06 NCMB316: PRELIM
Care of Clients with Problems in Nutritional & Gastrointestinal, Metabolism & Endocrine, Perception and
LECTURE Coordination (Acute & Chronic)
PRELIM TOPICS
• Disturbances in Ingestion, Digestion, and Absorption (pg.1)
• Diseases of the Upper Gastrointestinal Tract (pg.10)
o GERD, Gastritis, Peptic Ulcer, Dumping Syndrome
• Disturbances In Absorption and Elimination (pg.15)
o Intestinal Obstruction, Crohn’s Disease, Ulcerative
Colitis, Appendicitis, Peritonitis, Diverticular Disease,
Hemorrhoids
• Disorders of the Liver, Pancreas, and Gall Bladder (pg. 23)
o Hepatitis, Cirrhosis, Hepatic Encephalopathy,
Esophageal Varices, Cholelithiasis and Cholecystitis,
Pancreatitis (acute and chronic)
• Endocrine System and Pituitary Disorders (pg. 35)
o Hyperpituitarism, Hypopituitarism
DISTURBANCES IN INGESTION, DIGESTION, AND ABSORPTION
Functions of the Digestive System
• Food must be placed into the mouth before it can be acted
on; this is an active, voluntary process called ingestion.
• Propulsion. If foods are to be processed by more than one
digestive organ, they must be propelled from one organ to the
next; swallowing is one example of food movement that
depends largely on the propulsive process called peristalsis
(involuntary, alternating waves of contraction and relaxation of
the muscles in the organ wall).
• Food breakdown: Mechanical digestion prepares food for
further degradation by enzymes by physically fragmenting the
foods into smaller pieces, and examples of mechanical
digestion are: mixing of food in the mouth by the tongue,
churning of food in the stomach, and segmentation in the small
intestine.
• Food breakdown: The sequence of steps in which the large
food molecules are broken down into their building blocks by
enzymes is called chemical digestion.
• Transport of digested end products from the lumen of the GI
tract to the blood or lymph is absorption, and for absorption to
happen, the digested foods must first enter the mucosal cells
by active or passive transport processes.
• Defecation is the elimination of indigestible residues from the GI
tract via the anus in the form of feces.
Blood Supply
• Originates from the
aorta & branches
to the many
arteries throughout
the length of the
tract.
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Anatomy of the Digestive System
• The organs of the digestive system can be separated into two
main groups: those forming the alimentary canal and the
accessory digestive organs.
Organs of the Alimentary Canal
• The alimentary canal, also called the gastrointestinal tract, is a
continuous, hollow muscular tube that winds through the
ventral body cavity and is open at both ends. Its organs include
the following:
A. Mouth
Food enters the digestive tract through the mouth, or oral cavity, a
mucous membrane-lined cavity.
• The lips (labia) protect its
anterior opening.
• The cheeks form its lateral
walls.
• Palate. The hard palate
forms its anterior roof, and
the soft palate forms its
posterior roof.
• The uvula is a fleshy finger-
like projection of the soft
palate, which extends
inferiorly from the posterior edge of the soft palate.
• The space between the lips and the cheeks externally and the
teeth and gums internally are the vestibule.
• The area contained by the teeth is the oral cavity proper.
• The muscular tongue occupies the floor of the mouth and has
several bony attachments- two of these are to the hyoid bone
and the styloid processes of the skull.
• The lingual frenulum, a fold of mucous membrane, secures the
tongue to the floor of the mouth and limits its posterior
movements.
• At the posterior end of the oral cavity are paired masses of
lymphatic tissue, the palatine tonsils.
• The lingual tonsils cover the base of the tongue just beyond.
B. Pharynx
From the mouth, food passes posteriorly into the oropharynx and
laryngopharynx.
• The oropharynx is posterior to the oral cavity.
• The laryngopharynx is continuous with the esophagus below;
both of which are common passageways for food, fluids, & air.
C. Esophagus
The esophagus or gullet, runs from the pharynx through the
diaphragm to the stomach.
• Size. About 25 cm (10 inches) long, it is essentially a
passageway that conducts food by peristalsis to the stomach.
• Function: propel food & fluids from the pharynx to the stomach
and prevent reflux of gastric contents into the esophagus.
o Upper esophageal sphincter (UES) – closed when at rest to
prevent air in esophagus.
o Lower esophageal sphincter (LES) – normally closed when
at rest to prevent reflux of gastric contents into the
esophagus.
• Structure. The walls of the alimentary canal organs from the
esophagus to the large intestine are made up of the same four
basic tissue layers or tunics.
o The mucosa is the innermost layer, a moist membrane that
lines the cavity, or lumen, of the organ; it consists primarily
of a surface epithelium, plus a small amount of connective
tissue (lamina propria) and a scanty smooth muscle layer.
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o The submucosa is found just beneath the mucosa; it is a
soft connective tissue layer containing blood vessels,
nerve endings, lymph nodules, and lymphatic vessels.
o The muscularis externa is a muscle layer typically made up
of an inner circular layer and an outer longitudinal layer of
smooth muscle cells.
o The serosa is the outermost layer of the wall that consists of
a single layer of flat serous fluid-producing cells, the
visceral peritoneum.
• The alimentary canal wall contains two important intrinsic
nerve plexuses – the submucosal nerve plexus and the
myenteric nerve plexus, both of which are networks of nerve
fibers that are actually part of the autonomic nervous system
and help regulate the mobility and secretory activity of the GI
tract organs.
D. Stomach
Different regions of the stomach have been named, and they
include the following:
• Location. The C-shaped stomach is on the left side of the
abdominal cavity, nearly hidden by the liver and the
diaphragm.
• Function. The stomach acts as a temporary “storage tank” for
food as well as a site for food breakdown.
• Anatomic regions of the stomach:
o The cardiac region surrounds the cardio esophageal
sphincter, through which food enters the stomach from the
esophagus.
o The fundus is the expanded part of the stomach lateral to
the cardiac region.
o The corpus or body is the midportion, and as it narrows
inferiorly, it becomes the pyloric antrum, and then the
funnel-shaped pylorus.
o The pylorus or antrum is the terminal part of the stomach
and it is continuous with the small intestine through the
pyloric sphincter or valve.
• Size. The stomach varies from 15 to 25 cm in length, but its
diameter and volume depend on how much food it contains;
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when it is full, it can hold about 4 liters (1 gallon) of food, but
when it is empty it collapses inward on itself.
• The mucosa of the stomach is thrown into large folds called
rugae when it is empty.
• The convex lateral surface of the stomach is the greater
curvature.
• The concave medial surface is the lesser curvature.
• The lesser omentum, a double layer of peritoneum, extends
from the liver to the greater curvature.
• The greater omentum, another extension of the peritoneum,
drapes downward and covers the abdominal organs like a
lacy apron before attaching to the posterior body wall, and is
riddled with fat, which helps to insulate, cushion, and protect
the abdominal organs.
• Stomach mucosa. The mucosa of the stomach is a simple
columnar epithelium composed entirely of mucous cells that
produce a protective layer of bicarbonate-rich alkaline mucus
that clings to the stomach mucosa and protects the stomach
wall from being damaged by acid and digested by enzymes.
• Gastric glands. This otherwise smooth lining is dotted with
millions of deep gastric pits, which lead into gastric glands that
secrete the solution called gastric juice.
• Some stomach cells produce intrinsic factor, a substance
needed for the absorption of vitamin b12 from the small
intestine.
• The chief cells produce protein-digesting enzymes, mostly
pepsinogens.
• The parietal cells produce corrosive hydrochloric acid (HCL),
which makes the stomach contents acidic and activates the
enzymes.
• The enteroendocrine cells produce local hormones such as
gastrin, that are important to the digestive activities of the
stomach.
• After food has been processed, it resembles heavy cream and
is called chyme.
Three Phases of Gastric Secretion
1. Cephalic phase
- Begins with sight, smell and taste of food
- Vagus & GI nerve plexuses initiates secretory & contractile
activities
2. Gastric phase
- Begins with the presence of food in the stomach
- Gastric juice (HCL + hormones + enzymes) → FOOD →
CHYME
- G cells → hormone gastrin → promotes secretion of HCL &
pepsinogen
- HCL → converts pepsinogen to active pepsin (digestion of
CHONS)
- Mucus and bicarbonate secretions (protects stomach
from mechanical & chemical damage
3. Intestinal phase
- Begins as the chyme passes from the stomach into the
duodenum.
- Mediated by secretin (inhibits further acid production &
decreases gastric motility)
E. Small Intestine
The small intestine is the body’s major digestive organ.
• Location. The small intestine is a muscular tube extending from
the pyloric sphincter to the large intestine.
• Size. It is the longest section of the alimentary tube, with an
average length of 2.5 to 7 m (8 to 20 feet) in a living person.
• The small intestine has three subdivisions: the duodenum, the
jejunum, and the ileum, which contribute 5 percent, nearly 40
percent, and almost 60 percent of the small intestine,
respectively.
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• The ileum meets the large intestine at the ileocecal valve, • The saclike cecum is
which joins the large and small intestine. the first part of the
• The main pancreatic and bile ducts join at the duodenum to large intestine.
form the flask-like hepatopancreatic ampulla, literally, the • Hanging from the
”liver-pancreatic-enlargement”. cecum is the
• From there, the bile and pancreatic juice travel through the wormlike appendix, a
duodenal papilla and enter the duodenum together. potential trouble spot
• Microvilli are tiny projections of the plasma membrane of the because it is an ideal
mucosa cells that give the cell surface a fuzzy appearance, location for bacteria
sometimes referred to as the brush border; the plasma to accumulate and
membranes bear enzymes (brush border enzymes) that multiply.
complete the • The ascending colon
digestion of proteins travels up the right
and carbohydrates side of the
in the small intestine. abdominal cavity and makes a turn, the right colic (or hepatic)
• Villi are fingerlike flexure, to travel across the abdominal cavity.
projections of the • The ascending colon makes a turn and continuous to be the
mucosa that give it a transverse colon as it travels across the abdominal cavity.
velvety appearance • It then turns again at the left colic (or splenic) flexure, and
and feel, much like continues down the left side as the descending colon.
the soft nap of a • The intestine then enters the pelvis, where it becomes the S-
towel. shaped sigmoid colon.
• Within each villus is a • The anal canal ends at the anus which opens to the exterior.
rich capillary bed • The anal canal has an external voluntary sphincter, the external
and a modified anal sphincter, composed of skeletal muscle.
lymphatic capillary called a lacteal. • The internal involuntary sphincter is formed by smooth muscles.
• Circular folds, also called plicae circulares, are deep folds of
both mucosa and submucosa layers, and they do not Accessory Digestive Organs
disappear when food fills the small intestine. Other than the intestines and the stomach, the following are also
• Peyer’s patches. In contrast, local collections of lymphatic part of the digestive system:
tissue found in the submucosa increase in number toward the
end of the small intestine. G. Teeth
The role the teeth play in food
processing needs little
introduction; we masticate, or
chew, by opening and closing
our jaws and moving them from
side to side while continuously
using our tongue to move the
food between our teeth.
• Function. The teeth tear
and grind the food,
breaking it down into
smaller fragments.
NOTE: Intestinal cells produce cells that secretes enzymes & • The first set of teeth is the
hormones deciduous teeth, also called baby teeth or milk teeth, and they
• Secretin begin to erupt around 6 months, and a baby has a full set (20
o Secreted by duodenum in the presence of HCL teeth) by the age of 2 years.
o Stimulates secretion of pancreatic juice & bile in the liver • Permanent teeth. As the second set of teeth, the deeper
• Pancreozymin permanent teeth, enlarge and develop, the roots of the milk
o Secreted by duodenum in the presence of HCL & peptides teeth are reabsorbed, and between the ages of 6 to 12 years
o Stimulates secretion of pancreatic juice they loosen and fall out.
• Cholecystokinin • The chisel-shaped incisors are adapted for cutting.
o Secreted by duodenum in the presence of amino acids & • Canines. The fanglike canines are for tearing and piercing.
fatty acids • Premolars (bicuspids) and molars have broad crowns with
o Stimulates secretion of pancreatic enzymes & bile in the round cusps (tips) and are best suited for grinding.
gallbladder • The enamel-covered crown is the exposed part of the tooth
above the gingiva orgum.
F. Large Intestine
• Enamel is the hardest substance in the body and is fairly brittle
The large intestine is much larger in diameter than the small intestine
because it is heavily mineralized with calcium salts.
but shorter in length.
• The outer surface of the root is covered by a substance called
• Size. About 1.5 m (5 feet) long, it extends from the ileocecal
cementum, which attaches the tooth to the periodontal
valve to the anus.
membrane (ligament).
• Functions. Its major functions are to dry out indigestible food
• Dentin, a bonelike material, underlies the enamel and forms the
residue by absorbing water and to eliminate these residues
bulk of the tooth.
from the body as feces.
• It surrounds a central pulp cavity, which contains a number of
• It frames the small intestines on three sides and has the following
structures (connective tissue, blood vessels, and nerve fibers)
subdivisions: cecum, appendix, colon, rectum, and anal
collectively called the pulp.
canal.

