluids
 Replace blood volume
 Restlessness and tachycardia are the earliest manifestations of
hypovolemia
 Decreased urine output and should be monitored by a foley
catheter and hourly urine measurements
o Administer vasopressin
 Via an infusion pump
 Arterial administration of vasopressin can also control
hemorrhage
o Inject artery with emboli
 Selective arterial embolization with angiography. The emboli
may consist of autologous blood clots with or without an
absorbable gelatin sponge
o Maintain rest
56

 Rest decreases BP and GI tract activity. When bleeding stops,

the patient is allowed bathroom priviledges
 Narcotics (morphine sulfate) may calm the patient who is
extremely restless and apprehensive
o Maintain high gastric pH
 Gastric pH should be maintained between 5.5 and 7
 Monitor gastric pH at least each shift
 Give antacids 1hr before or 2hrs after the H2-receptor
antagonists so that the antacids do not interfere with
absorption of drugs. The patient may require antacids every 30
minutes after starting intake of food/fluids
o Stop bleeding surgically
 If bleeding continues beyond 48h, recurs, or is associated with
perforation/obstruction, surgery may be indicated
 Surgical procedures include gastric secretion, excision of the
ulcer, and vagotomy and pyloroplasty
o Perform multipolar electrocoagulation/heat-probe therapy
 In MPEC- a bipolar electric current cauterizes the bleeding
lesion
 In heat probe therapy, direct heat cauterizes the lesion

- Perforation
o When ulcer perforates, gastroduodenal contents empty through the
anterior wall of the stomach into the peritoneal cavity, resulting in
peritonitis, bacterial septicemia, and hypovolemic shock. Peristalsis
diminishes, and paralytic ileus develops
o Posterior perforation often results in pancreatitis, because the
pancreas plugs the perforation
o Assess pain
 Perforation occurs most frequently with duodenal ulcers
 The patient experiences sudden, sharp, severe pain beginning
in the midepigastrium
 As peritonitis develops, the pain spreads over the entire
abdomen, which becomes tender, hard, and rigid
 The pain often causes the patient to bend over or draw the
knees up the abdomen in an effort to decrease the tension on
the abdominal muscles
57

 When perforation erodes into the pancreas, manifestations of

pancreatitis
o Replace fluids
 If perforation occurs, the patient needs immediate
replacement of fluids, electrolyte, and blood as well as
administration of antibiotics
 Nasogastric suction should be instituted to drain gastric
secretions and thus prevent further peritoneal spillage
o Correct perforation surgically
 The surgeon, evacuates the escaped gastric contents, cleans
the peritoneal cavity by flushing it out with normal saline or an
antibiotic or both and closes the perforation by patching it with
omentum
 After surgery, antibiotics are given to combat peritonitis. NGT
remains in the stomach until peristalsis returns

- Obstruction
o Long-standing ulcer causes scarring because of repeated ulcerations
and healing
o Scarring at the pylorus frequently causes pyloric obstruction,
manifested most often by pain at night, when the stomach cannot be
emptied by peristalsis
o Pyloric obstruction can also lead to vomiting
o Surgery (pyloroplasty) is required to correct the problem

SURGICAL MANAGEMENT:
- Is usually recommended for patients with intractable ulcers, life-threatening
hemorrhage, perforation, or obstruction and for those with ZES not
responding to meds

- TYPES OF OPERATIONS:
o VAGOTOMY
 Performed to eliminate the acid-secreting stimulus to gastric
cells
58

 TRUNCAL VAGOTOMY – each vagus nerve is completely cut

 SELECTIVE VAGOTOMY – surgeon partially severs the nerves to
prescribe the hepatic and celiac branches
 PROXIMAL VAGOTOMY – only the parietal cell mass is
denervated ; reduces acid secretion

o VAGOTOMY WITH PYLOROPLASTY

 Cutting the right and left vagus nerves and widening the
existing exit of the stomach at the pylorus
 This procedure prevents stasis and enhances emptying,
thereby preventing belching, weight loss, and feeling of
fullness

o GASTROENTEROSTOMY / GASTRECTOMY
 Permits regurgitation of alkaline duodenal contents, thereby
neutralizing gastric acid. A drain is made in the bottom of the
stomach and sewn to an opening made in the jejunum
59

 Drainage also diverts acid away from the ulcerative area, which
facilitates healing
 Should be combined with vagotomy to reduce vagal influences
 60-80% of the stomach is removed

o ANTRECTOMY
 Removal of the entire antrum of the stomach which is the acid-
secreting portions of the stomach
 Cells that secrete gastrin are excised

o SUBTOTAL GASTRECTOMY
 Surgery that involves partial removal of the stomach, may be
accomplished by either a BILLROTH 1 / a BILLROTH 2 procedure