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• Where the pulp cavity extends into the root, it becomes the
root canal, which provides a route for blood vessels, nerves,
and other pulp structures to enter the pulp cavity of the tooth.
H. Salivary Glands
Three pairs of salivary glands empty their secretions into the mouth.
• The large parotid glands lie anterior to the ears and empty their
secretions into the mouth.
• The submandibular and sublingual glands empty their
secretions into the floor of the mouth through tiny ducts.
• The product of the salivary glands, saliva, is a mixture of mucus
and serous fluids.
• The clear serous portion contains an enzyme, salivary amylase,
in a bicarbonate-rich juice that begins the process of starch
digestion in the mouth.
I. Pancreas
Only the pancreas produces enzymes that break down all
categories of digestible foods.
• A fish shaped gland that lies retro-peritoneally in the upper
abdominal cavity behind the stomach and extends horizontally
from the duodenal C-loop to the spleen.
• Function:
o Exocrine: 80% of the organ; acinar cells secrete enzymes
o Endocrine: 20% of the organ; islets of Langerhans secrete
hormones.
• Location. The pancreas is a soft, pink triangular gland that
extends across the abdomen from the spleen to the
duodenum; but most of the pancreas lies posterior to the
parietal peritoneum, hence its location is referred to as
retroperitoneal.
• The pancreatic enzymes are secreted into the duodenum in an
alkaline fluid that neutralizes the acidic chyme coming in from
the stomach.
• The pancreas also has an endocrine function; it produces
hormones insulin and glucagon.
J. Liver
The liver is the largest gland in the body.
• Location. Located under the diaphragm, more to the right side
of the body, it overlies and almost completely covers the
stomach.
• 2 major regions: right & left lobe
• About 1500 ml of blood flows through the liver q min.
• Performs more than 400 functions in 3 major categories:
o Storage (copper, iron, magnesium, Vit.B2, B6, B12, A, D, E,
K, folic acid)
o Protection (phagocytic Kupffer cells, detoxifies potentially
harmful compounds such as drugs, chemicals & alcohol)
o Metabolism (breakdown of amino acids forming urea,
synthesis of plasma CHONS, CHO metabolism & Fat
metabolism)
• The liver has four lobes and is suspended from the diaphragm
and abdominal wall by a delicate mesentery cord, the
falciform ligament.
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• The liver’s digestive function is to produce bile – is a yellow-to-
green, watery solution containing bile salts, bile pigments,
cholesterol, phospholipids, and a variety of electrolytes.
• Bile does not contain enzymes but its bile salts emulsify fats by
physically breaking large fat globules into smaller ones, thus
providing more surface area for the fat-digesting enzymes to
work on.
K. Gallbladder
While in the gallbladder, bile is concentrated by the removal of
water.
• Location. The gallbladder is a small, thin-walled green sac that
snuggles in a shallow fossa in the inferior surface of the liver.
• When food digestion is not occurring, bile backs up the cystic
duct and enters the gallbladder to be stored.
Physiology of the Digestive System
Specifically, the digestive system takes in food (ingests it), breaks it
down physically and chemically into nutrient molecules (digests it),
and absorbs the nutrients into the bloodstream, then, it rids the body
of indigestible remains (defecates).
A. Activities Occurring in the Mouth, Pharynx, and Esophagus
The activities that occur in the mouth, pharynx, and esophagus are
food ingestion, food breakdown, and food propulsion.
Food Ingestion and Breakdown
Once food is placed in the mouth, both mechanical and chemical
digestion begin.
• First, the 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.
• When food enters the mouth, much larger amounts of saliva
pour out; however, the simple pressure of anything put into the
mouth and chewed will also stimulate the release of saliva.
• The pharynx and the esophagus have no digestive function;
they simply provide passageways to carry food to the next
processing site, the stomach.
o Food Propulsion – Swallowing and Peristalsis
o For food to be sent on its way to the mouth, it must first be
swallowed.
• Deglutition, or swallowing, is a complex process that involves
the coordinated activity of several structures (tongue, soft
palate, pharynx, and esophagus).
• Buccal phase of deglutition. The first phase, the voluntary
buccal phase, occurs in the mouth; once the food has been
chewed and well mixed with saliva, the bolus (food mass) is
forced into the pharynx by the tongue.
• Pharyngeal-esophageal phase. The second phase, the
involuntary pharyngeal-esophageal phase, transports food
through the pharynx and esophagus; the parasympathetic
division of the autonomic nervous system controls this phase
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and promotes the mobility of the digestive organs from this
point on.
• Food routes. All routes that the food may take, except the
desired route distal into the digestive tract, are blocked off; the
tongue blocks off the mouth; the soft palate closes off the nasal
passages; the larynx rises so that its opening is covered by the
flaplike epiglottis.
• Stomach entrance. Once food reaches the distal end of the
esophagus, it presses against the cardioesophageal sphincter,
causing it to open, and food enters the stomach.
B. Activities of the Stomach
It involves food breakdown and food propulsion.
Food Breakdown
The sight, smell, and taste of food stimulate parasympathetic
nervous system reflexes, which increase the secretion of gastric juice
by the stomach glands
• Secretion of gastric juice is regulated by both neural and
hormonal factors.
• The presence of food and a rising pH in the stomach stimulate
the stomach cells to release the hormone gastrin, which prods
the stomach glands to produce still more of the protein-
digesting enzymes (pepsinogen), mucus, & hydrochloric acid.
• The extremely acidic environment that hydrochloric acid
provides is necessary, because it activates pepsinogen to
pepsin, the active protein-digesting enzyme.
• Rennin, the second protein-digesting enzyme produced by the
stomach, works primarily on milk protein and converts it to a
substance that looks like sour milk.
• Food entry. As food enters and fills the stomach, its wall begins
to stretch (at the same time as the gastric juices are being
secreted).
• Stomach wall activation. Then the three muscle layers of the
stomach wall become active; they compress and pummel the
food, breaking it apart physically, all the while continuously
mixing the food with the enzyme-containing gastric juice so
that the semifluid chyme is formed.
o Food Propulsion – Peristalsis is responsible for the
movement of food towards the digestive site until the
intestines.
• Peristalsis. Once the food has been well mixed, a rippling
peristalsis begins in the upper half of the stomach, and the
contractions increase in force as the food approaches the
pyloric valve.
• Pyloric passage. The pylorus of the stomach, which holds about
30 ml of chyme, acts like a meter that allows only liquids and
very small particles to pass through the pyloric sphincter; and
because the pyloric sphincter barely opens, each contraction
of the stomach muscle squirts 3 ml or less of chyme into the
small intestine.
• When the duodenum is filled with chyme and its wall is
stretched, a nervous reflex, the enterogastric reflex, occurs; this
reflex “puts the brakes on” gastric activity and slows the
emptying of the stomach by inhibiting the vagus nerves and
tightening the pyloric sphincter, thus allowing time for intestinal
processing to catch up.
C. Activities of the Small Intestine
The activities of the small intestine are food breakdown and
absorption and food propulsion.
Food Breakdown and Absorption
Food reaching the small intestine is only partially digested.
• Digestion. Food reaching the small intestine is only partially
digested; carbohydrate and protein digestion has begun, but
virtually no fats have been digested up to this point.
• The microvilli of small intestine cells bear a few important
enzymes, the so-called brush border enzymes, that break down
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double sugars into simple sugars and complete protein
digestion.
• Foods entering the small intestine are literally deluged with
enzyme-rich pancreatic juice ducted in from the pancreas, as
well as bile from the liver; pancreatic juice contains enzymes
that, along with brush border enzymes, complete the digestion
of starch, carry out about half of the protein digestion, and are
totally responsible for fat digestion and digestion of nucleic
acids.
• Chyme stimulation. When chyme enters the small intestine, it
stimulates the mucosa cells to produce several hormones; two
of these are secretin and cholecystokinin which influence the
release of pancreatic juice and bile.
• Absorption of water and of the end products of digestion
occurs all along the length of the small intestine; most
substances are absorbed through the intestinal cell plasma
membranes by the process of active transport.
• Lipids or fats are absorbed passively by the process of diffusion.
• At the end of the ileum, all that remains are some water,
indigestible food materials, and large amounts of bacteria; this
debris enters the large intestine through the ileocecal valve.
o Food Propulsion – Peristalsis is the major means of
propelling food through the digestive tract.
• Peristalsis. The net effect is that the food is moved through the
small intestine in much the same way that toothpaste is
squeezed from the tube.
• Rhythmic segmental movements produce local constrictions of
the intestine that mix the chyme with the digestive juices, and
help to propel food through the intestine.
D. Activities of the Large Intestine
The activities of the large intestine are food breakdown and
absorption and defecation.
Food Breakdown and Absorption
What is finally delivered to the large intestine contains few nutrients,
but that residue still has 12 to 24 hours more to spend there.
• Metabolism. The “resident” bacteria that live in its lumen
metabolize some of the remaining nutrients, releasing gases
(methane and hydrogen sulfide) that contribute to the odor of
feces.
• About 50 ml of gas (flatus) is produced each day, much more
when certain carbohydrate- rich foods are eaten.
• Absorption by the large intestine is limited to the absorption of
vitamin K, some B vitamins, some ions, and most of the
remaining water.
• Feces, the more or less solid product delivered to the rectum,
contains undigested food residues, mucus, millions of bacteria,
and just enough water to allow their smooth passage.
o Propulsion of the Residue and Defecation
o When presented with residue, the colon becomes mobile,
but its contractions are sluggish or short-lived.
• The movements most seen in the colon are haustral
contractions, slow segmenting movements lasting about one
minute that occur every 30 minutes or so.
• Propulsion. As the haustrum fills with food residue, the distension
stimulates its muscle to contract, which propels the luminal
contents into the next haustrum.
• Mass movements are long, slow-moving, but powerful
contractile waves that move over large areas of the colon
three or four times daily and force the contents toward the
rectum.
• The rectum is generally empty, but when feces are forced into
it by mass movements and its wall is stretched, the defecation
reflex is initiated.
• The defecation reflex is a spinal (sacral region) reflex that
causes the walls of the sigmoid colon and the rectum to
contract and anal sphincters to relax.
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• Impulses. As the feces is forced into the anal canal, messages
reach the brain giving us time to make a decision as to whether
the external voluntary sphincter should remain open or be
constricted to stop passage of feces.
• Relaxation. Within a few seconds, the reflex contractions end
and rectal walls relax; with the next mass movement, the
defecation reflex is initiated again.
Summary of the Physiology of Digestion & Absorption:
1. Digestion: Physical/Mechanical & Chemical breakdown of
food into absorptive substances
a) Initiated in the mouth where food mixes with saliva and
starch is broken down
b) Food then passes into the esophagus where, it is propelled
into the stomach
c) In the stomach, food is processed by gastric secretions into
a substance called chyme
d) In the small intestine, CHO are hydrolyzed to
monosaccharide, fats to 2-glycerol and fatty acids; and
proteins to amino acids to complete the digestive process
e) When chyme enters the duodenum, mucus is secreted to
neutralize hydrochloric acid; in response to release of
secretin, pancreas releases bicarbonate to neutralize acid
chyme
f) Cholecystokinin and pancreozymin (CCK-PZ) are also
produced by the duodenal mucosa; stimulate contraction
of the gallbladder along with relaxation of the sphincter of
Oddi (to allow bile to flow from the common bile duct into
the duodenum), and stimulate release of pancreatic
enzymes
2. Absorption
a) intestinal cells to absorb nutrient molecules
(monosaccharides, amino acids and fatty acids)
b) villi increase the surface area for absorption, most
especially in the small intestine
Aging and the Digestive System
• Physiologic changes occur as individuals age, especially when
they become 65 years of age or older.
• Overall changes of the digestive system associated with aging
includes:
o Secretory mechanism
o Motility of the digestive organs
o Loss of strength & tone of the muscular tissue & it
supporting structures.
o Changes in neurosensory feedback regarding enzyme &
hormone release.
Assessment Techniques
History
• Demographic data – age, gender, culture, occupation
• Family history & genetic risk
• Previous G.I. disorders, abdominal surgeries
• Medications
o Aspirin, NSAIDs (PUD, GI bleeding)
o Laxatives & enemas (causes dependence on such
stimulation and cause constipation)
• Travel history
• Diet history
• Socioeconomic status
• Current health problem: PAIN (common complaint)
• The mnemonic PQRST may be helpful in assisting the nurse to
organize the current problem assessment
o Precipitating or palliative – What brings it on? What makes
it better?
o Quality or quantity – How does it look, feel or sound? How
intense/ severe is it?
o Region or radiation – Where is it? Does it spread anywhere?
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o Severity scale – How bad is it (on scale of 1 to 10)?
o Timing – Onset, duration & frequency
Physical Assessment
• Comprehensive examination of the client’s nutritional status,
the mouth & pharynx, the abdomen & the extremities
• Anthropometric measurement – evaluates nutritional status
height, weight, BMI
Abdomen
• Empty the bladder; lie in a supine position with knees bent,
keeping the arms at the sides (prevent abdominal muscle
tension)
• RUQ, LUQ, LLQ, RLQ
• If areas of pain are noted from the history, this area is examined
last in the examination sequence to prevent abdominal muscle
tension
• Observe the client’s face for signs of distress or pain
• 4 techniques used: IAPePa (usual: IPaPeA) – Inspection,
Auscultation, Percussion, Palpation
• Cullen’s sign – presence of ecchymosis (bruising) around the
umbilicus indicates intra-abdominal bleeding
• Observe also for abdominal movements
o Rarely seen on inspection
o Indicates intestinal obstruction
Auscultation
• High pitched gurgles air & fluid movement
o q 5-15 seconds / 5-30 sounds /min
o Diminished or absent (abdominal surgery, peritonitis,
paralytic ileus) Hypoactive – 1-2 sounds in 2 min.
Hyperactive – 30 sounds/min. Absent – no sounds in 3-
5min.
• Borborygmus – loud gurgling sounds due to hypermotility of the
bowel (diarrhea, gastroenteritis, above a complete intestinal
obstruction)
• Bruit “swooshing sounds” – Indicates aneurysm especially if
heard over the aorta; if heard, DO NOT percuss/palpate
abdomen.
Percussion
• Determine & estimate the size of solid organs (liver & spleen)
• detect presence of masses, fluid, and air.
• Tympanic – high pitched, loud musical sound of an air-filled
intestine.
• Dull – medium pitched, softer, thud-like sound over a solid
organ (liver).
Palpation
• Determine the size & location of abdominal organs & assess
presence of masses or tenderness
• Blumberg’s sign – rebound tenderness (pain felt on release of
fingers pushing & placed at a 90° angle in relation to the
abdomen)
Laboratory Assessments
Barium Swallow Test (Upper GI Series & Small Bowel Series)
• A barium swallow test
is a special type of
imaging test that uses
barium and X- rays to
create images of your
upper gastrointestinal
(GI) tract. Your upper
GI tract includes the
back of your mouth
and throat (pharynx)
and your esophagus.
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• Barium is used during a swallowing test to make certain areas
of the body show up more clearly on an X-ray. The radiologist
will be able to see size and shape of the pharynx and
esophagus. He or she will also be able see how you swallow.
These details might not be seen on a standard X-ray. Barium is
used only for imaging tests for the GI tract.
• A barium swallow test may be used by itself or as part of an
upper GI series. This series looks at your esophagus, stomach,
and the first part of the small intestine (duodenum). Fluoroscopy
is often used during a barium swallow test. Fluoroscopy (used
to trace the barium through the esophagus and stomach) is a
kind of X-ray “movie.” Barium is a white liquid that is visible on
X-rays. Barium passes through the digestive system and does
not cause a person any harm. As it passes through the body,
barium coats the inside of the food pipe, stomach, or bowel,
causing the outlines of the organs to appear on X-ray.
Why are barium swallow tests used?
• A barium swallow can help a doctor identify problems in the
food pipe, stomach, or bowel.
• A barium swallow test may be used if someone has any of the
following conditions:
o frequent, painful heartburn
o gastric reflux, where food or acid keeps coming back up
the food pipe
o difficulty eating, drinking, or swallowing
• This test can give a doctor information about how the person is
swallowing.
• It can also reveal if someone has any of the following in their
food pipe, stomach, or the first part of the bowel:
o ulcers
o abnormal growths
o blockages
o narrowing
• If someone has a tumor, this will show up on the X-ray as an
irregular outline that extends from the wall of the affected
organ.
Procedure
• People who are undergoing a barium swallow should not eat
or drink for a few hours before the test. In some cases, the
doctor may ask the person to stop taking medication before
the test. Some hospitals recommend not chewing gum, eating
mints, or smoking cigarettes after midnight the night before a
barium swallow test.
• The test takes around 60 minutes and will take place in the X-
ray department of the hospital. A person will need to change
into a hospital gown.
• In the X-ray room, the person drinks the barium liquid. It often
has a chalky taste but can sometimes be flavored.
• A person will lie on a tilting table for part of the examination.
• In some cases, a person will be given an injection to relax their
stomach.
• A person will be standing for some parts of the examination,
and lying down on a tilting table for other parts. This allows the
liquid to travel through the body, and for the radiologist and
radiographer to take a selection of images.
• People do not have to stay in hospital after the test and are
free to go home as soon as it is complete. The results usually
arrive within 1-2 weeks.
• After the procedure:
o Plenty of fluids to eliminate barium
o Mild laxative or stool softener can be given
o Advise client that stool may be chalky white for 24-48° as
barium is excreted
7 | 41
Barium Enema Test (Lower GI Series)
• A barium enema is an X-ray procedure used to examine the
rectum and colon, often used as a complement to lower
gastrointestinal (GI) endoscopy.
• It is a diagnostic tool for patients with, for example, lower GI
bleeding, altered bowel habit or abdominal pain, or to screen
for polyps and colorectal cancer.
• Contraindications include: acute colitis/diverticulitis, recent
polypectomy or colonic biopsy, older patients (>70 years old),
pregnancy, suspected colon perforation or fistula; cardiac
arrest when barium enter venous circulation.
How does it work?
• Contrast is passed into the rectum
to enhance X-ray pictures of the
bowel. Barium enemas may use a
single contrast (barium only) or
double contrast (barium and air).
Double-contrast studies are more
common and successful.
• Patient Preparation
• Bowel preparation: this varies, but
often involves a period of low-residue diet and oral/laxative
washout. Preparation is vital for good views of the bowel: the
patient should receive full instructions on preparation and the
procedure.
• The radiologist should be supplied with a full patient history.
The Procedure
• The patient is cannulated and may be given intravenous
antispasmodic medication (for example hyoscine butyl
bromide) to make the procedure more comfortable and to aid
the passage of barium.
• The patient is positioned in a left lateral position on an X-ray
table.
• A digital rectal examination is then performed.
• A rectal catheter is lubricated and inserted into the rectum. This
has two connectors. One connector is for passing barium and
the other is for insufflating air.
• The patient is placed prone.
• Liquid barium is passed via a giving set into the catheter. It is
passed slowly to prevent the patient experiencing discomfort
or an urge to defecate.
• X-ray screening takes place as the barium is passed so the
radiologist can observe filling. The amount instilled depends on
the patient. The radiologist stops once the rectum is filled and
the barium continues to pass around the colon. The radiologist
may change the patient’s position as necessary in order to aid
filling.
• Once the contrast reaches the splenic flexure, the patient
returns to the prone position and air is insufflated. As air enters,
the colon inflates and the images of the mucosa become
clearer.
• Radiography staff may assist in moving the patient to aid filling
and to provide reassurance.
• Screening continues until the radiologist identifies the caecum,
by seeing the appendix or by seeing barium entering the small
bowel.
• Once the entire colon is filled further pictures are taken in
individual positions to obtain complete views.
• The radiographer ensures all pictures are valid.
• The rectum is emptied of barium and the catheter removed.
• The patient passes barium for several hours after the
procedure.
• After the procedure:
o Advise client to drink plenty of water to assist in eliminating
the barium (chalky white stool for 24-72° until all barium is
expelled) and laxatives can be given.
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Risks and side effects
• Patients may feel nauseous after a barium swallow test or
become constipated. Drinking lots of fluids can help to relieve
constipation. Symptoms of nausea should improve as the
barium passes through the system.
• It is normal for people to have white-colored stools the first few
times they use the toilet after having a barium swallow test.
• Some people might worry about being exposed to radiation as
part of the X-ray process. However, the amount of radiation a
person is exposed to is minimal.
• Sometimes, the injection given to relax the stomach can cause
temporary blurred vision.
Special considerations
• People should not have a barium swallow test if they are
pregnant.
• If someone has glaucoma or heart problems and needs to
have a barium swallow, the doctor may not give the stomach-
relaxing injection.
• If someone has diabetes then the doctor will schedule a
morning appointment for the barium swallow.
• People who use insulin will be asked to miss their morning dose
and maybe the previous evening’s dose. They should bring
their insulin and some food to have after the test. However,
those who take long-acting insulin should continue taking this.
Major Complications
• Colonic perforation, Hemorrhage, Oversedation, Cardiac
arrhythmia.
Minor Complications
• Constipation, Abdominal discomfort, Rectal bleeding, Flatus.
Gastroscopy
• A gastroscopy is a procedure where a thin, flexible tube called
an endoscope is used to look inside the esophagus (gullet),
stomach and first part of the small intestine (duodenum). It's
also sometimes referred to as an upper gastrointestinal
endoscopy. The endoscope has a light and a camera at one
end. The camera sends images of the inside of your esophagus,
stomach and duodenum to a monitor.
Why a gastroscopy may be used
• A gastroscopy can be used to:
o Investigate problems such as difficulty swallowing
(dysphagia) or persistent abdominal (tummy) pain
o Diagnose conditions such as stomach ulcers or gastro-
esophageal reflux disease (GERD)
o Treat conditions such as bleeding ulcers, a blockage in the
esophagus, non-cancerous growths (polyps) or small
cancerous tumors
• A gastroscopy used to check symptoms or confirm a diagnosis
is known as a diagnostic gastroscopy. A gastroscopy used to
treat a condition is known as a therapeutic gastroscopy.
The gastroscopy procedure
• A gastroscopy often takes less than 15 minutes, although it may
take longer if it's being used to treat a condition.
• It's usually carried out as an outpatient procedure, which
means you won't have to spend the night in hospital.
• Before the procedure, your throat will be numbed with a local
anesthetic spray. You can also choose to have a sedative, if
you prefer. This means you will still be awake, but will be drowsy
and have reduced awareness about what's happening.
• The doctor carrying out the procedure will place the
endoscope in the back of your mouth and ask you to swallow
the first part of the tube. It will then be guided down your
esophagus and into your stomach.
8 | 41
• The procedure shouldn't be painful, but it may be unpleasant
or uncomfortable at times.
What are the risks?
• A gastroscopy is a very safe procedure, but like all medical
procedures it does carry a risk of complications. Possible
complications that can occur include:
o A reaction to the sedative, which can cause problems
with your breathing, heart rate and blood pressure
o Internal bleeding
o Tearing (perforation) of the lining of your esophagus,
stomach or duodenum
Esophagogastroduodenoscopy (EGD)
• Esophagogastroduodenoscopy (EGD) is a test to examine the
lining of the esophagus, stomach, and first part of the small
intestine (the duodenum).
How the Test is Performed
EGD is done in a hospital or medical center. The procedure uses an
endoscope. This is a flexible tube with a light and camera at the
end. The procedure is done as follows:
• During the procedure, breathing, heart rate, blood pressure,
and oxygen level are checked. Wires are attached to certain
areas of the body and then to machines that monitor these
vital signs.
• The patient receives medicine into a vein to help you relax. The
patient should feel no pain and not remember the procedure.
• A local anesthetic may be sprayed into the mouth to prevent
you from coughing or gagging when the scope is inserted.
• A mouth guard is used to protect the teeth and the scope.
Dentures must be removed before the procedure begins.
• The patient then lies on left side.
• The scope is inserted through the esophagus (food pipe) to the
stomach and duodenum. The duodenum is the first part of the
small intestine.
• Air is put through the scope to make it easier for the doctor to
see.
• The lining of the esophagus, stomach, and upper duodenum is
examined. Biopsies can be taken through the scope. Biopsies
are tissue samples that are looked at under the microscope.
• Different treatments may be done, such as stretching or
widening a narrowed area of the esophagus.
• After the test is finished, the client will not be able to have food
and liquid until their gag reflex returns (so you do not choke).
• The test lasts about 30 to 60 minutes.
• Before the Procedure
o Commonly used medications: Midazolam HCL,
Meperedine (Demerol) Sedation, Fentanyl, Atropine - dry
secretions, Local anesthetic - sprayed to inactivate gag
reflex & facilitate passage of tube
o Client is place in left lateral decubitus (Sim’s or side-lying)
position during the procedure.
• After the procedure
o Monitor VS q30mins until sedation wears off; put siderails up
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o NPO until gag reflex returns (usually in 1-2°) to avoid • No sedation is required
aspiration • Inform the client that mild gas pain & flatulence may be
o Monitor for signs of perforation: Pain, Bleeding, Fever experienced from the air instilled into the rectum during the
procedure.
Major Complications • If biopsy was obtained, a small amount of bleeding may be
• Colonic perforation, Hemorrhage, Oversedation, Cardiac observed; instruct the client that excessive bleeding should be
arrhythmia. reported immediately to the health care provider.

Minor Complications Gastric Analysis

• Constipation, Abdominal discomfort, Rectal bleeding, Flatus. • Measures the HCL & pepsin content for evaluation of
aggressive gastric & duodenal disorders (Zollinger-Ellison
Percutaneous Transhepatic Cholangiography (PTC) syndrome)
• Iodinated dye instilled via a percutaneous needle inserted • Alcohol, tobacco & medications that may affect gastric
through the liver into the intrahepatic ducts (needle is inserted secretion are avoided for 24° before the study
under x-ray visualization) • NGT is inserted & gastric residual contents are aspirated
• Rarely done as a diagnostic procedure anymore
• After the procedure: client is placed on the right side; observe Ultrasound
for signs of bleeding, hematoma, ecchymosis or bile leakage • Sound waves are passed through the body via a transducer
and echoes are converted into images and photograph for
Computed Tomography (CT Scan) analysis
• Noninvasive cross-sectional x-ray visualization detecting tissue • Commonly used to image soft tissues such as liver, spleen, the
densities & abnormalities in the abdomen & the structures in it pancreas, gallbladder (biliary system)
• Performed with (ask about allergies to seafood & iodine!!!) or • Full bladder is necessary for accurate visualization (1-2 l of fluid)
without contrast medium
• No particular follow-up care is needed after a CT scan unless Blood Tests
sedatives were administered; monitor VS until client is fully • CBC – GI bleeding; anemia
awake • PT – liver damage; prolonged PT (liver is the main site of all
proteins involved in coagulation)
Endoscopy • Serum é – GI malabsorption, excessive vomiting or diarrhea
• Direct visualization of the GI tract by means of a flexible • AST, ALT – liver disorders (ex; viral hepatitis)
fiberoptic endoscope • Serum amylase & lipase – best indicator of acute pancreatitis
• Usually done to evaluate bleeding, ulceration, inflammation, if elevated within 24° - 5 days
masses, tumors & cancerous lesions • Bilirubin – important in the evaluation of liver & biliary tract
functioning
Endoscopic Retrograde Cholangiopancreatography (ERCP)
• Serum ammonia – hepatic function; ammonia is normally used
• Visual and radiographic examination of the liver, gallbladder, to rebuild a.a. or is converted to urea for excretion
bile ducts & pancreas to identify cause & location of
obstruction; after cannula is inserted into the common bile Urine Tests
duct, radio-opaque dye is inserted followed by several x-ray • Urine amylase – acute pancreatitis; remains high even after
images serum levels return to normal
• Physician may perform a papillotomy, a small incision in the • Urobilinogen – hepatic & biliary obstruction
sphincter around the ampulla of vater, to remove gallstones
preparation: same as endoscopy Stool Tests
• FOBT (Fecal Occult Blood Test) – G.I. bleeding
Colonoscopy • Parasitic infection
• Endoscopic examination of the large bowel • Fecal fats (steatorrhea & malabsorption)
• Use to evaluate the cause of chronic diarrhea, locate the
source of bleeding, obtain tissue biopsy specimens or remove Plain abdominal X-ray Flat plate of abdomen
polyps • Masses, tumors & strictures or obstructions
• Preparation: • No special preparation of the client required
o Liquid diet for 12-24°, NPO 6-8° before the procedure
o Clean the bowel the evening before the procedure TERMINOLOGIES
(laxatives, suppositories, cleansing enemas) 1. Dyspepsia: Difficult digestion
o Sedation of client 2. Emesis (vomiting): Stomach contents expelled through the
o Atropine sulfate is kept available in case of bradycardia mouth
resulting from vasovagal response 3. Eructation: Act of belching or raising gas from stomach
• After the procedure: 4. Gastric ulcer: Lesion on wall of stomach; also known as peptic
o Check VS q15mins until stable; siderails up; observe signs of ulcer
perforation (pain & hemorrhage) 5. Gastritis: Inflammation of the stomach
6. Gastrodynia: Pain in the stomach
Proctosigmoidoscopy 7. Hematemesis: Vomiting of blood
• Endoscopic examination of the rectum & sigmoid colon using 8. Hiatal hernia: Protrusion of part of the stomach through the
flexible or rigid scope esophageal opening into diaphragm
• Purpose: screen for colon cancer, investigate source of GI 9. Hyperemesis: Excessive vomiting
bleeding, diagnose or monitor inflammatory bowel disease 10. Nasogastric: Pertaining to nose and stomach
• Preparation: liquid diet for at least 24° before the procedure; 11. Nausea: Urge to vomit
laxative (evening), cleansing enema (a.m. Before the 12. Regurgitation: Return of solids and fluids to mouth from stomach
procedure) 13. Ulcer: Sore or lesion of mucous membrane or skin
• Position: left side in the knee-chest position

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 NCMB316 – PRELIM
14. The liver, pancreas, and gallbladder all experience their own
specific conditions, the most common of which is good, old-
fashioned, often-painful gallstones.
15. Calculus (plural is calculi): Stones
16. Cholelithiasis: Condition of having gallstones
17. Duodenal ulcer: Erosion or ulceration in the lining of the
duodenum (first portion of the small intestine)
18. Gallstones: Hard collections of bile that form in gallbladder and
bile ducts
19. Hepatomegaly: Enlargement of liver
20. Hepatoma: Tumor of liver
DISEASES OF THE UPPER GASTROINTESTINAL TRACT
I. Gastroesophageal Reflux Disease (GERD)
• Some degree of gastroesophageal reflux (backflow of gastric
or duodenal contents into the esophagus resulting to
inflammatory changes of the esophageal mucosa) is normal in
both adults and children. Excessive reflux may occur because
of an incompetent lower esophageal sphincter, pyloric
stenosis, or a motility disorder. The incidence of GERD seems to
increase with aging.
• Hallmark of GERD: reflux esophagitis (acute symptoms of
inflammation)
Causes
• Inappropriate relaxation of the LES/ decrease tone of LES
• Gastric volume or intra-abdominal pressure is elevated
• Delayed gastric emptying
Assessment Findings
• Heartburn
o Substernal or retro- sternal burning sensation
o Pain radiates to the neck, jaw, back (mimic ANGINA or MI)
• Regurgitation
o Warm fluid traveling up the throat (sour or bitter taste)
o Danger for aspiration (note for crackles in the lungs)
• Hypersalivation “water brash”
• Dysphagia (Difficulty of swallowing)
• Odynophagia (Painful swallowing)
• Barrett’s epithelium
o Change of the normal squamous cell epithelium to
columnar epithelium
o More resistant to acid as a result of healing process
brought about by the inflammation
o Considered pre-malignant (high risk of cancer) in clients
with prolonged GERD
• Pyrosis (burning sensation in the esophagus)
• Dyspepsia (indigestion)
• Esophagitis
Other manifestations
• Chronic cough especially at night (due to position), asthma
• Eructation (belching)
• Flatulence (gas)
• Bloating after eating
• Nausea & Vomiting
10 | 41
Diagnostic Findings
• Diagnostic testing may include an endoscopy or barium
swallow to evaluate damage to the esophageal mucosa.
Ambulatory 12- to 36-hour esophageal pH monitoring is used to
evaluate the degree of acid reflux. Bilirubin monitoring (Bilitec)
is used to measure bile reflux patterns. Exposure to bile can
cause mucosal damage.
• Most accurate method: 24-hour ambulatory pH monitoring –
small catheter is placed through the nose into the distal
esophagus, pH is continuously monitored & recorded)
• Endoscopy (esophagogastroduodenoscopy)
• Esophageal manometry “motility testing” – water-filled
catheters are inserted via the client’s nose or mouth & slowly
withdrawn while measurements of LES pressure & peristalsis are
recorded); not specific enough to establish a diagnosis of
GERD
Management
• Management begins with teaching the patient to avoid
situations that decrease lower esophageal sphincter pressure
or cause esophageal irritation.
• Diet Therapy
o The patient is instructed to eat a low-fat diet; to avoid
caffeine, tobacco, beer, milk, foods containing
peppermint or spearmint, and carbonated beverages
o Limit or eliminate foods that decrease LES pressure
(chocolate, fatty foods, caffeinated beverages such as
coffee, tea, & cola, peppermints, alcohol)
o Restrict spicy & acidic foods (orange juice, tomatoes)
o Carbonated beverages increase pressure in the stomach
• Lifestyle changes
o Sleep in the left lateral (side-lying) position to minimize the
nighttime episodes of reflux
o avoid eating or drinking 2 hours before bedtime; maintain
normal body weight; avoid tight-fitting clothes; elevate
the head of the bed on 6- to 8-inch (15- to 20-cm) blocks;
and elevate the upper body on pillows.
• If reflux persists, antacids or H2 receptor antagonists, such as
famotidine (Pepcid), nizatidine (Axid), or ranitidine (Zantac),
may be prescribed.
o Antacids – neutralizes HCL & deactivating pepsin
(Aluminum Hydroxide, Magnesium Hydroxide, Maalox,
Mylanta)
o Histamine2 (H2) Receptor Antagonist – decrease acid
production of parietal cells (Famotidine, Ranitidine
(Zantac), Cimetidine (Tagamet), Nizatidine)
• Proton pump inhibitors (medications that decrease the release
of gastric acid, such as lansoprazole [Prevacid], rabeprazole
[AcipHex], esomeprazole [Nexium], omeprazole [Prilosec], and
pantoprazole [Protonix]) may be used; however, these
products may increase intragastric bacterial growth and the
risk of infection.
o Main treatment for GERD
o Inhibition of proton pump of the parietal cell thereby
decreases acid secretion
• In addition, the patient may receive prokinetic agents, which
accelerate gastric emptying. These agents include
bethanechol (Urecholine), domperidone (Motilium), and
metoclopramide (Reglan). Because metoclopramide
(increases gastric emptying) can have extrapyramidal side
effects that are increased in certain neuromuscular disorders,
such as Parkinson’s disease, it should be used only if no other
option exists, and the patient should be monitored closely.
• If medical management is unsuccessful, surgical intervention
may be necessary. Surgical management involves a Nissen
fundoplication (wrapping of a portion of the gastric fundus
around the sphincter area of the esophagus).
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• A Nissen fundoplication can be performed by the open
method or by laparoscopy.
• Endoscopic Therapy
o Stretta procedure – the physician applies radiofrequency
energy through needles placed near gastroesophageal
junction inhibiting the vagus nerve thus reducing the
discomfort of the client. It will reshape the ring of muscles
in the lower esophagus.
II. Gastritis
• Gastritis is inflammation of
the stomach mucosa.
• The incidence of gastritis is
highest in the fifth and sixth
decades of life; men are
more frequently affected
than women. The
incidence is greater in
clients who are heavy
drinkers and smokers.
Acute Gastritis
• Acute gastritis lasts several hours to a few days and is often
caused by dietary indiscretion (eating irritating food that is
highly seasoned or food that is infected). Other causes include
excessive use of aspirin and other nonsteroidal anti-
inflammatory drugs (NSAIDs), excessive alcohol intake, bile
reflux, and radiation therapy. A more severe form of acute
gastritis is caused by strong acids or alkali, which may cause
the mucosa to become gangrenous or to perforate. Gastritis
may also be the first sign of acute systemic infection.
Etiology and Risk Factors
• It usually stems from ingestion of a corrosive, erosive, or
infectious substance.
• Aspirin and other non-steroidal anti-inflammatory drugs
(NSAIDs), chemotherapeutic drugs, steroids, acute alcoholism
and food poisoning (typically caused by Staphylococcus
organisms) are common causes.
• Food substances including excessive amounts of tea,
carbonated drinks and pepper can precipitate acute gastritis.
Foods with a rough texture or those eaten at an extremely high
temperature can also damage the stomach mucosa.
• Acute gastritis is usually of short duration unless the gastric
mucosa has suffered extensive damage.
Pathophysiology
• The mucosal lining of the stomach normally protects it from the
action of gastric acid. This mucosal barrier is composed of
prostaglandins.
Due to any cause
↓ •
This barrier is penetrated
↓ older adults.
Hydrochloric acid comes into contact with the mucosa
↓ Pathophysiology
Injury to small vessels
↓ then becomes thin and atrophic.
Edema, hemorrhage, and possible ulcer formation
Clinical Manifestation
• Epigastric discomfort, feeling of fullness, early satiety, cramping
Belching (burping), flatulence, severe nausea and vomiting,
hematemesis.
• Sometimes GI bleeding is the only manifestation.
• When contaminated food is the cause of gastritis, diarrhea
usually develops within 5 hours of ingestion.
11 | 41
Diagnostic Findings
• Diagnosis is based on a detailed history of food intake,
medications taken, and any disorder related to gastritis.
• The physician may also perform a gastroscopy.
Medical Management
• Anti – emetic drugs like Inj. Perinorm or Tab, Domperidone are
frequently effective in vomiting.
• Antacids, H2 Blockers like cimetidine, Ranitidine, or Famotidine
are effective to reduce the pain.
• 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.
Diet Therapy
• Initially foods and fluids are withheld until nausea and vomiting
subside.
• Once the client tolerates food, the diet includes decaffeinated
tea, gelatin, toast, and simple bland foods.
• The client should avoid spicy foods, caffeine and large, heavy
meals.
• In the continued absence of nausea, vomiting and bloating,
the client can slowly return to a normal diet.
Chronic Gastritis
• Chronic gastritis is a prolonged inflammation of the stomach
that may be caused either by benign or malignant ulcers of the
stomach or by bacteria such as Helicobacter pylori. Chronic
gastritis may be associated with autoimmune diseases such as
pernicious anemia, dietary factors such as caffeine, the use of
medications such as NSAIDs or bisphosphonates (eg,
alendronate [Fosamax], risedronate [Actonel], ibandronate
[Boniva]), alcohol, smoking, or chronic reflux of pancreatic
secretions and bile into the stomach. Superficial ulceration may
occur and can lead to hemorrhage.
• 3 forms
o Superficial gastritis, which causes a reddened, edematous
mucosa with small erosions and hemorrhages.
o Atrophic gastritis, which 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.
o Hypertrophic gastritis, which produces a dull and nodular
mucosa with irregular, thickened, or nodular rugae;
hemorrhages occur frequently.
Etiological Factors
• Infection with Helicobacter pylori bacteria or gastric surgery
may lead to chronic gastritis.
• After gastric resection with a gastro- jejunostomy, bile and bile
acids may reflux into the remaining stomach, causing gastritis.
H. Pylori infection can lead to chronic atrophic gastritis.
• Age is also a risk factor; chronic gastritis is more common in
The stomach lining first becomes thickened and erythematous and
↓
Continued deterioration and atrophy
↓
Loss of function of the parietal cells
↓
Acid secretion decreases
↓
Inability to absorb vitamin B12
↓
Development of pernicious anemia
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Clinical Manifestation • If corrosion is extensive or severe, avoid emetics and lavage
• Manifestations are vague and may be absent because the
problem does not cause an increase in hydrochloric acid.
Assessment may reveal • Fiberoptic endoscopy may be necessary; emergency surgery
• Anorexia, feeling of fullness, dyspepsia, belching, vague
epigastric pain, nausea, vomiting, intolerance of spicy and
fatty foods
Complications
• Bleeding, Pernicious anemia, Gastric cancer
Medical Management
• Discomfort may lessen with a bland diet, small frequent meals,
antacids, H2 receptor antagonists, proton pump inhibitors, and • Reducing Anxiety
avoidance of food that cause manifestations.
• If H. pylori bacteria are present, anti-biotics and other
medications are administered to eliminate the bacteria.
• If 1 week of this regimen does not succeed in eliminating the
bacteria, the regimen may be repeated for an additional
week.
• If pernicious anemia develops, intramuscular injections of
vitamin B12 may be administered monthly for the remainder of
the client’s life.
• Promoting Optimal Nutrition
Nursing Management
• Nursing Diagnosis:
o Acute pain related to irritated stomach mucosa.
o Imbalanced nutrition, less than body requirement, related
to inadequate intake of nutrition.
o Risk for imbalanced fluid volume related to insufficient fluid
intake and excessive fluid loss subsequent to vomiting.
o Anxiety related to treatment.
o Deficient knowledge about dietary management and
disease process.
Clinical Manifestations
• Acute Gastritis
o May have rapid onset of symptoms: abdominal
discomfort, headache, lassitude, nausea, anorexia,
vomiting, and hiccupping • Promoting Fluid Balance
• Chronic Gastritis
o May be asymptomatic.
o Complaints of anorexia, heartburn after eating, belching,
a sour taste in the mouth, or nausea and vomiting.
o Patients with chronic gastritis from vitamin deficiency
usually have evidence of malabsorption of vitamin B12.
Assessment and Diagnostic Findings
• Gastritis is sometimes associated with achlorhydria or • Relieving Pain
hypochlorhydria (absence or low levels of hydrochloric acid) or
with high acid levels.
• Upper gastrointestinal (GI) x-ray series, endoscopy.
• Biopsy with histologic examination is performed.
• Serologic testing for antibodies to the H. pylori antigen and a
breath test may be performed.
Medical Management: Acute Gastritis
• The gastric mucosa is capable of repairing itself after an • A peptic ulcer is an excavation
episode of gastritis. As a rule, the patient recovers in about 1
day, although the appetite may be diminished for an
additional 2 or 3 days. The patient should refrain from alcohol
and eating until symptoms subside. Then the patient can
progress to a nonirritating diet. If symptoms persist, intravenous
fluids may be necessary. If bleeding is present, management is
similar to that of upper GI tract hemorrhage. If gastritis is due to
ingestion of strong acids or alkali, dilute and neutralize the acid
with common antacids (e.g., aluminum hydroxide); neutralize
alkali with diluted lemon juice or diluted vinegar.
12 | 41
because of danger of perforation. Supportive therapy may
include nasogastric intubation, analgesic agents and
sedatives, antacids, and IV fluids.
may be required to remove gangrenous or perforated tissue;
gastric resection (gastrojejunostomy) may be necessary to
treat pyloric obstruction. Chronic Gastritis Diet modification,
rest, stress reduction, avoidance of alcohol and NSAIDs, and
pharmacotherapy are key treatment measures. Gastritis
related to H. pylori infection is treated with selected drug
combinations.
Nursing Management
o Carry out emergency measures for ingestion of acids or
alkalies.
o Offer supportive therapy to patient and family during
treatment and after the ingested acid or alkali has been
neutralized or diluted.
o Prepare patient for additional diagnostic studies
(endoscopy) or surgery.
o Calmly listen to and answer questions as completely as
possible; explain all procedures and treatments.
o Provide physical and emotional support for patients with
acute gastritis.
o Help patient manage symptoms (e.g., nausea, vomiting,
heartburn, and fatigue).
o Avoid foods and fluids by mouth for hours or days until
acute symptoms subside.
o Offer ice chips and clear liquids when symptoms subside.
o Encourage patient to report any symptoms suggesting a
repeat episode of gastritis as food is introduced.
o Discourage caffeinated beverages (caffeine increases
gastric activity and pepsin secretion), alcohol, and
cigarette smoking (nicotine inhibits neutralization of gastric
acid in the duodenum).
o Refer patient for alcohol counseling and smoking
cessation when appropriate.
o Monitor daily intake and output for dehydration (minimal
intake of 1.5 L/day and urine output of 30 mL/h). Infuse
intravenous fluids if prescribed.
o Assess electrolyte values every 24 hours for fluid
imbalance.
o Be alert for indicators of hemorrhagic gastritis
(hematemesis, tachycardia, hypotension), and notify
physician.
o Instruct patient to avoid foods and beverages that may
be irritating to the gastric mucosa.
o Instruct patient in the correct use of medications to relieve
chronic gastritis.
o Assess pain and attainment of comfort through use of
medications and avoidance of irritating substances
III. Peptic Ulcer
formed in the mucosal wall of
the stomach, pylorus,
duodenum, or esophagus. It is
frequently referred to as a
gastric, duodenal, or
esophageal ulcer, depending
on its location. It is caused by
the erosion of a circumscribed
area of mucous membrane.
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Peptic ulcers are more likely to be in the duodenum than in the
stomach. They tend to occur singly, but there may be several
present at one time.
• It is an open sore that occurs in the protective lining of the
stomach (gastric ulcer), esophagus (esophageal ulcer) or
duodenum (duodenal ulcer). It can be caused by bacterial
infection, the use of some medications or other factors.
• Chronic ulcers usually occur in the lesser curvature of the
stomach, near the pylorus. Peptic ulcer has been associated
with bacterial infection, such as Helicobacter pylori. The
greatest frequency is noted in people between the ages of 40
and 60 years. After menopause, the incidence among women
is almost equal to that in men. Predisposing factors include
family history of peptic ulcer, blood type O, chronic use of
nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol
ingestion, excessive smoking, and, possibly, high stress.
• Esophageal ulcers result from the backward flow of
hydrochloric acid from the stomach into the esophagus.
Zollinger–Ellison syndrome (gastrinoma) is suspected when a
patient has several peptic ulcers or an ulcer that is resistant to
standard medical therapy. This syndrome involves extreme
gastric hyperacidity (hypersecretion of gastric juice), duodenal
ulcer, and gastrinomas (islet cell tumors). About 90% of tumors
are found in the gastric triangle. About one third of gastrinomas
are malignant. Diarrhea and steatorrhea (unabsorbed fat in
the stool) may be evident. These patients may have coexistent
parathyroid adenomas or hyperplasia and exhibit signs of
hypercalcemia. The most frequent complaint is epigastric pain.
• The presence of H. pylori is not a risk factor. Stress ulcer (not to
be confused with Cushing’s or Curling’s ulcers) is a term given
to acute mucosal ulceration of the duodenal or gastric area
that occurs after physiologically stressful events, such as burns,
shock, severe sepsis, and multiple organ trauma. Fiberoptic
endoscopy within 24 hours of trauma or injury shows shallow
erosions of the stomach wall; by 72 hours, multiple gastric
erosions are observed, and as the stressful condition continues,
the ulcers spread. When the patient recovers, the lesions are
reversed; this pattern is typical of stress ulceration.
Gastric Ulcer: Causes
• Break in the mucosal barrier
o Mucus & bicarbonate secretion (1st line of defense in pH
maintenance)
o Gastromucosal PG (increase barrier resistance to
ulceration)
o Adequate blood supply
o Pyloric sphincter dysfunction (bile may enter stomach &
cause damage to lipid plasma membrane of gastric
mucosa)
o Delayed gastric emptying
o H. pylori infection
• Note: There is normal gastric acid secretion!!!
Duodenal ulcer: causes
• Rapid emptying of food in the stomach
• Acid-bolus delivery, reduce buffering effect of food to
duodenum
• Increase secretion of acid is triggered also by CHON rich food,
Ca++, vagal excitation
• H. pylori produces urease
• Urease hydrolyzes urea to ammonia
• H+ ions are released in response to the presence of ammonia
→ further gastric mucosal damage
Other factors that contribute PUD:
• Drugs (aspirin, ibuprofen), cigarette smoking, chronic anxiety,
Type A personality
13 | 41
Clinical Manifestations
• Symptoms of an ulcer may last days, weeks, or months and may
subside only to reappear without cause. Many patients have
asymptomatic ulcers.
• Dull, gnawing pain and a burning sensation in the
midepigastrium or in the back are characteristic.
• Pain is relieved by eating or taking alkali; once the stomach has
emptied or the alkali wears off, the pain returns.
• Sharply localized tenderness is elicited by gentle pressure on
the epigastrium or slightly right of the midline.
• Other symptoms include pyrosis (heartburn) and a burning
sensation in the esophagus and stomach, which moves up to
the mouth, occasionally with sour eructation (burping).
• Vomiting is rare in uncomplicated duodenal ulcer; it may or
may not be preceded by nausea and usually follows a bout of
severe pain and bloating; it is relieved by ejection of the acid
gastric contents.
• Constipation or diarrhea may result from diet and medications.
• Bleeding (15% of patients with gastric ulcers) and tarry stools
may occur; a small portion of patients who bleed from an
acute ulcer have only very mild symptoms or none at all.
Complications of PUD
• Hemorrhage – most serious complications; hematemesis
(coffee-ground blood) usually indicates upper GI bleeding
• Perforation – surgical EMERGENCY!!!
• Gastroduodenal contents leak into the surrounding abdomen
• Sharp pain, client becomes apprehensive assuming knee-chest
position, chemical peritonitis occurs, bacterial septicemia &
hypovolemic shock follows.
• Peristalsis diminishes & paralytic ileus develops.
Assessment and Diagnostic Methods
• Physical examination (epigastric tenderness, abdominal
distention).
• Endoscopy (preferred, but upper gastrointestinal [GI] barium
study may be done) reveals ulceration; biopsy is usually done
to detect H. pylori infection & to rule out malignancy.
• Diagnostic tests include analysis of stool specimens for occult
blood ((+) occult blood in stool specimen test), gastric
secretory studies, and biopsy and histology with culture to
detect H. pylori (serologic testing, stool antigen tests, or a
breath
• ↓ Hgb/Hct (indicates bleeding)
• Gastric analysis: normal gastric acidity in gastric ulcer (↑ in
duodenal ulcer.
Medical Management
• The goals of treatment are to eradicate H. pylori and manage
gastric acidity.
Pharmacologic Therapy
• Antibiotics combined with proton pump inhibitors and bismuth
salts to suppress H. pylori.
• H2-receptor antagonists (in high doses in patients with Zollinger–
Ellison syndrome) to decrease stomach acid secretion;
maintenance doses of H2-receptor antagonists are usually
recommended for 1 year. Proton pump inhibitors may also be
prescribed.
• Cytoprotective agents (protect mucosal cells from acid or
NSAIDs).
• Antacids in combination with cimetidine (Tagamet) or
ranitidine (Zantac) for treatment of stress ulcer and for
prophylactic use. Lifestyle Changes
• Stress reduction and rest are priority interventions. The patient
needs to identify situations that are stressful or exhausting (e.g.,
rushed lifestyle and irregular schedules) and implement
changes, such as establishing regular rest periods during the
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day in the acute phase of the disease. Biofeedback, hypnosis,
behavior modification, massage, or acupuncture may also be
useful.
• Smoking cessation is strongly encouraged because smoking
raises duodenal acidity and significantly inhibits ulcer repair.
Support groups may be helpful.
• Dietary modification may be helpful. Patients should eat
whatever agrees with them; small, frequent meals are not
necessary if antacids or histamine blockers are part of therapy.
Over secretion and hypermotility of the GI tract can be
minimized by avoiding extremes of temperature and
overstimulation by meat extracts. Alcohol and caffeinated
beverages such as coffee (including decaffeinated coffee,
which stimulates acid secretion) should be avoided. Diets rich
in milk and cream should be avoided also because they are
potent acid stimulators. The patient is encouraged to eat three
regular meals a day
Surgical Management
• With the advent of H2-receptor antagonists, surgical
intervention is less common.
• If recommended, surgery is usually for intractable ulcers
(particularly with Zollinger–Ellison syndrome), life threatening
hemorrhage, perforation, or obstruction.
• Gastroduodenostomy (Billroth I): distal end of the stomach is
removed, and the remainder is anastomosed to the
duodenum.
• Gastrojejunostomy (Billroth II): removal of the antrum and distal
portion of the stomach and duodenum with anastomosis of the
remaining portion of the stomach to the jejunum
• Vagotomy: Transection of vagus nerve that eliminates the acid
secreting stimulus to gastric cells & causing a decrease gastric
acid secretion.
• Pyloroplasty: performed in conjunction with vagotomy to
widen the exit of pylorus to facilitate emptying of stomach
contents
• Subtotal Gastrectomy: removal of 75% - 85% of the stomach
• Antrectomy: removal of the antrum of the stomach to eliminate
the gastric phase of digestion
• Gastroenterostomy: creating a passage between the body of
the stomach & the jejunum to permit neutralization of gastric
acid by regurgitation of alkaline duodenal contents into the
stomach
• Esophagojejunostomy (total gastrectomy): removal of the
entire stomach with a loop of jejunum anastomosed to the
esophagus.
Routine preoperative nursing care
• Informed consent, NPO, Medications
Postoperative nursing care
• Provide routine post-op care
• Ensure adequate function of NG tube
• Measure drainage accurately to determine necessity for fluid
and electrolyte replacement; notify physician if there is no
drainage. Anticipate frank, red bleeding for 12-24°; Do not
manipulate the tube and ensure its patency
• Promote adequate pulmonary ventilation
• Place client in mid- or high-Fowler’s position to promote chest
expansion; Teach client to splint high upper abdominal incision
before turning, coughing, and deep breathing
• Promote adequate nutrition.
o After removal of NG tube, provide clear liquids with
gradual introduction of small amounts of bland food at
frequent intervals; Monitor weight daily. Assess for
regurgitation; if present, instruct client to eat smaller
amounts of food at a slower pace
• Provide client teaching and discharge planning concerning
14 | 41
o Gradually increasing food intake until able to tolerate 3-
meals/day
o Daily monitoring of weight
o Stress-reduction measures
o Need to report signs of complications to physician
immediately (hematemesis, vomiting, diarrhea, pain,
melena, weakness, feeling of abdominal
fullness/distension)
o Methods of controlling
Nursing Process the Patient with Peptic Ulcer
• Assessment
o Assess pain and methods used to relieve it; take a
thorough history, including a 72-hour food intake history.
o If patient has vomited, determine whether emesis is bright
red or coffee ground in appearance. This helps identify
source of the blood.
o Ask patient about usual food habits, alcohol, smoking,
medication use (NSAIDs), and level of tension or
nervousness.
o Ask how patient expresses anger (especially at work and
with family), and determine whether patient is
experiencing occupational stress or family problems.
o Obtain a family history of ulcer disease.
o Assess vital signs for indicators of anemia (tachycardia,
hypotension).
o Assess for blood in the stools with an occult blood test.
o Palpate abdomen for localized tenderness.
• Diagnosis Nursing Diagnoses
o Acute pain related to the effect of gastric acid secretion
on damaged tissue
o Anxiety related to coping with an acute disease
o Imbalanced nutrition related to changes in diet
o Deficient knowledge about preventing symptoms and
managing the condition
• Collaborative Problems/Potential Complications
o Hemorrhage: upper GI
o Perforation
o Penetration
o Pyloric obstruction (gastric outlet obstruction)
• Planning and Goals
o The major goals of the patient may include relief of pain,
reduced anxiety, maintenance of nutritional requirements,
knowledge about the management and prevention of
ulcer recurrence, and absence of complications.
Nursing Interventions
• Relieving Pain and Improving Nutrition
o Administer prescribed medications.
o Avoid aspirin, which is an anticoagulant, and foods and
beverages that contain acid-enhancing caffeine (colas,
tea, coffee, chocolate), along with decaffeinated coffee.
o Encourage patient to eat regularly spaced meals in a
relaxed atmosphere; obtain regular weights and
encourage dietary modifications.
o Encourage relaxation techniques.
• Reducing Anxiety
o Assess what patient wants to know about the disease, and
evaluate level of anxiety; encourage patient to express
fears openly and without criticism.
o Explain diagnostic tests and administering medications on
schedule.
o Interact in a relaxing manner, help in identifying stressors,
and explain effective coping techniques and relaxation
methods.
o Encourage family to participate in care, and give
emotional support.
• Monitoring and Managing Complications
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o If hemorrhage is a concern
◦ Assess for faintness or dizziness and nausea, before or
with bleeding; test stool for occult or gross blood;
monitor vital signs frequently (tachycardia,
hypotension, and tachypnea).
◦ Insert an indwelling urinary catheter and monitor
intake and output; insert and maintain an IV line for
infusing fluid and blood.
◦ Monitor laboratory values (hemoglobin and
hematocrit).
◦ Insert and maintain a nasogastric tube and monitor
drainage; provide lavage as ordered.
◦ Monitor oxygen saturation and administering oxygen
therapy.
◦ Place the patient in the recumbent position with the
legs elevated to prevent hypotension, or place the
patient on the left side to prevent aspiration from
vomiting.
◦ Treat hypovolemic shock as indicated.
o If perforation and penetration are concerns
◦ Note and report symptoms of penetration (back and
epigastric pain not relieved by medications that were
effective in the past).
◦ Note and report symptoms of perforation (sudden
abdominal pain, referred pain to shoulders, vomiting
and collapse, extremely tender and rigid abdomen,
hypotension and tachycardia, or other signs of
shock).
IV. Dumping Syndrome
• Constellation of vasomotor symptoms after eating, especially
following after billroth II procedure
• There is rapid gastric emptying into the small intestine causing
abdominal distention (shifting of fluids to the GUT)
• Early manifestation:
o Occur w/in 30mins
o Symptoms: vertigo, tachycardia, syncope, sweating,
pallor, palpitations & desire to lie down
• Late dumping syndrome:
o Occurs 1½ - 3hrs p.c.
o Due to rapid entry of high-CHO food into the jejunum →
Hyperglycemia → ↑ insulin release → Rebound
hypoglycemia
o Symptoms: dizziness, light-headedness, palpitations,
diaphoresis & confusion
• Dietary Management:
o Decrease the amount of food taken at one time &
eliminating liquids ingested with meals
o Instruct client to consume a high-CHON (↑ colloidal
osmotic pressure), high-fat, low- to moderate-CHO diet
15 | 41
DISTURBANCES IN ABSORPTION AND ELIMINATION
I. Intestinal Obstruction
• Intestinal obstruction exists when blockage prevents the normal
flow of intestinal contents through the intestinal tract. Two types
of processes can impede this flow:
1. Mechanical obstruction
• An intraluminal obstruction or a mural obstruction from pressure
on the intestinal wall occurs. Examples are intussusception,
polypoid tumors and neoplasms, stenosis, strictures, adhesions,
hernias, and abscesses.
• Physical blockage of the passage of intestinal contents with
subsequent distension by fluid and gas.
• Causes:
o Adhesions (bands of granulation & scar tissue that
develop as a result of an inflammatory response encircling
the intestines & constricting its lumen)
o Hernias – protrusion of an organ or structure thru a
weakened abdominal muscle, can be congenital or
acquired defect
o Volvulus (twisting of the intestine)
o Intussusceptions (telescoping of a segment of the intestine
within itself)
o Inflammatory bowel disease, foreign bodies, strictures,
neoplasms, fecal impaction
2. Functional obstruction
• The intestinal musculature cannot propel the contents along
the bowel. Examples are amyloidosis, muscular dystrophy,
endocrine disorders such as diabetes mellitus, or neurologic
disorders such as Parkinson’s disease. The blockage also can
be temporary and the result of the manipulation of the bowel
during surgery. The obstruction can be partial or complete. Its
severity depends on the region of bowel affected, the degree
to which the lumen is occluded, and especially the degree to
which the vascular supply to the bowel wall is disturbed.
• “paralytic”, “neurogenic” or “adynamic ileus”
• Brought about by interference with the nerve supply to the
intestine resulting in decreased or absent peristalsis
• Causes:
o Handling of the intestine during abdominal surgery
o Hypokalemia
o Peritonitis
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o Shock Drug Therapy/Surgery