 BILLROTH 1 / GASTRODUODENOSTOMY
 Surgeon removes part of the distal portion of the
stomach, including the antrum. The remainder of the
stomach is anastomosed to the duodenum
 This combined procedure is more properly called
gastroduodenostomy
60

 It decreases the incidence of dumping syndrome that

often occurs after a Billroth 2 procedure

 BILLROTH 2 / GASTROJEJUNOSTOMY
 Resection involves anastomosis of the proximal remnant
of the stomach to the proximal jejunum
 Surgeons prefer this technique for treatment of
duodenal ulcer because recurrent ulceration develops
less frequently after this surgery
61

o TOTAL GASTRECTOMY / ESOPHAGOJEJUNOSTOMY

 Total resection of the stomach is the principal intervention for
extensive gastric cancer. This surgery involves removal of the
stomach, with anastomosis of the esophagus to the jejunum,
an esophagojejunotomy
 Removal of the entire stomach with a loop of jejunum
anastomosed to the esophagus
62

COMPLICATIONS OF GASTRIC SURGERIES:

1. HEMORRHAGE
- Bleeding is usually caused by a splenic injury / slippage of a ligature. Assess
the patient post-operatively for manifestations of bleeding and
intraperitoneal hemorrhage

2. ALKALINE REFLUX GASTRITIS

- Caused by duodenal contents
- Usually associated after vagotomy which decreases gastric motility, allowing
reflux of duodenal contents into the stomach

3. ACUTE GASTRIC DILATION

- In the immediate post-op period, distention of the stomach produces
epigastric pain, tachycardia, and hypotension
- Patient complains of a feeling of fullness, hiccups, or gagging
- Rapidly improves after insertion of a NGT or clearing of a plugged NGT

4. NUTRITIONAL PROBLEMS
- Vit. B12 and folic acid deficiency
- Calcium metabolism disorders
- Reduced absorption of calcium and vitamin D; such problems result from a
shortage of intrinsic factor and inadequate absorption because of rapid
entry of blood into the bowel

5. DUMPING SYNDROME
- Postprandial problem
- Occurs after gastrojejunostomy because ingested food rapidly enter the
jejunum without proper mixing and without the normal duodenal digestive
processing
- Usually subsides in 6-12 months
- Early manifestations, which occur 5-30 minutes after eating, involve the
vasomotor disturbances of vertigo, tachycardia, syncope, sweating, pallor,
palpitation, diarrhea, nausea with a desire to lie down, weakness
- Dumping syndrome is most common after Billroth 2 procedure
- Intestinal manifestations include:
63

o Epigastric fullness
o Distention
o Abdominal discomfort
o Tenesmus
o Abdominal cramping
o Nausea
o Borborygmi
- Early manifestations are probably caused by rapid movement of
extracellular fluids into the bowel to convert the rapidly entering hypertonic
bolus into an isotonic mixture. This rapid fluid shift decreases the circulating
blood volume
- A jejunum distended with food and fluid increases intestinal peristalsis and
motility
- Late manifestations, which occur 2-3h after eating, are a result of rapid
entry of high-carbohydrate food into the jejunum, a rise in blood glucose
level, and excessive insulin level

- MANAGEMENT:
o Decreasing the amount of food taken at one time and maintaining a
high protein, high fat, low carbohydrate, dry diet
o Gastric emptying can be delayed by eating in a recumbent / semi-
recumbent position, lying down after meals, increasing the fat
content in diet, and avoiding fluids 1 hour before, or 2hours after
meals
o Patient may also be given sedatives and anti-spasmodic agents to
delay gastric emptying
o If manifestations persists, surgical intervention may include reducing
the size of the gastroenterostomy/converting a Billroth 2 to Billroth 1
by inserting a short segment of jejunum between the duodenal
stump and the stomach

6. GASTROJEJUNOCOLIC FISTULA
- Arise from perforation of a recurrent ulceration at the gastrojejunal
anastomosis site
- The perforation forms a fistula between the ulcer and adjacent bowel
- Manifestations include :
64

o Fecal vomiting
o Diarrhea
o Weight loss and anorexia
- Manifestations are caused by bacterial overgrowth in the small intestine

7. PYLORIC OBSTRUCTION
- Manifested by vomiting, occurs at the pylorus and is caused by scarring,
edema, inflammation, or a combination of these conditions
- A patient vomits persistently is usually hospitalized to receive IV fluids with
electrolyte added
- Management focuses on restoring fluids and electrolyte and decompressing
the dilated stomach; if necessary, surgical intervention is instituted