o Vascular obstructions – interference with the blood supply • Antiemetic
to a portion of the intestine, resulting in intestinal ischemia • Antispasmodic
and gangrene of the bowel; caused by an embolus, • Pain reliever- narcotic analgesic
atherosclerosis • Antibiotic
• Most bowel obstructions occur in the small intestine. Adhesions • Anthelminthic- if caused by bolus of ascaris
are the most common cause of small bowel obstruction, • Electrolyte replacement
followed by hernias and neoplasms. Other causes include • Surgery – depends on the cause
intussusception, volvulus (i.e., twisting of the bowel), and o Exploratory Laparotomy
paralytic ileus. Most obstructions in the large bowel occur in the o Removal of the tumor – with end-to-end anastomosis
sigmoid colon. The most common causes are carcinoma, o Adhesiolysis
diverticulitis, inflammatory bowel disorders, and benign tumors.
Table 38-5 and Figure 38-7 list mechanical causes of obstruction
and describe how they occur.

Small Bowel Obstruction

Pathophysiology
• Intestinal contents, fluid, and gas accumulate above the
intestinal obstruction. The abdominal distention and retention
of fluid reduce the absorption of fluids and stimulate more
gastric secretion. With increasing distention, pressure within the
intestinal lumen increases, causing a decrease in venous and
arteriolar capillary pressure. This causes edema, congestion,
necrosis, and eventual rupture or perforation of the intestinal
Assessment Findings wall, with resultant peritonitis.
• High-pitched bowel sounds above the level of the obstruction • Reflux vomiting may be caused by abdominal distention.
Decreased or absent bowel sound below the obstruction Vomiting results in loss of hydrogen ions and potassium from the
stomach, leading to reduction of chlorides and potassium in
Complete Intestinal Obstruction the blood and to metabolic alkalosis. Dehydration and acidosis
• Cardinal Signs and Symptoms develop from loss of water and sodium. With acute fluid losses,
o Abdominal pain, Abdominal distention, Vomiting, hypovolemic shock may occur.
Obstipation
• Other signs/sx Clinical Manifestations
o Malnutrition, Flatulence, Weakness, Electrolyte • The initial symptom is usually crampy pain that is wavelike and
Imbalances, Ascites colicky. The patient may pass blood and mucus but no fecal
matter and no flatus. Vomiting occurs. If the obstruction is
Diagnostic Tests complete, the peristaltic waves initially become extremely
• Flat-plate & upright abdominal x-rays reveal the presence of vigorous and eventually assume a reverse direction, with the
gas and fluid intestinal contents propelled toward the mouth instead of
• ↑ Hgb/Hct, BUN & Creatinine (indicative of dehydration) toward the rectum. If the obstruction is in the ileum, fecal
• ↓ Serum Na+, Cl-, K+ vomiting takes place. First, the patient vomits the stomach
• Sigmoidoscopy, colonoscopy, barium enema, CT scan contents, then the bile-stained contents of the duodenum and
the jejunum, and finally, with each paroxysm of pain, the
Nursing Interventions
darker, fecal-like contents of the ileum. The signs of dehydration
• Monitor F&E balance, prevent further imbalance; keep client become evident: intense thirst, drowsiness, generalized
NPO and administer IV fluids as ordered malaise, aching, and a parched tongue and mucous
• Most clients w/ an obstruction have at least an NGT. Accurately membranes.
measure the drainage from NG/intestinal tube • The abdomen becomes distended. The lower the obstruction is
• Put in fowler’s position (alleviate pressure on diaphragm) in the GI tract, the more marked the abdominal distention. If
• Encourage nasal breathing to minimize swallowing of air and the obstruction continues uncorrected, hypovolemic shock
further abdominal distension occurs from dehydration and loss of plasma volume.
• Institute comfort measures associated with NG intubation and
intestinal decompression Assessment and Diagnostic Findings
• Diagnosis is based on the symptoms described previously and
Prevent complications
on imaging studies. Abdominal x-ray and CT findings include
• Measure abdominal girth daily to assess for increasing abnormal quantities of gas, fluid, or both in the intestines.
abdominal distension Laboratory studies (i.e., electrolyte studies and a complete
• Assess for sign and symptoms of peritonitis blood cell count) reveal a picture of dehydration, loss of
• Monitor urinary output plasma volume, and possible infection.

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Medical Management
• Decompression of the bowel through a nasogastric tube is
successful in most cases. When the bowel is completely
obstructed, the possibility of strangulation and tissue necrosis
(i.e., tissue death) warrants surgical intervention. Before surgery,
IV fluids are necessary to replace the depleted water, sodium,
chloride, and potassium.
• The surgical treatment of intestinal obstruction depends on the
cause of the obstruction. For the most common causes of
obstruction, such as hernia and adhesions, the surgical
procedure involves repairing the hernia or dividing the
adhesion to which the intestine is attached. In some instances,
the portion of affected bowel may be removed and an
anastomosis performed. The complexity of the surgical
procedure depends on the duration of the intestinal
obstruction and the condition of the intestine.
Nursing Management
• Nursing management of the nonsurgical patient with a small
bowel obstruction includes maintaining the function of the
nasogastric tube, assessing and measuring the nasogastric
output, assessing for fluid and electrolyte imbalance,
monitoring nutritional status, and assessing improvement (e.g.,
return of normal bowel sounds, decreased abdominal
distention, subjective improvement in abdominal pain and
tenderness, passage of flatus or stool). The nurse reports
discrepancies in intake and output, worsening of pain or
abdominal distention, and increased nasogastric output. If the
patient’s condition does not improve, the nurse prepares him
or her for surgery. Nursing care of the patient after surgical
repair of a small bowel obstruction is similar to that for other
abdominal surgeries.
Large Bowel Obstruction
Pathophysiology
• As in small bowel obstruction, large bowel obstruction results in
an accumulation of intestinal contents, fluid, and gas proximal
to the obstruction. It can lead to severe distention and
perforation unless some gas and fluid can flow back through
the ileal valve. Large bowel obstruction, even if complete, may
be undramatic if the blood supply to the colon is not disturbed.
However, if the blood supply is cut off, intestinal strangulation
and necrosis occur; this condition is life-threatening. In the large
intestine, dehydration occurs more slowly than in the small
intestine because the colon can absorb its fluid contents and
can distend to a size considerably beyond its normal full
capacity.
• Adenocarcinoid tumors account for the majority of large
bowel obstructions. Most tumors occur beyond the splenic
flexure, making them accessible with a flexible sigmoidoscope.
Clinical Manifestations
• Large bowel obstruction differs clinically from small bowel
obstruction in that the symptoms develop and progress
relatively slowly. In patients with obstruction in the sigmoid
colon or the rectum, constipation may be the only symptom for
months. The shape of the stool is altered as it passes the
obstruction that is gradually increasing in size. Blood loss in the
stool may result in iron deficiency anemia. The patient may
experience weakness, weight loss, and anorexia. Eventually,
the abdomen becomes markedly distended, loops of large
bowel become visibly outlined through the abdominal wall,
and the patient has crampy lower abdominal pain. Finally,
fecal vomiting develops. Symptoms of shock may occur.
Assessment and Diagnostic Findings
• Diagnosis is based on symptoms and on imaging studies.
Abdominal x-ray and abdominal CT or MRI findings reveal a
17 | 41
distended colon and pinpoint the site of the obstruction. Barium
studies are contraindicated.
Medical Management
• Restoration of intravascular volume, correction of electrolyte
abnormalities, and nasogastric aspiration and decompression
are instituted immediately. A colonoscopy may be performed
to untwist and decompress the bowel. A cecostomy, in which
a surgical opening is made into the cecum, may be performed
in patients who are poor surgical risks and urgently need relief
from the obstruction. The procedure provides an outlet for
releasing gas and a small amount of drainage. A rectal tube
may be used to decompress an area that is lower in the bowel.
However, the usual treatment is surgical resection to remove
the obstructing lesion. A temporary or permanent colostomy
may be necessary. An ileoanal anastomosis may be performed
if removal of the entire large bowel is necessary.
Nursing Management
• The nurse’s role is to monitor the patient for symptoms that
indicate that the intestinal obstruction is worsening and to
provide emotional support and comfort. The nurse administers
IV fluids and electrolytes as prescribed. If the patient’s condition
does not respond to nonsurgical treatment, the nurse prepares
the patient for surgery. This preparation includes preoperative
teaching as the patient’s condition indicates. After surgery,
general abdominal wound care and routine postoperative
nursing care are provided.
II. Regional Enteritis (Crohn’s Disease)
• Regional enteritis is a subacute and chronic inflammation of
the gastrointestinal (GI) tract wall that extends through all
layers. Crohn’s disease is usually first diagnosed in adolescents
or young adults but can appear at any time of life. Although
the most common areas in which it is found are the distal ileum
and colon, it can occur anywhere along the GI tract. Fistulas,
fissures, and abscesses form as the inflammation extends into
the peritoneum. In advanced cases, the intestinal mucosa has
a cobblestone like appearance. As the disease advances, the
bowel wall thickens and becomes fibrotic and the intestinal
lumen narrows. The clinical course and symptoms vary. In some
patients, periods of remission and exacerbation occur, but in
others, the disease follows a fulminating course.
• An idiopathic inflammatory disease of the small intestine (60%),
the colon (20%), or both
• Terminal ileum: the site most often affected
• Causes:
o Unknown, thought to be autoimmune
o M. paratuberculosis
o Genetic predisposition (1st degree & identical twins)
Pathology
• Deep fissures & ulceration develops → bowel fistulas → diarrhea
& malabsorption
• Chronic pathologic changes include thickening of the bowel
wall → narrowed lumen & strictures → obstruction
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Clinical Manifestations Rectal 20% 100%

• Onset of symptoms is usually insidious, with prominent right involvement
lower quadrant abdominal pain and diarrhea unrelieved by Diarrhea 5 – 6 soft loose stool/ 20 – 30 watery stool/
defecation. day day
• Abdominal tenderness and spasm. Abdominal + +
• Crampy pains occur after meals; the patient tends to limit pain
intake, causing weight loss, malnutrition, and secondary Weight loss + +
anemia. Intervention TPN Diet, TPN
• Chronic diarrhea may occur, resulting in a patient who is Steroids Steroids
uncomfortable and is thin and emaciated from inadequate Azulfidine Azulfidine
food intake and constant fluid loss. The inflamed intestine may (Sulfasalazine) (Sulfasalazine)
perforate and form intra-abdominal and anal abscesses. Ileostomy Ileostomy
• Fever and leukocytosis occur. Proctocolectomy
• Abscesses, fistulas, and fissures are common. Crohn’s Disease VS Ulcerative Colitis
• Symptoms extend beyond the GI tract to include joint disorders
(e.g., arthritis), skin lesions (e.g., erythema nodosum), ocular
disorders (e.g., conjunctivitis), and oral ulcers.
• Abdominal distention, masses, visible peristalsis
• Diarrhea (steatorrhea is common & sometimes bloody)
• Constant abdominal pain
• Low-grade fever
• Weight loss (80% of clients)
• Be aware NURSE!!! to detect clinical manifestations of
peritonitis, bowel obstruction & nutritional & fluid imbalances!!!

Assessment and Diagnostic Methods

• Barium study of the upper GI tract is the most conclusive
diagnostic aid; shows the classic “string sign” of the terminal
ileum (constriction of a segment of intestine) as well as
cobblestone appearance, fistulas, and fissures.
• Endoscopy, colonoscopy, and intestinal biopsies may be used
to confirm the diagnosis.
• Proctosigmoidoscopic examination, computed tomography
(CT) scan.
• Stool examination for occult blood and steatorrhea.
• Complete blood cell count (decreased Hgb and Hct),
sedimentation rate (elevated), albumin, and protein levels
(usually decreased due to malnutrition).

III. Ulcerative Colitis

• Ulcerative and inflammatory condition of affecting the
mucosal lining of the colon or rectum
Nursing Interventions
• Cause: unknown
• Assessment findings: • Maintain NPO during the active phase
o Anorexia, Weight loss, Fever, Severe diarrhea with Rectal • Monitor for complications like severe bleeding, dehydration,
electrolyte imbalance
bleeding, Anemia, Dehydration, Abdominal pain and
• Monitor bowel sounds, stool and blood studies
cramping
• Restrict activities
• Administer IVF, electrolytes and TPN if prescribed
• Instruct the patient to avoid gas-forming foods, milk products
and foods such as whole grains, nuts, RAW fruits and
vegetables (SPINACH), pepper, alcohol and caffeine
• Diet progression- clear liquid LOW residue, high protein diet
• Administer drugs
o Anti-inflammatory, Antibiotics, Steroids, Bulk-forming
agents and vitamin/iron supplements
Regional ENTERITIS Ulcerative Colitis
(Crohn’s Disease) IV. Appendicitis
Characteristic Transmural Mucous Ulceration • The appendix is a small, finger-like appendage attached to the
cecum just below the ileocecal valve. Because it empties into
Ileum Rectum/Cerum
the colon inefficiently and its lumen is small, it is prone to
Unknown Unknown
becoming obstructed and is vulnerable to infection
Cause Familial Familial
(appendicitis). The obstructed appendix becomes inflamed
Environmental Emotional stress
and edematous and eventually fills with pus. It is the most
Age/ Peak 15 – 40 years 15 – 25 years
common cause of acute inflammation in the right lower
Incidence 55 – 65 years
quadrant of the abdominal cavity and the most common
Bleeding ↓; stool with pus and Severe; stool with
cause of emergency abdominal surgery. Although it can occur
mucus blood, pus and mucus
at any age, it more commonly occurs between the ages of 10
and 30 years.

18 | 41 I. BAISA
 NCMB316 – PRELIM
• Inflammation of the vermiform appendix that prevents mucus
from passing into the cecum; if untreated, ischemia, gangrene,
rupture, and peritonitis occur
• Occurs in about 7% of the population and affects males more
often than females
• Causes:
o Mechanical obstruction (fecaliths, calcium-phosphate
rich mucus & inorganic salts, worms, tumors, viral infection,
inflammation)
o May be related to decreased fiber in the diet and high
intake of refined carbohydrates
o Linking of appendix
Pathophysiology
Obstruction of the appendix lumen (mucosa continues to
secrete fluids until pressure w/in the lumen exceeds venous
pressure)
↓ deficit, reducing anxiety, eliminating infection due to the
blood flow to appendix, mucosal Inflammation and bacterial
proliferation
↓ •
gangrene develops w/in 24-36° due to hypoxia
↓ of paralytic ileus). Do not administer an enema or laxative
Abscess
↓ •
Peritonitis
Clinical Manifestations
• Lower right quadrant pain usually accompanied by low grade
fever, nausea, and sometimes vomiting; loss of appetite is
common; constipation can occur.
• Pain starts at the epigastric or umbilical region & becomes
localized in the “Mc Burney’s point”
• At McBurney’s point (located halfway between the umbilicus
and the anterior spine of the ilium), local tenderness with
pressure and some rigidity of the lower portion of the right
rectus muscle.
• Rebound tenderness may be present; location of appendix
dictates amounts of tenderness, muscle spasm, and
occurrence of constipation or diarrhea.
• Rovsing’s sign (elicited by palpating left lower quadrant, which
paradoxically causes pain in right lower quadrant).
• Blumberg sign = Rebound tenderness
• Psoas sign = pain with extension of right hip
• Obturator sign = pain on passive internal rotation of the flexed
thigh
• If appendix ruptures, pain becomes more diffuse; abdominal
distention
• Decreased bowel sounds
• High grade fever = Ruptured!!
19 | 41
Assessment and Diagnostic Findings
• Diagnosis is based on a complete physical examination and
laboratory and imaging tests.
• Elevated WBC count (above 10,000/cu.mm) with an elevation
of the neutrophils; abdominal radiographs, ultrasound studies,
and CT scans may reveal right lower quadrant density or
localized distention of the bowel.
Medical Management
• Surgery (conventional or laparoscopic) is indicated if
appendicitis is diagnosed and should be performed as soon as
possible to decrease risk of perforation.
• Administer antibiotics and IV fluids until surgery is performed.
• Analgesic agents can be given after diagnosis is made.
Complications of Appendectomy
• The major complication is perforation of the appendix, which
can lead to peritonitis, abscess formation (collection of
purulent material), or portal pylephlebitis.
• Perforation generally occurs 24 hours after the onset of pain.
Symptoms include a fever of 37.7C (100F) or greater, a toxic
appearance, and continued abdominal pain or tenderness.
Nursing Management
• Nursing goals include relieving pain, preventing fluid volume
potential or actual disruption of the GI tract, maintaining skin
integrity, and attaining optimal nutrition.
Preoperatively, prepare patient for surgery, start IV line,
administer antibiotic, and insert nasogastric tube (if evidence
(could cause perforation).
Postoperatively, place patient in high Fowler’s position, give
narcotic analgesic as ordered, administer oral fluids when
tolerated, give food as desired on day of surgery (if tolerated).
If dehydrated before surgery, administer IV fluids.
• If a drain is left in place at the area of the incision, monitor
carefully for signs of intestinal obstruction, secondary
hemorrhage, or secondary abscesses (e.g., fever, tachycardia,
and increased leukocyte count).
V. Peritonitis
• Peritonitis, inflammation of the peritoneum, is usually the result
of bacterial infection, with the organisms coming from disease
of the GI tract, or, in women, the internal reproductive organs.
It can also result from external sources, such as injury or trauma
or an inflammation from an extraperitoneal organ, such as the
kidney.
Pathophysiology
• Peritonitis is caused by leakage of contents from abdominal
organs into the abdominal cavity, usually as a result of
inflammation, infection, ischemia, trauma, or tumor
perforation. The most common bacteria implicated are
Escherichia coli, and Klebsiella, Proteus, and Pseudomonas
species. Other common causes are appendicitis, perforated
ulcer, diverticulitis, and bowel perforation. Peritonitis may also
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be associated with abdominal surgical procedures and
peritoneal dialysis. Sepsis is the major cause of death from
peritonitis (shock, from sepsis or hypovolemia). Intestinal
obstruction from bowel adhesions may develop.
• Initial response
o Edema
o Vascular congestion
o Hypermotility of the bowel and outpouring of plasma-like
fluid from the extracellular
o Vascular
o Interstitial compartments into the peritoneal space
• Later response
o Abdominal distension leading to respiratory compromise
o Hypovolemia results in decreased urinary output
o Intestinal motility gradually decreases and progresses to
paralytic ileus
• Causes
o Caused by trauma (blunt or penetrating)
o Inflammatory conditions
o Ulcerative colitis, diverticulitis, pelvic inflammatory disease
o Ischemia
o Ruptured appendix
o Perforated peptic ulcer
o UTI
o Bowel obstruction (volvulus, intestinal obstruction)
o Bacterial invasion
o Peritoneal dialysis
Clinical Manifestations
Clinical features depend on the location and extent of
inflammation.
• Diffuse pain becomes constant, localized, and more intense
near site of the process.
• Pain is aggravated by movement.
• Severe abdominal pain, absent bowel sounds,
• Affected area of the abdomen becomes extremely tender
and distended, and muscles become rigid.
• Rebound tenderness and paralytic ileus may be present.
• Anorexia, nausea, and vomiting occur and peristalsis is
diminished.
• Temperature and pulse increase; hypotension may develop.
• Shallow respirations; decreased urinary output; weak, rapid
pulse; fever
• Signs of shock: Tachycardia, Tachypnea, Oliguria, Restlessness,
Weakness, Pallor, Diaphoresis
Assessment and Diagnostic Methods
• WBC elevated WBC (20,000/cu. mm. or higher)
• Hct elevated (if hemoconcentration)
• Serum electrolytes (altered potassium, sodium and chloride)
• Abdominal x-rays, ultrasound, CT scan, MRI, and peritoneal
aspiration with culture and sensitivity studies
Medical Management
• Fluid, colloid, and electrolyte replacement with an isotonic
solution is the major focus of medical management.
• Analgesics are administered for pain; antiemetics are
administered for nausea and vomiting.
• Intestinal intubation and suction are used to relieve abdominal
distention.
• Oxygen therapy by nasal cannula or mask is instituted to
improve ventilatory function.
• Occasionally, airway intubation and ventilatory assistance are
required.
• Massive antibiotic therapy may be instituted (sepsis is the major
cause of death).
20 | 41
• Surgical objectives include removal of infected material;
surgery is directed toward excision (appendix), resection
(intestine), repair (perforation), or drainage (abscess).
o Laparotomy: opening made through the abdominal wall
into the peritoneal cavity to determine the cause of
peritonitis
o Depending on cause, bowel resection may be necessary
Nursing Management
• Monitor the patient’s blood pressure by arterial line if shock is
present.
• Monitor central venous or pulmonary artery pressures and urine
output frequently.
• NPO with fluid replacement
• NGT is inserted to relieve abdominal distention
• Provide ongoing assessment of pain, GI function, and fluid and
electrolyte balance.
• Assess nature of pain, location in the abdomen, and shifts of
pain and location.
• Administer analgesic medication and position for comfort (e.g.,
on side with knees flexed to decrease tension on abdominal
organs).
• Record intake and output and CVP and/or pulmonary artery
pressures.
• Administer and monitor IV fluids closely; nasogastric intubation
may be necessary.
• Observe for decrease in temperature and pulse rate, softening
of the abdomen, return of peristaltic sounds, and passage of
flatus and bowel movements, which indicate peritonitis is
subsiding.
• Increase food and oral fluids gradually, and decrease
parenteral fluid intake when peritonitis subsides.
• Observe and record character of drainage from postoperative
wound drains if inserted; take care to avoid dislodging drains.
• Postoperatively, prepare patient and family for discharge;
teach care of incision and drains if still in place at discharge.
• Refer for home care if necessary.
VI. Diverticular Disease
• A diverticulum is a saclike herniation of the lining of the bowel
that extends through a defect in the muscle layer. Diverticula
may occur anywhere in the small intestine or colon but most
commonly occur in the sigmoid colon. Diverticulosis exists
when multiple diverticula are present without inflammation or
symptoms. It is most common in people older than 80 years. A
low intake of dietary fiber is considered a major predisposing
factor. Diverticulitis results when food and bacteria retained in
the diverticulum produce infection and inflammation that can
impede draining and lead to perforation or abscess. It may
occur in acute attacks or persist as a chronic, smoldering
infection. A congenital predisposition is likely when the disorder
is present in those younger than 40 years. Complications of
diverticulitis include abscess, fistula (abnormal tract) formation,
obstruction, perforation, peritonitis, and hemorrhage.
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Clinical Manifestations
Diverticulosis
• Frequently, no problematic symptoms are noted; chronic
constipation often precedes development.
• Bowel irregularity with intervals of diarrhea, nausea and
anorexia, and bloating or abdominal distention.
• Cramps, narrow stools, and increased constipation or at times
intestinal obstruction.
• Weakness, fatigue, and anorexia.
Diverticulitis
• Acute onset of mild to severe pain in the left lower quadrant,
worsens with movement, coughing or straining
• Nausea, vomiting, low-grade fever, chills, and leukocytosis
• If untreated, peritonitis and septicemia
• Chronic constipation with episodes of diarrhea
• Abdominal distention and tenderness
• Occult bleeding, rectal bleeding, change in bowel movement
Diverticulitis
• Acute inflammation and infection caused by trapped fecal
material and bacteria
• Diverticulum is outpouching of the mucosal lining of the GI tract
commonly in the colon
• Diverticula/ Diverticulosis are multiple outpouchings
• Causes: Low fiber diet, chronic constipation, obesity
Assessment and Diagnostic Findings
• Colonoscopy and possibly barium enema studies (Barium
enema is NOT usually ordered in cases of acute inflammation
because of possibility of perforation)
• Sigmoidoscopy
• Visualization of diverticula
• Computed tomography (CT) scan with contrast agent
• Abdominal x-ray
• Laboratory tests: complete blood cell count, revealing an
elevated white blood cell count, and elevated erythrocyte
sedimentation rate (ESR)
Nursing Management
• High fiber diet
• Liberal fluid intake of 2,500 to 3,000 ml/day.
• Avoid nuts and seeds which can be trapped in the diverticula.
• Bulk – forming laxatives are ordered to restore normal bowel
pattern
• IVF and medications
• During an acute episode:
o Bed rest
o NPO, then clear liquids to rest the bowel
o Avoid high fiber foods to prevent further irritation of the
mucosa
o Gradually increase the fiber when the infection/
inflammation subsides
Medical Management
Dietary and Pharmacologic Management
• Diverticulitis can usually be treated on an outpatient basis with
diet and medication; symptoms treated with rest, analgesics,
and antispasmodics.
• The patient is instructed to ingest clear liquids until inflammation
subsides, then a high-fiber, low-fat diet. Antibiotics are
prescribed for 7 to 10 days and a bulk-forming laxative is also
prescribed.
• Patients with significant symptoms and often those who are
elderly, immunocompromised, or taking corticosteroids are
hospitalized. The bowel is rested by withholding oral intake,
administering IV fluids, and instituting nasogastric suctioning.
21 | 41
• Broad-spectrum antibiotics and analgesics are prescribed and
an opioid is prescribed for pain relief. Oral intake is increased
as symptoms subside. A low-fiber diet may be necessary until
signs of infection decrease.
• Antispasmodics such as propantheline bromide and
oxyphencyclimine (Daricon) may be prescribed.
• Normal stools can be achieved by administering bulk
preparations (psyllium), stool softeners, warm oil enemas, and
evacuant suppositories.
VII. Hemorrhoids
Hemorrhoids are vascular masses that protrude into the lumen of
the lower rectum or perianal area.
• They result when increased intra-abdominal pressure causes
engorgement in the vascular tissue lining the anal canal.
• Loosening of vessels from surrounding connective tissue occurs
with protrusion or prolapse into the anal canal.
• There are two main types of hemorrhoids: external hemorrhoids
appear outside the external sphincter, and internal
hemorrhoids appear above the internal sphincter.
• When blood within the hemorrhoids becomes clotted because
of obstruction, the hemorrhoids are referred to as being
thrombosed.
• Predisposing factors include pregnancy, prolonged sitting or
standing, straining stool, chronic constipation or diarrhea, anal
infection, obesity, wearing constricting clothing, rectal surgery
or episiotomy, genetic predisposition, alcoholism, portal
hypertension (cirrhosis), coughing, sneezing, or vomiting, loss of
muscle tone attributable to old age, and anal intercourse.
• Complications include hemorrhage, anemia, incontinence of
stool, and strangulation.
• Hemorrhoids are the most common of a variety of anorectal
disorders.
Causes/Risk Factors
Modifiable
• Some factors that are associated with hemorrhoids are
occupations that require prolonged sitting or standing; heart
failure; anorectal infections; anal intercourse; alcoholism;
pregnancy; colorectal cancer; and hepatic disease such as
cirrhosis, amoebic abscesses, or hepatitis.
• Straining because of constipation, diarrhea, coughing,
sneezing, or vomiting and loss of muscle tone because of
aging, rectal surgery, or episiotomy can also cause
hemorrhoids.
Assessment
• Pain (more so with external hemorrhoids), sensation of
incomplete fecal evacuation, constipation, and anal itching.
Sudden rectal pain may occur if external hemorrhoids are
thrombosed.
• Bleeding may occur during defecation (hematochezia); bright
red blood on stool caused by injury of mucosa covering
hemorrhoid.
• Visible and palpable masses at anal area.
• Mucous secretion from the anus
• Internal hemorrhoids may prolapse, usually painless.
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• External hemorrhoids are usually painful
Diagnostic Evaluation
• External examination with anoscope or proctoscope shows
single or multiple hemorrhoids.
• Barium edema or colonoscopy rules out more serious colonic
lesions causing rectal bleeding such as polyps.
Primary Nursing Diagnosis
• Pain (acute or chronic) related to rectal swelling and prolapse
Therapeutic Intervention / Medical Management
• High-fiber diet to keep stools soft, liberal fluid intake, laxatives
• Warm sitz baths to ease pain and combat swelling.
• Reduction of prolapsed external hemorrhoid manually.
Surgical Interventions:
• Injection of sclerosing solutions to produce scar tissue and
decrease prolapse is an office procedure.
• Cryodestruction (freezing) of hemorrhoids is an office
procedure.
• Surgery may be indicated in presence of prolonged bleeding,
disabling pain, intolerable itching, and general unrelieved
discomfort.
• Hemorrhoidectomy
• Sclerotherapy (5% phenol in oil)
• Pre-op Care
o Low residue diet to reduce the bulk of stool
o Stool softeners
• Post-op Care
o Promotion of comfort
◦ Analgesics as prescribed
◦ Post-op position: Side – lying position or prone position
◦ Hot sitz bath 12 to 24 hrs. post-op to promote comfort
and hasten healing
o Promotion of elimination
◦ Stool softeners are given as prescribed
◦ Analgesic before initial defecation
◦ Encourage the client to defecate as soon as the urge
occurs
◦ Enema as prescribed, using a small – bore rectal tube
Pharmacologic Intervention
1. Stool softeners to keep stools soft and relieve symptoms.
2. Topical creams, suppositories or other preparation such as
Anusol, Preparation H, and witch- hazel compresses to reduce
itching and provide comfort.
3. Oral analgesics may be needed.
Nursing Intervention
1. After thrombosis or surgery, assist with frequent repositioning
using pillow support for comfort.
2. Provide analgesics, warm sitz baths, or warm compresses to
reduce pain and inflammation.
3. Apply witch-hazel dressing to perianal area or anal creams or
suppositories, if ordered, to relieve discomfort.
4. Observe anal area postoperatively for drainage and bleeding.
5. Administer stool softener or laxative to assist with bowel
movements soon after surgery, to reduce risk of stricture.
6. Teach anal hygiene and measures to control moisture to
prevent itching.
7. Encourage the patient to exercise regularly, follow a high fiber
diet, and have an adequate fluid intake (8 to 10 glasses per
day) to avoid straining and constipation, which predisposes to
hemorrhoid formation.
8. Discourage regular use of laxatives; firm, soft stools dilate the
anal canal and decrease stricture formation after surgery.
9. Tell patient to expect a foul-smelling discharge for 7 to 10 days
after cryodestruction.
22 | 41
10. Determine the patient’s normal bowel habits and identify
predisposing factors to educate patient about preventing
recurrence of symptoms.
Documentation Guidelines
1. Physical findings: Rectal examination, urinary retention,
bleeding, and mucous drainage
2. Wound healing: Drainage, color, swelling
3. Pain management: Pain (location, duration, frequency),
response to interventions
4. Postoperative bowel movements: Tolerance for first bowel
movement
Discharge and Home Healthcare Guidelines
• Teach the patient the importance of a high-fiber diet,
increased fluid intake, mild exercise, and regular bowel
movements. Be sure the patient schedules a follow-up visit to
the physician. Teach the patient which analgesic applications
for local pain may be used. If the patient has had surgery,
teach her or him to recognize signs of urinary retention, such as
bladder distension and hemorrhage, and to contact the
physician at their appearance.
Patient Teaching
• Clean rectal area thoroughly after each defecation
• Sitz bath at home especially after defecation
• Avoid constipation by adhering to this practice:
o High – fiber diet, High fluid intake, Regular exercise
o Regular time for defecation, use stool softener until healing
is complete
• Notify physician for the following:
o Rectal bleeding, suppurative drainage, continued pain on
defecation and continued constipation
TERMINOLOGIES
1. Ascites: Abnormal accumulation of fluid in peritoneal cavity
caused by cirrhosis, tumors, and infection
2. Borborygmus: Rumbling, gurgling sound made by movement
of gas in intestine
3. Cathartic: Strong laxative
4. Colonic polyposis: Polyps, small growths protruding from
mucous membrane of colon
5. Constipation: Difficult or delayed defecation caused by low
peristalsis movement, over-absorption of water as contents sits
too long in the intestine, or by dehydration
6. Diarrhea: Frequent discharge of liquid stool (feces)
7. Diverticula: Abnormal side pockets in hollow structure, such as
intestine, sigmoid colon, and duodenum
8. Flatus: Gas expelled through the anus
9. Hemorrhoids: Swollen or twisted veins either outside or just inside
the anus
10. Hernia: A protrusion of an organ or part through the wall of the
cavity that contains it
11. Ileus: Intestinal obstruction that can be caused by failure of
peristalsis following surgery, hernia, tumor, adhesions, and often
by peritonitis
12. Inguinal hernia: A small loop of bowel protruding through a
weak place in the inguinal ring, an opening in the lower
abdominal wall, which allows blood vessels to pass into the
scrotum
13. Intussusception: Telescoping of the intestine; common in
children
14. Laxative: Medication encouraging movement of feces
15. Melena: Black stool; feces containing blood
16. Polyposis: Condition of polyps in the intestinal wall
17. Pruritus ani: Intense itching of the anal area
18. Steatorrhea: Excessive fat in feces
19. Volvulus: Twisting of intestine upon itself
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DISORDERS OF THE LIVER, PANCREAS, AND GALL BLADDER Vitamin and Iron Storage
ASSESSMENT OF THE LIVER Vitamins A, B, and D and several of the B-complex vitamins are
• Liver function is complex, and liver dysfunction affects all body stored in large amounts in the liver. Certain substances, such as iron
systems. For this reason, the nurse must understand how the liver and copper, are also stored in the liver.
functions and must have expert clinical assessment and
Bile Formation
management skills to care for patients undergoing complex
diagnostic and treatment procedures. The nurse also must Bile is continuously formed by the hepatocytes and collected in the
understand technologic advances in the management of liver canaliculi and bile ducts. It is composed mainly of water and
disorders. Liver disorders are common and may result from a electrolytes such as sodium, potassium, calcium, chloride, and
virus, exposure to toxic substances such as alcohol, or tumors. bicarbonate, and it also contains significant amounts of lecithin,
fatty acids, cholesterol, bilirubin, and bile salts. Bile is collected and
Anatomic and Physiologic Overview stored in the gallbladder and is emptied into the intestine when
• The liver, the largest gland of the body, can be considered a needed for digestion.
chemical factory that manufactures, stores, alters, and
Bilirubin Excretion
excretes a large number of substances involved in metabolism.
The location of the liver is essential in this function because it Bilirubin is a pigment derived from the breakdown of hemoglobin by
cells of the reticuloendothelial system, including the Kupffer cells of
receives nutrient-rich blood directly from the gastrointestinal
the liver. Hepatocytes remove bilirubin from the blood and
(GI) tract and then either stores or transforms these nutrients into
chemically modify it through conjugation to glucuronic acid, which
chemicals that are used elsewhere in the body for metabolic
makes the bilirubin more soluble in aqueous solutions.
needs. The liver is especially important in the regulation of
glucose and protein metabolism. Drug Metabolism
• The liver manufactures and secretes bile, which has a major
The liver metabolizes many medications, such as barbiturates,
role in the digestion and absorption of fats in the GI tract. The
opioids, sedatives, anesthetics, and amphetamines. Metabolism
liver removes waste products from the bloodstream and
generally results in drug inactivation, although activation may also
secretes them into the bile. The bile produced by the liver is
occur. One of the important pathways for medication metabolism
stored temporarily in the gallbladder until it is needed for
involves conjugation (binding) of the medication with a variety of
digestion, at which time the gallbladder empties and bile
compounds, such as glucuronic acid or acetic acid, to form more
enters the intestine.
soluble substances.
Anatomy of the Liver
Major Functions of The Liver
• The liver is a large, highly vascular organ located behind the
• Bile production and excretion
ribs in the upper right portion of the abdominal cavity. It weighs
• Excretion of bilirubin, cholesterol, hormones and drugs
between 1200 and 1500 g and is divided into four lobes. A thin
• Metabolism of CHO, CHON and fats
layer of connective tissue surrounds each lobe, extending into
• Storage of glycogen, vitamins and minerals
the lobe itself and dividing the liver mass into small, functional
• Synthesis of plasma proteins, such as albumin and clotting
units called lobules. The circulation of the blood into and out of
factors
the liver is of major importance to liver function. The blood that
• Detoxification
perfuses the liver comes from two sources. Approximately 80%
of the blood supply comes from the portal vein, which drains I. Hepatitis, Viral: Types A, B, C, D, E, and G
the GI tract and is rich in nutrients but lacks oxygen. • Infectious inflammation of the liver parenchyma caused by
viruses.
Functions of the Liver
• Widespread inflammation of the liver tissue
Glucose Metabolism
• Liver cell damage due to hepatic cell degeneration and
The liver plays a major role in the metabolism of glucose and the necrosis
regulation of blood glucose concentration. After a meal, glucose is • Proliferation and enlargement of the Kupffer cells
taken up from the portal venous blood by the liver and converted • Inflammation of the periportal areas causing interruption of bile
into glycogen, which is stored in the hepatocytes. flow.
Ammonia Conversion
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. Ammonia produced
by bacteria in the intestines is also removed from portal blood for
urea synthesis.