FOLLOW-UP CARE:
- Recurrence within 1 year may be prevented with the prophylactic use of H2
Receptor Antagonists given at a reduced dose
- The likelihood of recurrence is reduced if the patient avoids smoking, coffee
(including decaffeinated) and other caffeinated beverages, alcohol, and
ulcerative medications

NURSING MANAGEMENT:
1. Assessment
- Ask patient to describe the pain and the methods used to relieve it (eg.
food, antacids). The patient usually describes peptic ulcer pain as
burning/gnawing; it occurs about 2h after a meal and frequently awakens
the patient between midnight and 3 am

- Gastric ulcer pain located in left epigastrium, with possible radiation to the
back; usually occurs 1-2hours after meals
- Duodenal ulcer pain located midepigastrium and described as burning,
cramping; usually occurs 2-4hours after meals and is relieved by food
- Characteristics of vomitus
- Usual food intake for a 72h period and to describe food habits
- Lifestyle and habits
- Patient’s level of anxiety and his/her perception of current stressors
65

- Weight loss
- Hemoglobin and hematocrit decreased (if anemic)
- Endoscopy reveals ulceration
- Gastric analysis: normal gastric acidity in gastric ulcer; increased in
duodenal ulcer
- Upper GI series: confirms presence of ulcer

2. Relieving pain
- Meds
- Avoid aspirin, foods and beverages that contain caffeine and decaffeinated
coffee, and meals should be eaten at regularly paced intervals in a relaxed
setting
- Relaxation techniques
- Smoking cessation

3. Reducing anxiety
- Appropriate information is provided at the patient’s level of understanding,
all questions are answered, and the patient is encouraged to express fears
openly
- Explaining diagnostic tests and administering meds on schedule also help to
reduce anxiety
- Nurse interacts with the patient in a relaxed manner, helps identify
stressors, and explain various coping techniques and relaxation methods

4. Provide teaching
- Pre-op teaching should include explanation of surgery
- Explain that the patient will have either an NGT or gastrostomy tube with
suction
- IV line until surgical site heals
- Demonstrate and discuss the importance of deep-breathing exercises/use
of an incentive spirometer or both

5. Monitoring and managing potential complications

- Hemorrhage
66

o When hemorrhage is large (2000-3000ml) most the blood is vomited.

When hemorrhage is small, much/all of the blood is passed in the
stools, which will appear tarry black because of digested hemoglobin
o Assess patient for faintness/dizziness and nausea which may
precede/accompany bleeding
o Monitor vital signs frequently; evaluate for tachycardia, hypotension,
and tachypnea
o Monitor hemoglobin and hematocrit, testing the stool for
gross/occult blood
o Signs of bleeding include tachycardia, tachypnea, hypotension,
mental confusion, thirst, and oliguria. If bleeding recurs within 48h,
medical therapy has begun, or if more than 6-10 units of blood are
required within 24 hours to maintain blood volume, the patient is
likely to require surgery

- Perforation and penetration

o Perforation is the erosion of the ulcer through the gastric serosa into
the peritoneal cavity without warning. It is an abdominal catastrophe
and requires immediate surgery
o Penetration is erosion of the ulcer through gastric serosa into
adjacent structures such as the pancreas, biliary tract, or
gastrohepatic omentum. Symptoms of penetration include back and
epigastric pain not relieved by meds that were effective in the past

o Signs of symptoms of perforation:

 Sudden, severe upper abdominal pain; pain may be referred to
the shoulders especially the right shoulder, because of
irritation of phrenic nerve in the diaphragm
 Vomiting and fainting
 Extremely tender and rigid abdomen
 Hypotension and tachycardia, indicating shock

o Assess for peritonitis/localized infection:

 Increased temperature
 Abdominal pain
 Paralytic ileus
 Increased BP/absent bowel sounds
67

 Abdominal distention
o Antibiotic therapy is administered parenterally as prescribed

- Pyloric obstruction
o Also called gastric outlet obstruction (GOO)
o Occurs when the area distal to the pyloric sphincter becomes scarred
and stenosed from spasm/edema or from scar tissue that forms
when an ulcer alternately heals and breaks down
o Patient has nausea and vomiting, constipation, epigastric fullness,
anorexia, and later, weight loss
o First consideration is insertion of NGT to decompress the stomach,
confirmation that obstruction is the cause of the discomfort is
accomplished by assessing the amount of fluid aspirated from the NG
tube. A residual of more than 400ml strongly suggests obstruction
o Upper GI study/endoscopy is performed to confirm gastric outlet
obstruction