Protein Metabolism
The liver also plays an important role in protein metabolism. It
synthesizes almost all of the plasma proteins (except gamma-
globulin), including albumin, alpha-globulins and beta-globulins,
blood clotting factors, specific transport proteins, and most of the
plasma lipoproteins.

Fat Metabolism
The liver is also active in fat metabolism. Fatty acids can be broken
down for the production of energy and ketone bodies (acetoacetic
acid, beta-hydroxybutyric acid, and acetone). Ketone bodies are
small compounds that can enter the bloodstream and provide a
source of energy for muscles and other tissues.

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Hepatitis A
• Hepatitis A is caused by an RNA virus of the genus Enterovirus.
This form of hepatitis is transmitted primarily through the fecal–
oral route, by the ingestion of food or liquids infected by the
virus.
• The virus is found in the stool of infected patients before the
onset of symptoms and during the first few days of illness. The
incubation period is estimated to be 2 to 6 weeks, with a mean
of approximately 4 weeks. The course of illness may last 4 to 8
weeks. The virus is present only briefly in the serum; by the time
jaundice appears, the patient is likely to be noninfectious. A
person who is immune to hepatitis A may contract other forms
of hepatitis. Recovery from hepatitis A is usual; it rarely
progresses to acute liver necrosis and fulminant hepatitis. No
carrier state exists, and no chronic hepatitis is associated with
hepatitis A. Poor hygiene or contaminated food and shellfish
increase risk of transmission, practice food hygiene can prevent
hepatitis A.
• Flies may carry diseases such as Hepatitis A, typhoid, amebic
dysentery and polio by contamination food or water.
Clinical Manifestations
• Many patients are anicteric (without jaundice) and
symptomless.
• When symptoms appear, they are of a mild, flulike, upper
respiratory infection, with low-grade fever.
• Anorexia is an early symptom and is often severe.
• Later, jaundice and dark urine may be apparent.
• Indigestion is present in varying degrees.
• Liver and spleen are often moderately enlarged for a few days
after onset.
• Patient may have an aversion to cigarette smoke and strong
odors; symptoms tend to clear when jaundice reaches its peak.
• Symptoms may be mild in children; in adults, they may be more
severe, and the course of the disease prolonged.
Assessment and Diagnostic Methods
• Stool analysis for hepatitis A antigen
• Serum hepatitis A virus antibodies; immunoglobulin
Prevention
• Scrupulous hand washing, safe water supply, proper control of
sewage disposal.
• Hepatitis vaccine.
• Administration of immune globulin, if not previously vaccinated,
to prevent hepatitis A if given within 2 weeks of exposure.
• Immune globulin is recommended for household members and
for those who are in sexual contact with people with heap A.
• Preexposure prophylaxis is recommended for those traveling to
developing countries or settings with poor or uncertain
sanitation conditions who do not have sufficient time to
acquire protection by administration of hepatitis A vaccine.
Management
• Bed rest during the acute stage; encourage a nutritious diet.
• Give small, frequent feedings supplemented by IV glucose if
necessary, during period of anorexia.
• Promote gradual but progressive ambulation to hasten
recovery. Patient is usually managed at home unless symptoms
are severe.
• Assist patient and family to cope with the temporary disability
and fatigue that are common problems in hepatitis.
• Teach patient and family the indications to seek additional
health care if the symptoms persist or worsen.
24 | 41
• Instruct patient and family regarding diet, rest, follow-up blood
work, avoidance of alcohol, and sanitation and hygiene
measures (hand washing) to prevent spread of disease to other
family members.
• Teach patient and family about reducing risk for contracting
hepatitis A: good personal hygiene with careful hand washing;
environmental sanitation with safe food and water supply and
sewage disposal.
Hepatitis B
• Hepatitis B virus (HBV) is a DNA virus transmitted primarily
through blood. The virus has been found in saliva, semen, and
vaginal secretions and can be transmitted through mucous
membranes and breaks in the skin. Hepatitis B has a long
incubation period (1 to 6 months). It replicates in the liver and
remains in the serum for long periods, allowing transmission of
the virus. Those at risk include all health care workers, patients
in hemodialysis and oncology units, sexually active homosexual
and bisexual men, and IV drug users. About 10% of patients
progress to a carrier state or develop chronic hepatitis.
• Hepatitis B remains a major worldwide cause of cirrhosis and
hepatocellular carcinoma.
• Risk factors: people who share needles and health workers who
are exposed to infected blood.
Clinical Manifestations
• Symptoms may be insidious and variable; subclinical episodes
frequently occur; fever and respiratory symptoms are rare;
some patients have arthralgias and rashes.
• Loss of appetite, dyspepsia, abdominal pain (upper right
quadrant), general aching, malaise, fatigue, nausea and
vomiting, and weakness may occur.
• Jaundice may or may not be evident. With jaundice, there are
light-colored stools and dark urine.
• Liver may be tender and enlarged; spleen is enlarged and
palpable in a few patients. Posterior cervical lymph nodes may
also be enlarged.
Assessment and Diagnostic Findings
• Hepatitis B surface antigen appears in blood of up to 90% of
patients. Additional antigens help to confirm diagnosis.
Prevention
• Screening of blood donors
• Good personal hygiene
• Education
• Hepatitis B vaccine protects against serious disease-causing
inflammation and damage to the liver.
Medical Management
• Alpha-interferon has shown promising results.
• Lamivudine (Epivir) and adefovir (Hepsera).
• Bed rest and restriction of activities until hepatic enlargement
and elevation of serum bilirubin and liver enzymes have
disappeared.
• Maintain adequate nutrition; restrict proteins when the ability of
the liver to metabolize protein byproducts is impaired.
• Administer antacids and antiemetics for dyspepsia and
general malaise; avoid all medications if patient is vomiting.
• Provide hospitalization and fluid therapy if vomiting persists.
Nursing Management
• Convalescence may be prolonged and recovery may take 3
to 4 months; encourage gradual activity after complete
clearing of jaundice.
• Identifies psychosocial issues and concerns, particularly the
effects of separation from family and friends if the patient is
hospitalized; if not hospitalized, the patient will be unable to
work and must avoid sexual contact.
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• Include family in planning to help reduce their fears and
anxieties about the spread of the disease.
• Educate patient and family in home care and convalescence.
• Instruct patient and family to provide adequate rest and
nutrition.
• Inform family and intimate friends about risks of contracting
hepatitis B.
• Arrange for family and intimate friends to receive hepatitis B
vaccine or hepatitis B immune globulin as prescribed.
• Caution patient to avoid drinking alcohol and eating raw
shellfish.
• Inform family that follow-up home visits by home care nurse are
indicated to assess progress and understanding, reinforce
teaching, and answer questions.
• Encourage patient to use strategies to prevent exchange of
body fluids, such as avoiding sexual intercourse or using
condoms.
• Emphasize importance of keeping follow-up appointments and
participating in other health promotion activities and
recommended health screenings.
hygiene (hand washing). The effectiveness of immune globulin
in protecting against hepatitis E virus is uncertain.
• The risk of fulminant disease has been described mainly in
pregnant patients.
Hepatitis G
• Hepatitis G (the latest form) is a posttransfusion hepatitis with an
incubation period of 14 to 145 days. Autoantibodies are absent.
• The new virus, tentatively named hepatitis G virus (HGV) and
known to be closely related to GB virus C (GBV-C), is
transmitted by blood and blood products, intravenous drug use
and other behavior associated with a high risk of parenteral
exposure to blood (credits from google).

Hepatitis C
• A significant portion of cases of viral hepatitis are not A, B, or D;
they are classified as hepatitis C. It is the primary form of
hepatitis associated with parenteral means (sharing
contaminated needles, needlesticks or injuries to health care
workers, blood transfusions) or sexual contact. The incubation
period is variable and may range from 15 to 160 days. The
clinical course of hepatitis C is similar to that of hepatitis B;
symptoms are usually mild. A chronic carrier state occurs
frequently. There is an increased risk for cirrhosis and liver
cancer after hepatitis C. A combination therapy using ribavirin Assessment findings
(Rebetol) and interferon (Intron-A) is effective for treating • Preicteric stage (prodromal phase) = 1 week
patients with hepatitis C and in treating relapses. o Anorexia (major manifestation), N&V, fatigue, constipation
• RNA virus generally transmitted predominantly by blood or diarrhea, weight loss.
products and it is currently the most common hepatitis among o RUQ discomfort, hepatomegaly, splenomegaly,
IV drug abusers and in prisons. lymphadenopathy.
• Icteric stage
Hepatitis D
o Fatigue, weight loss, light-colored stools, dark urine
• Hepatitis D (delta agent) occurs in some cases of hepatitis B.
o Continued hepatomegaly with tenderness,
Because the virus requires hepatitis B surface antigen for its
lymphadenopathy, splenomegaly
replication, only patients with hepatitis B are at risk. It is common
o Jaundice, pruritus
in IV drug users, hemodialysis patients, and recipients of multiple
• Posticteric stage
blood transfusions. Sexual contact is an important mode of
o Fatigue, but an increased sense of well-being,
transmission of hepatitis B and D. Incubation varies between 30
hepatomegaly gradually decreasing.
and 150 days. The symptoms are similar to those of hepatitis B
except that patients are more likely to have fulminant hepatitis Collaborative Management
and progress to chronic active hepatitis and cirrhosis. • Promotion of rest to relieve fatigue
Treatment is similar to that for other forms of hepatitis. • Maintenance of food and fluid intake
• RNA virus that infects either simultaneously with hepatitis B or as • 3,000 ml/day of fluids for fever and vomiting; monitor I and O,
a super-infection in a person with chronic hepatitis B weight
• Hepatitis D infection cannot occur unless there is current and • Well-balanced diet; encourage fruit juices & noncarbonated
ongoing replication of the hepatitis B virus beverages
• Overall, this infection carries the highest risk among acute viral • Fats may need to be restricted
hepatitis for fulminant disease; the risk is even greater in super- • Alcoholic beverages should be avoided
infection • Prevention of injury
• Predominantly seen in patients exposed to blood products • Advise client to use soft toothbrush or swabs
(drug addicts and hemophiliacs). If anti-hbs antibodies are • Administer Vitamin K as ordered
present, then that person is immune to hepatitis B and D • Provision of comfort measures
• Relaxing baths, backrubs, fresh linens and quiet dark
Hepatitis E
environment
• The hepatitis E virus is transmitted by the fecal–oral route,
• Relieve pruritus through the following measures:
principally through contaminated water and poor sanitation.
o Use of cool, light, non-restrictive clothing
Incubation is variable and is estimated to range between 15
o Use of soft, dry, clean bedding, use of warm baths
and 65 days. In general, hepatitis E resembles hepatitis A. It has
o Application of emollient creams and lotions to dry skin.
a self-limited course with an abrupt onset. Jaundice is almost
o Maintenance of a cool environment
always present. Chronic forms do not develop. The major
o Administration of antihistamines as ordered
method of prevention is avoiding contact with the virus through
o Use of diversional activities, e.g. reading, TV and radio

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II. Cirrhosis, Hepatic
• Cirrhosis is a chronic disease characterized by replacement of
normal liver tissue with diffuse fibrosis that disrupts the structure
and function of the liver. Cirrhosis, or scarring of the liver, is
divided into three types: alcoholic, most frequently due to
chronic alcoholism and the most common type of cirrhosis; post
necrotic, a late result of a previous acute viral hepatitis; and
biliary, a result of chronic biliary obstruction and infection (least
common type of cirrhosis).
Types
• Laennec’s cirrhosis – associated with alcohol abuse and
malnutrition; characterized by an accumulation of fat in the
liver cells, progressing to widespread scar formation.
• Post necrotic cirrhosis – results in severe inflammation with
massive necrosis as a complication of viral hepatitis
• Cardiac cirrhosis – occurs as a consequence of RSHF;
manifested by hepatomegaly with some fibrosis.
• Biliary cirrhosis – associated with biliary obstruction, usually in
the common bile duct; results in chronic impairment of bile
excretion.
Clinical Manifestations
• Compensated cirrhosis: usually found secondary to routine
physical examination; vague symptoms.
• Decompensated cirrhosis: symptoms of decreased proteins,
clotting factors, and other substances and manifestations of
portal hypertension.
• Liver enlargement early in the course (fatty liver); later in
course, liver size decreases from scar tissue.
• Portal obstruction and ascites: Organs become the seat of
chronic passive congestion; indigestion and altered bowel
function result.
• Infection and peritonitis: Clinical signs may be absent,
necessitating paracentesis for diagnosis.
• Gastrointestinal varices: prominent, distended abdominal
blood vessels; distended blood vessels throughout the GI tract;
varices or hemorrhoids; hemorrhage from the stomach.
• Edema.
• Vitamin deficiency (A, C, and K) and anemia.
• Mental deterioration with impending hepatic encephalopathy
and hepatic coma.
Assessment
• Anorexia, weakness, weight loss (liver is unable to metabolize
nutrients and store fat-soluble vitamins)
• Fever (in response to tissue injury)
• Jaundice, pruritus, tea colored urine (due to increase bilirubin
in the blood)
• Remember!!! bilirubin is conjugated initially before excretion
• Increased Bleeding tendencies. (Liver is unable to store Vit. K.
There is also impaired production of clotting factors)
Diagnostic Methods
• Liver function tests (e.g., serum alkaline phosphatase, aspartate
aminotransferase [AST] [serum glutamic oxaloacetic
transaminase (SGOT)], alanine aminotransferase [ALT] [serum
glutamic pyruvic transaminase (SGPT)], GGT, serum
cholinesterase, and bilirubin), prothrombin time, ABGs, biopsy
26 | 41
• Ultrasound scanning
• CT scan
• MRI
• Radioisotopic liver scans
Medical Management
Medical management is based on presenting symptoms.
• Treatment includes antacids, vitamins and nutritional
supplements, balanced diet; potassium- sparing diuretics (for
ascites); avoidance of alcohol.
• Colchicine may increase the length of survival in patients with
mild to moderate cirrhosis.
Nursing Management
• Promoting Rest
o Position bed for maximal respiratory efficiency; provide
oxygen if needed.
o Initiate efforts to prevent respiratory, circulatory, and
vascular disturbances.
o Encourage patient to increase activity gradually and plan
rest with activity and mild exercise.
• Improving Nutritional Status
o Provide a nutritious, high-protein diet supplemented by
Bcomplex vitamins and others, including A, C, and K.
o Encourage patient to eat: Provide small, frequent meals,
consider patient preferences, and provide protein
supplements, if indicated.
o Provide nutrients by feeding tube or total PN if needed.
o Provide patients who have fatty stools (steatorrhea) with
water-soluble forms of fat-soluble vitamins A, D, and E, and
give folic acid and iron to prevent anemia.
o Provide a low-protein diet temporarily if patient shows signs
of impending or advancing coma; restrict sodium if
needed.
• Providing Skin Care
o Change patient’s position frequently.
o Avoid using irritating soaps and adhesive tape.
o Provide lotion to soothe irritated skin; take measures to
prevent patient from scratching the skin.
• Reducing Risk of Injury
o Use padded side rails if patient becomes agitated or
restless.
o Orient to time, place, and procedures to minimize
agitation.
o Instruct patient to ask for assistance to get out of bed.
o Carefully evaluate any injury because of the possibility of
internal bleeding.
o Provide safety measures to prevent injury or cuts (electric
razor, soft toothbrush).
o Apply pressure to venipuncture sites to minimize bleeding.
• Monitoring and Managing Complications
o Monitor for bleeding and hemorrhage.
o Monitor the patient’s mental status closely and report
changes so that treatment of encephalopathy can be
initiated promptly.
o Carefully monitor serum electrolyte levels are and correct
if abnormal.
o Administer oxygen if oxygen desaturation occurs; monitor
for fever or abdominal pain, which may signal the onset of
bacterial peritonitis or other infection.
o Assess cardiovascular and respiratory status; administer
diuretics, implement fluid restrictions, and enhance patient
positioning, if needed.
o Monitor intake and output, daily weight changes,
changes in abdominal girth, and edema formation.
o Monitor for nocturia and, later, for oliguria, because these
states indicate increasing severity of liver dysfunction.
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Portal Hypertension

Pathology
1. In portal hypertension
- plasma shift into interstitial spaces within the liver due to III. Hepatic Encephalopathy
the increase pressure. The collection of fluids shifts out of • Accumulation of ammonia because the liver cannot convert
the Glisson’s capsule and accumulate in the peritoneal ammonia into urea that can lead to hepatic coma (Ammonia
cavity is by product of CHON metabolism)
2. The liver is unable to metabolize protein, thereby • Initial manifestations: BEHAVIORAL changes and MENTAL
hypoalbuminemia occurs changes
- result to decreased oncotic pressure, fluids shift out of the • Other findings in advanced stages are:
IVC, and accumulate in the peritoneal cavity. o asterixis – flapping tremors of the hands
3. The liver is unable to excrete adrenal cortex hormone, one of o confusion / disorientation
which is aldosterone o delirium / hallucination
- Hyperaldosteronism leads to retention of sodium and o fetor hepaticus – disagreeable odor from the mouth
water o coma
4. Esophageal varices = 2° to backpressure
5. Internal hemorrhoids, leg varicosities, and dependent edema Diagnostic tests
- due to venous stasis, increasing hydrostatic pressure. This • SGOT or AST, SGPT, LDH, alkaline phosphatase increased
leads to shifting of plasma into interstitial space • Serum bilirubin increased
• PT prolonged
Consequences of Portal HPN • Serum albumin decreased
• Hepatomegaly= initially, then the liver shrinks in size as fibrosis • Hgb/Hct decrease
replaces the liver parenchyma
• Splenomegaly= due to increased backpressure of the blood Medical Management
• Caput medusae (dilated veins over the abdomen) • Bedrest
• Spider angioma (telangiectasia / dilated capillaries over the • Hepatic protector – Essentiale, Godex
face and anterior trunk) = due to increased estrogen • Betablockers
• Palmar erythema. This is also due to elevated estrogen level in • Blood transfusion
males. • Diuretic
• Ascites • Vitamin K
• Males (increase estrogen) will result to: • Antibiotics - Neomycin
o Decreased libido, Impotence, Fall of body hair, Atrophy • Paracentesis
of testicles, gynecomastia • Albumer infusion
• Females (increase androgen) • Antihistamine
o Hirsutism, acne, deepening of voice • Laxative
o Virilism (development or premature development of • Enema
male secondary sexual characteristics) • Diet - low sodium, high CHO, Low CHON, Low fat

Nursing interventions
• Provide sufficient rest and comfort
o Provide bed rest with bathroom privileges.

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o Encourage gradual, progressive, increasing activity with • Assist in NGT and Sengstaken-Blakemore tube insertion for
planned rest periods. balloon tamponade.
o Institute measures to relieve pruritus.
◦ Do not use soaps and detergents
◦ Bathe in tepid water followed by application of an
emollient lotion.
◦ Provide cool, light, nonrestrictive clothing.
◦ Keep nails short to avoid skin excoriation from
scratching.
◦ Apply cool, moist compresses to pruritic areas.
• Promote nutritional intake
o Encourage small frequent feedings.
o Promote a high-calorie, low- to moderate- protein, high
CHO, low-fat diet, with supplemental vitamin therapy
(vitamins A, B- complex, C, D, K, and folic acid)
• Never leave the patient unattended during esophageal
Prevent infection balloon tamponade
• Prevent skin breakdown by frequent turning and skin care. • Closely monitor the lumen pressure
• Provide reverse isolation for clients with severe leukopenia; pay • Check VS q30 minutes. Maintain drainage and suction on the
special attention to hand-washing technique. suction’s ports
• Monitor WBC. • Watch for signs of respiratory distress while the tube is in place.
• Monitor/prevent bleeding. If this will happen, call another nurse to notify the physician and
• Administer diuretics as ordered quickly pinch the tube at the patient’s nose and cut it with
• Provide client teaching & D/C planning concerning: scissors, remove the tube
• Avoidance of agents that may be hepatotoxic (sedatives, • Deflate the esophageal balloon for about 30 minutes every 8-
opiates, or OTC drugs detoxified by the liver) 12 hours
• How to assess for weight gain and increased abdominal girth • Provide frequent mouth and nose care
• Avoidance of persons with upper respiratory infections
Surgical Management
• Recognition and reporting of signs of recurring illness (liver
• Endoscopic sclerotherapy – sclerosing agent is injected directly
tenderness, increased jaundice, increased fatigue, anorexia)
into the varix with a flexible fiberoptic endoscope to promote
• Avoidance of all alcohol
thrombosis & sclerosis of bleeding sites
• Avoidance of straining at stool, vigorous blowing of nose and
• Endoscopic Variceal ligation (variceal banding)
coughing, to decrease the incidence of bleeding
• Shunt procedures
o Dilated tortuous veins usually found in the submucosa of
the lower esophagus; however, they may develop higher IV. Esophageal Varices, Bleeding
in the esophagus or extend into the stomach
Bleeding or hemorrhage from esophageal varices is one of the
• Causes:
major causes of death in patients with cirrhosis. Esophageal varices
o Commonly caused by portal hypertension secondary to
are dilated tortuous veins usually found in the submucosa of the
liver cirrhosis
lower esophagus; they may develop higher in the esophagus or
extend into the stomach. The condition is nearly always caused by
portal hypertension. Risk factors for hemorrhage include muscular
strain from heavy lifting; straining at stool; sneezing, coughing, or
vomiting; esophagitis or irritation of vessels (rough food or irritating
fluids); reflux of stomach contents (especially alcohol); and
salicylates or any drug that erodes the esophageal mucosa.

Assessment Findings
• Hematemesis (vomiting of bright red blood)
• Melena (passing out of black, tarry stools)
• Hepatomegaly
• Splenomegaly
• Jaundice
• Ascites
• Signs of SHOCK!!! (Tachycardia, Hypotension, Tachypnea, Cold
clammy skin) Clinical Manifestations
• Hematemesis, melena, or general deterioration in mental or
Diagnostic Evaluation physical status; often a history of alcohol abuse.
• Upper GI endoscopy to identify the cause & site of bleeding • Signs and symptoms of shock (cool clammy skin, hypotension,
• Serum liver function test tachycardia) may be present

Nursing Interventions Assessment and Diagnostic Methods

• Monitor VS strictly (note: signs of shock), LOC • Endoscopy, barium swallow, ultrasonography, CT, and
• Maintain NPO, Monitor blood studies angiography
• Administer O2, Blood Transfusion, Vasopressin (Pitressin) • Neurologic and portal hypertension assessment

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• Liver function tests (serum aminotransferases, bilirubin, alkaline
phosphatase, and serum proteins)
• Splenoportography, hepatoportography, and celiac
angiography.
Medical Management
• Aggressive medical care includes evaluation of extent of
bleeding and continuous monitoring of vital signs when
hematemesis and melena are present.
• Signs of potential hypovolemia are noted; blood volume is
monitored with a central venous catheter or pulmonary artery
catheter.
• Oxygen is administered to prevent hypoxia and to maintain
adequate blood oxygenation, and IV fluids and volume
expanders are administered to restore fluid volume and
replace electrolytes.
• Transfusion of blood components may also be required.
• Nonsurgical treatment is preferred because of the high
mortality associated with emergency surgery to control
bleeding from esophageal varices and because of the poor
physical condition of most of these patients. Nonsurgical
measures include:
o Pharmacologic therapy: vasopressin (Pitressin),
vasopressin with nitroglycerin, somatostatin and
octreotide (Sandostatin), beta-blocking agents, and
nitrates
o Balloon tamponade, saline lavage, and endoscopic
sclerotherapy
o Esophageal banding therapy and variceal band ligation
o Transjugular intrahepatic portosystemic shunting (TIPS)
Surgical Management
If necessary, surgery may involve the following:
• Direct surgical ligation of varices
• Splenorenal, mesocaval, and portacaval venous shunts
• Esophageal transection with devascularization.
Nursing Management
Provide postoperative care similar to that for any thoracic or
abdominal operation.
• Monitor patient’s physical condition and evaluate emotional
responses and cognitive status.
• Monitor and record vital signs. Assess nutritional status.
• Perform a neurologic assessment, monitoring for signs of
hepatic encephalopathy (findings may range from drowsiness
to encephalopathy and coma).
• Treat bleeding by complete rest of the esophagus. Initiate
parenteral nutrition (PN) as ordered.
• Assist patient to avoid straining and vomiting. Maintain gastric
suction to keep the stomach as empty as possible.
• Provide frequent oral hygiene and moist sponges to the lips to
relieve thirst.
• Closely monitor blood pressure.
• Provide vitamin K therapy and multiple blood transfusions as
ordered for blood loss.
• Provide a quiet environment and calm reassurance to reduce
anxiety and agitation. Provide emotional support and pertinent
explanations regarding medical and nursing interventions.
• Monitor closely to detect and manage complications,
including hypovolemic or hemorrhagic shock, hepatic
encephalopathy, electrolyte imbalance, metabolic and
respiratory alkalosis, alcohol withdrawal syndrome, and
seizures.
ANATOMIC AND PHYSIOLOGIC OVERVIEW
The Gallbladder
• The gallbladder, a pear-shaped, hollow, saclike organ, 7.5 to
10 cm (3 to 4 in) long, lies in a shallow depression on the inferior
29 | 41
surface of the liver, to which it is attached by loose connective
tissue. The capacity of the gallbladder is 30 to 50 mL of bile. Its
wall is composed largely of smooth muscle. The gallbladder is
connected to the common bile duct by the cystic duct.
• The gallbladder functions as a storage depot for bile. Between
meals, when the sphincter of Oddi is closed, bile produced by
the hepatocytes enters the gallbladder. During storage, a large
portion of the water in bile is absorbed through the walls of the
gallbladder, so that bile in the gallbladder is five to 10 times
more concentrated than that originally secreted by the liver.
When food enters the duodenum, the gallbladder contracts
and the sphincter of Oddi (located at the junction of the
common bile duct with the duodenum) relaxes.
• Relaxation of this sphincter allows the bile to enter the intestine.
This response is mediated by secretion of the hormone
cholecystokinin- pancreozymin (CCK-PZ) from the intestinal
wall. Bile is composed of water and electrolytes (sodium,
potassium, calcium, chloride, and bicarbonate) along with
significant amounts of lecithin, fatty acids, cholesterol, bilirubin,
and bile salts. The bile salts, together with cholesterol, assist in
emulsification of fats in the distal ileum. They are then
reabsorbed into the portal blood for return to the liver, after
which they are once again excreted into the bile. This pathway
from hepatocytes to bile to intestine and back to the
hepatocytes is called the enterohepatic circulation. Because
of this circulation, only a small fraction of the bile salts that enter
the intestine are excreted in the feces. This decreases the need
for active synthesis of bile salts by the liver cells.
• Approximately half of the bilirubin, a pigment derived from the
breakdown of red blood cells, is a component of bile. It is
converted by the intestinal flora into urobilinogen, a highly
soluble substance. Urobilinogen is either excreted in the feces
or returned to the portal circulation, where it is reexcreted into
the bile. About 5% is normally absorbed into the general
circulation and then excreted by the kidneys. If the flow of bile
is impeded (e.g., by gallstones in the bile ducts), bilirubin does
not enter the intestine. As a result, blood levels of bilirubin
increase. This causes increased renal excretion of urobilinogen,
which results from conversion of bilirubin in the small intestine,
and decreased excretion in the stool. These changes produce
many of the signs and symptoms seen in gallbladder disorders.
The Pancreas
• The pancreas, located in the upper abdomen, has endocrine
as well as exocrine functions. The exocrine functions include
secretion of pancreatic enzymes into the gastrointestinal (GI)
tract through the pancreatic duct. The endocrine functions
include secretion of insulin, glucagon, and somatostatin
directly into the bloodstream.
The Exocrine Pancreas
• The secretions of the exocrine portion of the pancreas are
collected in the pancreatic duct, which joins the common bile
duct and enters the duodenum at the ampulla of Vater.
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Surrounding the ampulla is the sphincter of Oddi, which partially
controls the rate at which secretions from the pancreas and the
gallbladder enter the duodenum. The secretions of the
exocrine pancreas are digestive enzymes high in protein
content and an electrolyte-rich fluid.
• The secretions, which are very alkaline because of their high
concentration of sodium bicarbonate, are capable of
neutralizing the highly acid gastric juice that enters the
duodenum. The enzyme secretions include amylase, which
aids in the digestion of carbohydrates; trypsin, which aids in the
digestion of proteins; and lipase, which aids in the digestion of
fats. Other enzymes that promote the breakdown of more
complex foodstuffs are also secreted. Hormones originating in
the GI tract stimulate the secretion of these exocrine
pancreatic juices. The hormone secretin is the major stimulus for
increased bicarbonate secretion from the pancreas, and the
major stimulus for digestive enzyme secretion is the hormone
CCK-PZ. The vagus nerve also influences exocrine pancreatic
secretion.
The Endocrine Pancreas
• The islets of Langerhans, the endocrine part of the pancreas,
are collections of cells embedded in the pancreatic tissue.
They are composed of alpha, beta, and delta cells. The
hormone produced by the beta cells is called insulin; the alpha
cells secrete glucagon, and the delta cells secrete
somatostatin.
Insulin
• A major action of insulin is to lower blood glucose by permitting
entry of glucose into the cells of the liver, muscle, and other
tissues, where it is either stored as glycogen or used for energy.
Insulin also promotes the storage of fat in adipose tissue and
the synthesis of proteins in various body tissues. In the absence
of insulin, glucose cannot enter the cells and is excreted in the
urine. This condition, called diabetes mellitus, can be
diagnosed by high levels of glucose in the blood. In diabetes
mellitus, stored fats and protein are used for energy instead of
glucose, causing loss of body mass. (Diabetes mellitus is
discussed in detail in Chapter 41.) The level of glucose in the
blood normally regulates the rate of insulin secretion from the
pancreas.
Glucagon
• The effect of glucagon (opposite to that of insulin) is chiefly to
raise the blood glucose by converting glycogen to glucose in
the liver. Glucagon is secreted by the pancreas in response to
a decrease in the level of blood glucose.
Somatostatin
• Somatostatin exerts a hypoglycemic effect by interfering with
release of growth hormone from the pituitary and glucagon
from the pancreas, both of which tend to raise blood glucose
levels.
Endocrine Control of Carbohydrate Metabolism
• Glucose required for energy is derived by metabolism of
ingested carbohydrates and also from proteins by the process
of gluconeogenesis. Glucose can be stored temporarily in the
form of glycogen in the liver, muscles, and other tissues. The
endocrine system controls the level of blood glucose by
regulating the rate at which glucose is synthesized, stored, and
moved to and from the bloodstream. Through the action of
hormones, blood glucose is normally maintained at less than
100 mg/dL (5.5 mmol/L).
Insulin is the primary hormone that lowers the blood glucose level.
Hormones that raise the blood glucose level are glucagon,
epinephrine, adrenocorticosteroids, growth hormone, and thyroid
30 | 41
hormone. The endocrine and exocrine functions of the pancreas
are interrelated. The major exocrine function is to facilitate digestion
through secretion of enzymes into the proximal duodenum. Secretin
and CCK-PZ are hormones from the GI tract that aid in the digestion
of food substances by controlling the secretions of the pancreas.
Neural factors also influence pancreatic enzyme secretion.
Considerable dysfunction of the pancreas must occur before
enzyme secretion decreases and protein and fat digestion become
impaired. Pancreatic enzyme secretion is normally 1500 to 2500
mL/day.
V. Cholelithiasis and Cholecystitis
• In cholelithiasis, calculi (gallstones) usually form in the
gallbladder from solid constituents of bile and vary greatly in
size, shape, and composition. There are two major types of
gallstones: pigment stones, which contain an excess of
unconjugated pigments in the bile, and cholesterol stones (the
more common form), which result from bile supersaturated with
cholesterol due to increased synthesis of cholesterol and
decreased synthesis of bile acids that dissolve cholesterol.
• Risk factors for pigment stones include cirrhosis, hemolysis, and
infections of the biliary tract. These stones cannot be dissolved
and must be removed surgically. Risk factors for cholesterol
stones include gender (women are two to three times more
likely to develop cholesterol stones); use of oral contraceptives,
estrogens, and clofibrate; age (usually older than 40 years);
multiparous status; and obesity. There is also an increased risk
related to diabetes, GI tract disease, T-tube fistula, and ileal
resection or bypass. FAT, FEMALE, FORTY, FERTILE
• Cholecystitis, an acute complication of cholelithiasis, is an
acute infection of the gallbladder. Most patients with
cholecystitis have gallstones (calculous cholecystitis). A
gallstone obstructs bile outflow and bile in the gallbladder
initiates a chemical reaction, resulting in edema, compromise
of the vascular supply, and gangrene. In the absence of
gallstones, cholecystitis (acalculous) may occur after surgery,
severe trauma, or burns, or with torsion, cystic duct obstruction,
multiple blood transfusions, and primary bacterial infections of
the gallbladder. Infection causes pain, tenderness, and rigidity
of the upper right abdomen and is associated with nausea and
vomiting and the usual signs of inflammation. Purulent fluid
inside the gallbladder indicates an empyema of the
gallbladder.
• Theory of Stone formation: Metabolic factors (obesity,
pregnancy, DM, hypothyroidism, stasis) may all lead to
stagnation of bile in the gallbladder → excessive absorption of
water → precipitation of salts (stones)
• Gallstones are composed primarily of cholesterol (80%), bile
salts, Ca++, bilirubin & CHONs
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Clinical Manifestations
• May be silent, producing no pain and only mild GI symptoms
• May be acute or chronic with epigastric distress (fullness,
abdominal distention, and vague upper right quadrant pain);
may follow a meal rich in fried or fatty foods
• If the cystic duct is obstructed, the gallbladder becomes
distended, inflamed, and eventually infected; fever and
palpable abdominal mass; biliary colic with epigastric pain
lasting approximately 30min, excruciating RUQ abdominal
pain, radiating to back or right shoulder with nausea and
vomiting several hours after a heavy meal; restlessness and
constant or colicky pain and leukocytosis (↑WBC)
• Jaundice, accompanied by marked itching, with obstruction
of the common bile duct, in a small percentage of patients
• Pruritus, easy bruising, very dark urine; grayish or clay-colored
stool.
• Deficiencies of vitamins A, D, E, and K (fat-soluble vitamins)
• Charcot triad: fever, jaundice, pain in RUQ pain (ascending
cholangitis)
• Intolerance for fatty foods (steatorrhea, N&V, sensation of
fullness)
Assessment and Diagnostic Methods
• Cholecystogram, cholangiogram; celiac axis arteriography
• Laparoscopy, Ultrasonography; EUS
• Helical CT scans and MRI; ERCP
• Serum alkaline phosphatase; gamma-glutamyl (GGT),
gamma-glutamyl transpeptidase (GGTP), LDH
• Cholesterol levels
• Direct bilirubin, transaminase, alkaline phosphatase, WBC,
amylase, lipase: all increased
• Oral cholecystogram (gallbladder series): positive for gallstone
Gerontologic Considerations
• Surgical intervention for disease of the biliary tract is the most
common operation performed in the elderly.
• Biliary disease may be accompanied or preceded by
symptoms of septic shock: oliguria, hypotension, mental
changes, tachycardia, and tachypnea.
• Cholecystectomy is usually well tolerated and carries a low risk
if expert assessment and care are provided before, during, and
after surgery.
• Mortality from serious complications is high. Risk of
complications and shorter hospital stays make it essential that
older patients and their family members receive specific
information about signs and symptoms of complications and
measures to prevent them.
Nursing Intervention
• Administer pain medications as ordered & monitor for effects.
• Administer IV fluids as ordered.
• Provide small, frequent meals of modified diet, low fat (if oral
intake allowed)
• Provide care to relieve pruritus
• Provide care for the client with a cholecystectomy or
choledochostomy
Medical Management
• Major objectives of medical therapy are to reduce the
incidence of acute episodes of gallbladder pain and
cholecystitis by supportive and dietary management and, if
possible, to remove the cause by pharmacotherapy,
endoscopic procedures, or surgical intervention.
• Supportive treatment: NPO with NG intubation and IV fluids
• Diet modification with administration of fat- soluble vitamins
• Drug therapy
o NSAIDS – Ketorolac
o Narcotic analgesics for pain
31 | 41
o Morphine vs Demerol
o Anticholinergics (atropine) may be used for pain
o Antiemetics
Nutritional and Supportive Therapy
• Achieve remission with rest, IV fluids, nasogastric suction,
analgesia, and antibiotics.
• Diet immediately after an episode is usually low-fat liquids with
high protein and carbohydrates followed by solid soft foods as
tolerated, avoiding eggs, cream, pork, fried foods, cheese, rich
dressings, gas- forming vegetables, and alcohol.
Pharmacologic Therapy
• Ursodeoxycholic acid (UDCA [Urso, Actigall]) and
chenodeoxycholic acid (chenodiol or CDCA [Chenix]) are
effective in dissolving primarily cholesterol stones.
• Patients with significant, frequent symptoms; cystic duct
occlusion; or pigment stones are not candidates for therapy
with UDCA.
Nonsurgical Removal of Gallstones
• In addition to dissolving gallstones, they can be removed by
other instrumentation (e.g., catheter and instrument with a
basket attached are threaded through the T-tube tract or
fistula formed at the time of T-tube insertion, ERCP endoscope),
intracorporeal lithotripsy (laser pulse), or extracorporeal shock
wave therapy (lithotripsy or extracorporeal shock wave
lithotripsy [ESWL]).
Surgical Management
Goal of surgery is to relieve persistent symptoms, to remove the
cause of biliary colic, and to treat acute cholecystitis.
• Laparoscopic cholecystectomy: performed through a small
incision or puncture made through the abdominal wall in the
umbilicus. Performed via laparoscopy for uncomplicated cases
when client has not had previous abdominal surgery.
• Cholecystectomy: Gallbladder is removed through an
abdominal incision (usually right subcostal) after ligation of the
cystic duct and artery.
• Minicholecystectomy: Gallbladder is removed through a small
incision.
• Choledochostomy: incision into the common duct for stone
removal and insertion of a t-tube.
• Cholecystostomy (surgical or percutaneous): Gallbladder is
opened, and the stone, bile, or purulent drainage is removed.
• Cholecystectomy with choledochotomy: removal of the
gallbladder with insertion of a T-tube into the common bile duct
if common bile duct exploration is performed.
Nursing Interventions
• Provide routine pre-op care
• Provide routine post-op care
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• Position client in semi-Fowler’s or side-lying positions; reposition
frequently.
• Splint incision when turning, coughing, and deep breathing
• Maintain/monitor functioning of T-tube
o Ensure that T-tube is connected to closed gravity
drainage.
o Avoid kinks, clamping, or pulling of the tube.
o Measure and record drainage every shift
o Expect 300 – 500 ml bile-colored drainage for the 1st 24°
then 200 ml/24° for 3 - 4 days
o Assess for signs of peritonitis
o Monitor color of urine and stools (stools will be light colored
if bile is flowing through T tube but normal color should
reappear as drainage diminishes)
o Assess skin around T-tube; cleanse frequently and keep dry
• Provide client teaching and discharge planning concerning
o Adherence to dietary restrictions
o Resumption of ADL
◦ Avoid heavy lifting for at least 6 weeks
◦ Resume sexual activity as desired unless ordered
otherwise by physician: clients having laparoscopy
cholecystectomy usually resume normal activity
within two weeks
◦ Recognition and reporting of signs of complications
(fever, jaundice, pain, dark urine, pale stools, pruritus)
VI. Pancreatitis, Acute
• Pancreatitis (inflammation of the pancreas) is a serious disorder
that can range in severity from a relatively mild, self-limiting
disorder to a rapidly fatal disease that does not respond to any
treatment.
• Acute pancreatitis is commonly described as an autodigestion
of the pancreas by the exocrine enzymes it produces,
principally trypsin. Eighty percent of patients with acute
pancreatitis have biliary tract disease or a history of long-term
alcohol abuse. Other less common causes of pancreatitis
include bacterial or viral infection, with pancreatitis
occasionally developing as a complication of mumps virus.
Many disease processes and conditions have been associated
with an increased incidence of pancreatitis, including surgery
on or near the pancreas, medications, hypercalcemia, and
hyperlipidemia.
• Up to 10% of cases are idiopathic, and there is a small
incidence of hereditary pancreatitis. Mortality is high because
of shock, anoxia, hypotension, or fluid and electrolyte
imbalances. Attacks of acute pancreatitis may result in
complete recovery, may recur without permanent damage, or
may progress to chronic pancreatitis.
Clinical Manifestations
Severe abdominal pain is the major symptom.
• Pain in the midepigastrium may be accompanied by
abdominal distention; a poorly defined, palpable abdominal
32 | 41
mass; decreased peristalsis; and vomiting that fails to relieve
the pain or nausea.
• Pain is frequently acute in onset (24 to 48 hours after a heavy
meal or alcohol ingestion); may be more severe after meals
and unrelieved by antacids.
• Patient appears acutely ill.
• Abdominal guarding; rigid or board-like abdomen (generally
an ominous sign, usually indicating peritonitis).
• Ecchymosis in the flank or around the umbilicus, which may
indicate severe hemorrhagic pancreatitis.
• Nausea and vomiting, fever, jaundice, mental confusion,
agitation.
• Hypotension related to hypovolemia and shock.
• May develop tachycardia, cyanosis, and cold, clammy skin.
• Acute renal failure common.
• Respiratory distress and hypoxia.
• May develop diffuse pulmonary infiltrates, dyspnea,
tachypnea, and abnormal blood gas values.
• Myocardial depression, hypocalcemia, hyperglycemia, and
disseminated intravascular coagulation (DIC).
Assessment and Diagnostic Findings
• Diagnosis is based on history of abdominal pain, the presence
of known risk factors, physical examination findings, and
diagnostic findings (increased urine amylase level and white
blood cell [WBC] count; hypocalcemia; transient
hyperglycemia; glucosuria and increased serum bilirubin levels
in some patients). X-rays of abdomen and chest, ultrasound,
and contrast-enhanced computed tomography (CT) scan
may be performed. Hematocrit and hemoglobin levels are
used to monitor the patient for bleeding.
• Serum amylase and lipase levels are most indicative (elevated
within 24 hours; amylase returns to normal within 48 to 72 hours;
lipase remains elevated for longer period). Peritoneal fluid is
evaluated for increase in pancreatic enzymes.
Medical Management: Acute Phase
During the acute phase, management is symptomatic and directed
toward preventing or treating complications.
• Oral intake is withheld to inhibit pancreatic stimulation and
secretion of pancreatic enzymes.
• Parenteral nutrition (PN) is administered to the debilitated
patient.
• Nasogastric suction is used to relieve nausea and vomiting and
to decrease painful abdominal distention and paralytic ileus.
• Histamine-2 (H2) receptor antagonists (cimetidine, ranitidine)
or, sometimes, proton pump inhibitors are given to decrease
hydrochloric acid secretion.
• Adequate pain medication, such as morphine, is administered.
Antiemetic agents may be prescribed to prevent vomiting.
• Correction of fluid, blood loss, and low albumin levels is
necessary.
• Antibiotics are administered if infection is present. Insulin is
necessary if significant hyperglycemia occurs.
• Aggressive respiratory care is provided for pulmonary infiltrates,
effusion, and atelectasis.
• Biliary drainage (drains and stents) results in decreased pain
and increased weight gain.
• Surgical intervention may be performed for diagnosis,
drainage, resection, or debridement.
Medical Management: Post-acute Phase
• Antacids are given when the acute episode begins to resolve.
• Oral feedings low in fat and protein are initiated gradually.
• Caffeine and alcohol are eliminated.
• Medications (e.g., thiazide diuretics, glucocorticoids, or oral
contraceptives) are discontinued.
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Nursing Management • Administer prescribed fluids, medications, and blood products.