6. Provide patient teaching and discharge planning concerning

- Medical regimen
o Take meds at prescribed times
o Have antacids available at all times
o Recognize situations that would increase the need for antacids
o Avoid ulcerogenic drugs (salicylates, steroids)
o Know proper dosage, action, and side effects
- Proper diet
o Bland diet consisting of 6 small meals/day
o Eat meals slowly
o Avoid acid-producing substances
o Avoid stressful situations at mealtime
o Plan for rest periods after meals
o Avoid late bedtime snacks
- Avoidance of stress-producing situations and development of stress-
reduction methods (relaxation, exercise, biofeedback)

4. GASTRIC CANCER / CANCER OF THE STOMACH

68

- Most often develops in the distal 3rd and may spread through the walls of
the stomach into adjacent tissues, lymphatics, regional lymph nodes and
other abdominal organs, or through the bloodstream to the lungs and
bones
- Adenocarcinoma – most common
- Affects men twice as often as women
- Commonly occurs between ages 50 and 70

ETIOLOGY AND RISK FACTORS:

- Excessive intake of highly salted or smoked foods
- Diet low in quantity of vegetables and fruits
- Atrophic gastritis
- Achlorhydria
- H. Pylori infection
- Pernicious anemia
- Smoking
- Genetic factors
- Nitrite food preservatives
- Overheated fat products

PATHOPHYSIOLOGY:
- Some tumors penetrate, some ulcerate and some spread along the tissue
planes
- Gastric cancer begins as a localized lesion then progresses to involve the
mucosa or submucosa
- Lesions may spread by direct extension to surrounding tissues, the liver in
particular
- The lesion may ulcerate or appear as a polypoid (polyp-like) mass
- Lymph node involvement and metastasis occur early due to the rich blood
and lymphatic supply to the stomach
- Metastatic lesions are often found in the liver, lungs, ovaries, and
peritoneum

MANIFESTATIONS:
69

- Because clinical manifestations occur late in the course of the disease,

stomach cancer is seldom detected in an early stage
- Presence of palpable epigastric mass, ascites or bone pain caused by
metastasis – may be the first manifestation
- If cancer grows near the cardia, the patient may experience dysphagia
because of early involvement of the esophagus. If cancer is near the
pylorus, symptoms may result from obstruction
- Weight loss, vague indigestion, anorexia, or a feeling of fullness/mild
discomfort so insidious. Discomfort may be brought on/relieved by eating
- Anemia from blood loss commonly occurs

DIAGNOSTIC FINDINGS:
1. CBC – detects anemia, hematocrit and hemoglogin decrease
2. Upper GI x-ray with barium swallow –identify lesions
3. Ultrasound – identify a mass
4. Upper endoscopy and biopsy – provides the definite diagnosis

MEDICAL MANAGETMENT:
1. Chemotherapy
2. Radiation therapy
3. Surgical resection – primary treatment

SURGICAL MANAGEMENT:
- Only intervention that treats stomach cancer. Unfortunately because the
diagnosis is usually late, surgery is more often palliative than curative
o SUBTOTAL GASTRECTOMY (BILLROTH 1 AND 2)
o TOTAL GASTRECTOMY
o GASTROENTEROSTOMY
 Surgical creation of a passage between the stomach and small
intestine

NURSING MANAGEMENT:
1. Assessment
- Health history: anorexia, early satiety, indigestion, vomiting, epigastric pain
after meals, recent unintentional weight loss
- Physical exam:
70

o General appearance
o Weight , height
o Abdominal distention/palpable upper abdominal mass
o Occult blood in stool/vomitus

2. PAIN RELATED TO TUMOR MASS PRESSING ON NERVES

- Administer analgesics as prescribed
- An opioid may be necessary for severe pain
- Assess the frequency, intensity, and duration of the pain to determine the
effectiveness of analgesics
- Suggest non-pharmacologic methods for pain relief

3. IMBALANCED NUTRITION: LESS THAN BODY REQUIREMENTS, RELATED TO

ANOREXIA
- Encourage patient to eat small, frequent, non-irritating foods to decrease
gastric irritation
- Food supplements should be high in calories, as well as vitamins A, C and
iron, to enhance tissue repair
- If vitamin is unable to meet nutritional requirements, parenteral nutrition
may be necessary

4. ANXIETY RELATED TO DISEASE AND ANTICIPATED TREATMENT

- A relaxed, non-threatening atmosphere so that patients can express fears,
concerns, and possible anger about the diagnosis and prognosis
- Encourage the family to support the patient, offering reassurance, and
supporting positive coping measures
- Advise patient about any procedures and treatments so that the patient
knows what to expect
- Suggest talking to a support person (spiritual adviser)