Relieving Pain and Discomfort • Assist with supportive management, such as mechanical
• Administer analgesics as prescribed. Current recommendation ventilation.
for pain management is parenteral opioids, including
Shock and Multiple Organ Failure
morphine, hydromorphone, or fentanyl via patient-controlled
• Monitor patient closely for early signs of neurologic,
analgesia or bolus.
cardiovascular, renal, and respiratory dysfunction.
• Frequently assess pain and the effectiveness of the
• Prepare for rapid changes in patient status, treatment, and
pharmacologic interventions.
therapies; respond quickly.
• Withhold oral fluids to decrease formation and secretion of
• Inform family of status and progress of patient; allow time with
secretin.
patient.
• Use nasogastric suctioning to remove gastric secretions and
relieve abdominal distention; provides frequent oral hygiene VII. Pancreatitis, Chronic
and care to decrease discomfort from the nasogastric tube
• Chronic pancreatitis is an inflammatory disorder characterized
and relieve dryness of the mouth.
by progressive anatomic and functional destruction of the
• Maintain patient on bed rest to decrease metabolic rate and
pancreas. Cells are replaced by fibrous tissue with repeated
to reduce secretion of pancreatic enzymes; report increased
attacks of pancreatitis. The end result is obstruction of the
pain (may be pancreatic hemorrhage or inadequate
pancreatic and common bile ducts and duodenum.
analgesic dosage).
• In addition, there is atrophy of the epithelium of the ducts,
• Provide frequent and repeated but simple explanations about
inflammation, and destruction of the secreting cells of the
treatment; patient may have clouded sensorium from pain,
pancreas. Alcohol consumption in Western societies and
fluid imbalances, and hypoxemia.
malnutrition worldwide are the major causes. The incidence of
Improving Breathing Pattern pancreatitis among alcoholics is 50 times the rate in the
nondrinking population.
• Maintain patient in semi-Fowler’s position to decrease pressure
on diaphragm.
• Change position frequently to prevent atelectasis and pooling
of respiratory secretions.
• Assess respiratory status frequently (pulse oximetry, arterial
blood gas [ABG] values), and teach patient techniques of
coughing and deep breathing and the use of incentive
spirometry.

Improving Nutritional Status

• Assess nutritional status and note factors that alter the patient’s
nutritional requirements (e.g., temperature elevation, surgery,
drainage).
• Monitor laboratory test results and daily weights.
• Provide enteral nutrition or PN as prescribed.
• Monitor serum glucose level every 4 to 6 hours.
• Introduce oral feedings gradually as symptoms subside.
Pathophysiology
• Avoid heavy meals and alcoholic beverages.
• Long-term alcohol consumption causes hypersecretion of
Maintaining Skin Integrity protein in pancreatic secretions, resulting in protein plugs and
• Assess the wound, drainage sites, and skin carefully for signs of calculi within the pancreatic ducts. Alcohol has a direct toxic
infection, inflammation, and breakdown. effect on the cells of the pancreas. Damage is more severe in
• Carry out wound care as prescribed, and take precautions to patients with diets low in protein and very high or very low in fat.
protect intact skin from contact with drainage; consult with a Smoking is another factor in the development of chronic
wound–ostomy–continence nurse as needed to identify pancreatitis. Because heavy drinkers usually smoke, it is difficult
appropriate skin care devices and protocols. to separate the effects of the alcohol abuse and smoking.
• Turn patient every 2 hours; use of specialty beds may be
Clinical Manifestations
indicated to prevent skin breakdown.
• Recurring attacks of severe upper abdominal and back pain,
Monitoring and Managing Complications accompanied by vomiting; opioids may not provide relief.
Fluid and Electrolyte Disturbances • Risk of addiction to opiates is high because of the severe pain.
• There may be continuous severe pain or dull, nagging,
• Assess fluid and electrolyte status by noting skin turgor and
constant pain.
moistness of mucous membranes.
• Weight loss is a major problem
• Weigh daily; measure all fluid intake and output.
• Altered digestion (malabsorption) of foods (proteins and fats)
• Assess for other factors that may affect fluid and electrolyte
results in frequent, frothy, and foul- smelling stools with a high
status, including increased body temperature and wound
fat content (steatorrhea).
drainage.
• As disease progresses, calcification of the gland may occur
• Observe for ascites, and measure abdominal girth.
and calcium stones may form within the ducts.
• Administer intravenous (IV) fluids and blood or blood products
to maintain volume and prevent or treat shock. Assessment and Diagnostic Methods
• Report decreased blood pressure, reduced urine output, and
• Endoscopic retrograde cholangiopancreatography (ERCP) is
low serum calcium and magnesium.
the most useful study.
Pancreatic Necrosis • Various imaging procedures, including magnetic resonance
imaging (MRI), CT scans, and ultrasound.
• Transfer patient to intensive care unit for close monitoring.

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• A glucose tolerance test evaluates pancreatic islet cell
function.
• Steatorrhea is best confirmed by laboratory analysis of fecal fat
content.
Medical Management
Treatment is directed toward preventing and managing acute
attacks, relieving pain and discomfort, and managing exocrine and
endocrine insufficiency of pancreatitis.
• Endoscopy to remove pancreatic duct stones, correct
strictures, and drain cysts may be effective in selected patients
to manage pain and relieve obstruction.
• Pain and discomfort are relieved with analgesics; yoga may be
an effective nonpharmacologic method for pain reduction
and for relief of other coexisting symptoms.
• Patient should avoid alcohol and foods that produce
abdominal pain and discomfort. No other treatment will relieve
pain if patient continues to consume alcohol.
• Diabetes mellitus resulting from dysfunction of pancreatic islet
cells is treated with diet, insulin, or oral hypoglycemic agents.
Patient and family are taught the hazard of severe
hypoglycemia related to alcohol use.
• Pancreatic enzyme replacement therapy is instituted for
malabsorption and steatorrhea.
• Surgery is done to relieve abdominal pain and discomfort,
restore drainage of pancreatic secretions, and reduce
frequency of attacks (pancreaticojejunostomy).
• Morbidity and mortality after surgical procedures are high
because of patient’s poor physical condition before surgery
and concomitant occurrence of cirrhosis.
TERMINOLOGIES
1. Albumin: A protein made in the liver that assists in maintaining
blood volume in the arteries and veins. If the liver is damaged,
then the albumin can drop to very low levels, which may cause
fluid to leak into the tissues from the blood vessels, resulting in
edema or swelling. In acute liver failure, there is an
accumulation of fluid in the abdomen that is known as
“ascites”.
2. Ascites: A large, abnormal accumulation of fluid in the
abdomen that can occur due to liver failure, cirrhosis and liver
cancer. This condition requires immediate medical attention.
3. Cholate: The major primary bile acid produced in the liver that
facilitates fat absorption and cholesterol excretion.
4. Cirrhosis: A serious liver condition characterized by irreversible
scarring of the liver that can lead to liver failure and death.
Alcohol and chronic viral hepatitis (such as chronic hepatitis B
and C) can cause continuous inflammation of the liver, which
can lead to excess scar formation or fibrosis. Scarring results in
the loss of liver cells and impairs liver function.
5. Decompensation: Term for describing the development of
measurable deterioration or clinical complication in patients
with chronic liver disease.
6. Encephalopathy: Serious brain function abnormalities
experienced by some patients with advanced liver disease.
Symptoms most commonly include confusion, disorientation,
insomnia, and may progress to a coma.
7. Endoscopy: A medical procedure where a doctor puts a tube-
like instrument into the body to look inside. Unlike most other
medical imaging devices, endoscopes are inserted directly
into the organ. There are many types of endoscopy, each of
which is designed for looking at a certain part of the body.
8. Enzymes: Naturally occurring chemical substances in the
human body that help chemical reaction take place.
9. Fibrosis: Growth of fibrous tissue in the liver where there is usually
liver cell damage or destruction. Fibrosis can lead to cirrhosis,
an even more serious liver disease.
34 | 41
10. Gastroenterology: The field of medicine that focuses on the
function and disorders of the GI system, which includes the
esophagus, stomach, pancreas, intestines, and liver.
11. Hemochromatosis: is a disorder that interferes with the body’s
ability to break down iron, and results in too much iron being
absorbed from the gastrointestinal tract.
12. Hepatic Impairment: Liver failure is the inability of the liver to
perform its normal synthetic and metabolic function as part of
normal physiology.
13. Hepatic Venous Pressure Gradient (HVPG): Currently, the most
commonly used parameter to directly measure portal pressure
is the Hepatic Venous Pressure Gradient (HVPG). HVPG
represents the gradient between pressures in the portal vein
and the intra-abdominal portion of inferior vena cava.
14. Hepatitis B: Formerly called “serum hepatitis”, it is caused by the
hepatitis B virus (HBV). It is spread primarily through blood,
unprotected sex, shared needles, and from an infected mother
to her newborn during the delivery process. There is a safe
vaccine for HBV.
15. Hepatitis C: Formerly known as “non-A, non-B hepatitis”, it is
caused by the hepatitis C virus (HCV). It is spread through
infected blood, primarily in those who use illicit street drugs and
those who received blood transfusions prior to 1992 (the first
year that a blood test for HCV became available for screening
the blood supply). There is no vaccine.
16. Hepatology: is the medical specialty focusing on treatment of
diseases, disorders, and conditions of the liver. Hepatology is a
subspecialty of internal medicine, and is often practiced in
conjunction with gastroenterology, another subspecialty of
internal medicine. Hepatologists treat liver diseases such as all
types of hepatitis, and cirrhosis of the liver.
17. Liquid Chromatography-Mass Spectrometry (LC-MS): An
analytical chemistry technique that combines the physical
separation capabilities of liquid chromatography (or HPLC)
with the mass analysis capabilities of mass spectrometry. LC-MS
is a powerful technique with has very high sensitivity and
specificity. Generally, its application is oriented towards the
specific detection and potential identification of chemicals in
the presence of other chemicals (in a complexmixture).
18. Liver Biopsy: The removal of a small piece of tissue from the liver
using a special needle. The tissue is examined under a
microscope to look for the presence of inflammation or liver
damage.
19. Portal Circulation refers to the circulation of the blood from the
small intestine to the liver, via the portal vein.
20. Portal Vein: The hepatic portal vein is a vein in the abdominal
cavity that drains blood from the gastrointestinal tract and
spleen to the liver.
21. Varices: Enlarged veins within the gastrointestinal tract that
form as a result of cirrhosis.
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ANATOMY AND PHYSIOLOGY OF THE ENDOCRINE SYSTEM
Functions of the Endocrine System
• Composed of ductless glands that releases hormones directly
into the bloodstream
• Hypothalamus control most of the endocrinal activity of the
pituitary gland
• Secretes RELEASING HORMONES: GHRH, CRH, TRH, GnRH, PRH
• Despite the huge variety of hormones, there are really only two
mechanisms by which hormones trigger changes in cells.
1. Water equilibrium. The endocrine system controls water
equilibrium by regulating the solute concentration of the blood.
2. Growth, metabolism, and tissue maturation. The endocrine
system controls the growth of many tissues, like the bone and
muscle, and the degree of metabolism of various tissues, which
aids in the maintenance of the normal body temperature and
normal mental functions. Maturation of tissues, which appears
in the development of adult features and adult behavior, are
also determined by the endocrine system.
3. Heart rate and blood pressure management. The endocrine
system assists in managing the heart rate and blood pressure
and aids in preparing the body for physical motion.
4. Immune system control. The endocrine system helps regulate
the production and functions of immune cells.
5. Reproductive function controls. The endocrine system regulates
the development and the functions of the reproductive
systems in males and females.
6. Uterine contractions and milk release. The endocrine system
controls uterine contractions throughout the delivery of the
newborn and stimulates milk release from the breasts in
lactating females.
7. Ion management. The endocrine system regulates Na+, K+,
and Ca2+ concentrations in the blood.
8. Blood glucose regulator. The endocrine system controls blood
glucose levels and other nutrient levels in the blood.
9. Direct gene activation. Being lipid-soluble molecules, the
steroid hormones can diffuse through plasma membranes of
their target cells; once inside, the steroid hormone enters the
nucleus and binds to a specific receptor protein there; then,
the hormone-receptor complex binds to specific sites on the
cell’s DNA, activating certain genes to transcribe messenger
RNA; the mRNA then is translated in the cytoplasm, resulting in
the synthesis of new proteins.
10. Second messenger system. Water-soluble, nonsteroidal
hormones-protein, and peptide hormones- are unable to enter
the target cells, so instead, they bind to receptors situated on
the target cell’s plasma membrane and utilize a second
messenger system.
Anatomy of the Endocrine System
Compared to other organs of the body, the organs of the endocrine
system are small and unimpressive, however, functionally the
endocrine organs are very impressive, and when their role in
maintaining body homeostasis is considered, they are true giants.
35 | 41
Hypothalamus
The major endocrine organs of the body include the pituitary,
thyroid, parathyroid, adrenal, pineal and thymus glands, the
pancreas, and the gonads.
• The hypothalamus, which is part of the nervous system, is also
considered as a major endocrine organ because it produces
several hormones. It is an important autonomic nervous system
and endocrine control center of the brain located inferior to
the thalamus.
• Mixed functions. Although the function of some hormone-
producing glands is purely endocrine, the function of others
(pancreas and gonads) is mixed- both endocrine and
exocrine.
Pituitary Gland
The pituitary gland is approximately the size of a pea.
• Location. The pituitary gland hangs by a stalk from the inferior
surface of the hypothalamus of the brain, where it is snugly
surrounded by the “Turk’s saddle” of the sphenoid bone.
• Lobes. It has two functional lobes – the anterior pituitary
(glandular tissue) and the posterior pituitary (nervous tissue).
o Anterior Pituitary (Adenohypophysis)
◦ 70% of the gland
◦ Found in the sella turcica, a depression in the
sphenoid bone at the base of the brain
o Posterior Pituitary (Neurohypophysis)
◦ Stores & secretes ADH & Oxytocin produced by the
hypothalamus
Hormones of the Anterior Pituitary
There are several hormones of the anterior pituitary hormones that
affect many body organs.
• Growth hormone (GH) is a general metabolic hormone;
however, its major effects are directed to the growth of skeletal
muscles and long bones of the body; it is a protein- sparing and
anabolic hormone that causes amino acids to be built into
proteins and stimulates most target cells to grow in size and
divide.
• Prolactin (PRL) is a protein hormone structurally similar to growth
hormone; its only known target in humans is the breast
because, after childbirth, it stimulates and maintains milk
production by the mother’s breast.
• Adrenocorticotropic hormone (ACTH) regulates the endocrine
activity of the cortex portion of the adrenal gland.
• Thyroid-stimulating hormone (TSH) also called thyrotropin
hormone influences the growth and activity of the thyroid
gland.
• Gonadotropic hormones regulate the hormonal activity of
gonads (ovaries and testes).
• Follicles-stimulating hormone (FSH) stimulates follicle
development in the ovaries; as the follicles mature, they
produce estrogen and eggs that are readied for ovulation; in
men, FSH stimulates sperm development by the testes.
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• Luteinizing hormone (LH) triggers ovulation of an egg from the
ovary and causes the ruptured follicle to produce
progesterone and some estrogen; in men, LH stimulates
testosterone production by the interstitial cells of the testes.
• Melanocyte-stimulating hormone (MSH) is a peptide hormone
secreted by the cells of the anterior pituitary, particularly the
corticotrophic cell. Corticotrophic cells are one of the different
types of cells in the anterior pituitary (credits from google).
Hormones of the Posterior Pituitary
The posterior pituitary is not an endocrine gland in the strict sense
because it does not make the peptide hormones it releases, but it
simply acts as a storage area for hormones made by hypothalamic
neurons.
• Oxytocin is released in significant amount only during childbirth
and in nursing women; it stimulates powerful contractions of the
uterine muscle during labor, during sexual relations, and during
breastfeeding and also causes milk ejection (let-down reflex) in
a nursing woman.
• Antidiuretic hormone (ADH) causes the kidneys to reabsorb
more water from the forming of urine; as a result, urine volume
decreases and blood volume increases; in larger amounts, ADH
also increases blood pressure by causing constriction of the
arterioles, so it is sometimes referred to as vasopressin.
additional
• Disorders are generally grouped into:
o HYPER – when the gland secretes excessive hormones
o HYPO – when the gland does not secrete enough
hormones
• Hyper and Hypo can be classified as:
o PRIMARY – when the Gland itself is the problem
o SECONDARY – when the problem is the pituitary or the
hypothalamus.
• Growth hormone (Somatotropin) – Growth of body tissues and
bone
o Hypersecretion:
◦ Gigantism (children)
◦ Acromegaly (adults)
◦ Hypo-secretion of GH: Dwarfism
• Prolactin (Mammotropic/ Lactotropic Hormone) – Mammary
tissue growth and lactation.
o Hypersecretion:
◦ Galactorrhea (abnormal breast-milk production)
o Hyposecretion:
◦ Absence of milk during lactation
• ACTH (Adrenocorticotropic Hormone) – Stimulates adrenal
cortex to secrete the adrenal hormones cortisol & aldosterone
o Hypersecretion:
◦ Cushing’s Syndrome
o Hyposecretion:
◦ Addison’s Disease
• TSH (Thyroid Stimulating Hormone) - Stimulates the thyroid gland
to secrete T3 and T4
o Hypersecretion:
◦ Hyperthyroidism
o Hyposecretion:
◦ Hypothyroidism
• Gonadotropin (FSH/ LH) – Affect growth, maturity and
functioning of primary and secondary sex characteristics. They
influence the gonads (ovaries and testes) to secrete gonadal
hormones- estrogen, progesterone, testosterone
o Hypersecretion:
◦ precocious puberty
o Hyposecretion
◦ Males: impotence, decrease production of
spermatozoa
◦ Females: no ovulation, no menstruation, infertility
36 | 41
• MSH (Melanocyte Stimulating Hormone) – Stimulates the skin
melanocytes to produce the pigment melanin
o Hypersecretion:
◦ Bronze appearance of the skin (hyperpigmentation)
o Hyposecretion:
◦ Albinism (hypopigmentation)
• ADH (Antidiuretic Hormone / Vasopressin) – causes the renal
retention of water (not affecting sodium) in the renal tubules. It
can also cause vasoconstriction; “vasopressin”
o Hypersecretion:
◦ SIADH – excessive retention of water by the renal
tubules:
o Hyposecretion:
◦ DI – inability of the renal tubules to retain water
o Diagnostic Test: Water deprivation test
• Oxytocin – released during childbirth to cause uterine
contraction and responsible for the “let-down” reflex of milk
ejection
Thyroid Gland
The thyroid gland is a hormone-producing gland that is familiar to
most people primarily because many obese individuals blame their
overweight condition on their “glands” (thyroid).
• Location. The thyroid gland is located at the base of the throat,
just inferior to the Adam’s apple, where it is easily palpated
during a physical examination.
• Lobes. It is a fairly large gland consisting of two lobes joined by
a central mass, or isthmus.
• Composition. Internally, the thyroid gland is composed of
hollow structures called follicles, which store a sticky colloidal
material.
• Types of thyroid hormones. Thyroid hormone often referred to
as the body’s major metabolic hormone, is actually two active,
iodine-containing hormones, thyroxine or T4, and
triiodothyronine or T3.
• Thyroxine is the major hormone secreted by the thyroid follicles.
• Most triiodothyronine is formed at the target tissues by
conversion of the thyroxine to triiodothyronine.
• Function. Thyroid hormone controls the rate at which glucose is
“burned” oxidized, and converted to body heat and chemical
energy; it is also important for normal tissue growth and
development.
• Calcitonin decreases blood calcium levels by causing calcium
to be deposited in the bones; calcitonin is made by the so-
called parafollicular cells found in the connective tissues
between the follicles.
Parathyroid Glands
The parathyroid glands are mostly tiny masses of glandular tissue.
• Location. The parathyroid glands are located on the posterior
surface of the thyroid gland.
• The parathyroids secrete parathyroid hormone (PTH) or
parathormone, which is the most important regulator of
calcium ion homeostasis of the blood; PTH is a hypercalcemic
hormone (that is, it acts to increase blood levels of calcium),
whereas calcitonin is a hypocalcemic hormone.; PTH also
stimulates the kidneys and intestines to absorb more calcium.
Adrenal Glands
Although the adrenal gland looks like a single organ, it is structurally
and functionally two endocrine organs in one.
Hormones of the Adrenal Cortex
The adrenal cortex produces three major groups of steroid
hormones, which are collectively called corticosteroids–
mineralocorticoids, glucocorticoids, and sex hormones.
• The mineralocorticoids, primarily aldosterone, are produced by
the outermost adrenal cortex cell layer; mineralocorticoids are
important in regulating the mineral (or salt) content of the
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blood, particularly the concentrations of sodium and potassium
ions and they also help in regulating the water and electrolyte
balance in the body.
• Renin, an enzyme produced by the kidneys when the blood
pressure drops, also cause the release of aldosterone by
triggering a series of reactions that form angiotensin II, a potent
stimulator of aldosterone release.
• Atrial natriuretic peptide (ANP) prevents aldosterone release, its
goal being to reduce blood volume and blood pressure.
• The middle cortical layer mainly produces glucocorticoids,
which include cortisone and cortisol; glucocorticoids promote
normal cell metabolism and help the body to resist long-term
stressors, primarily by increasing blood glucose levels, thus it is
said to be a hyperglycemic hormone; it also reduces pain and
inflammation by inhibiting some pain-causing molecules called
prostaglandins.
• Both male and female sex hormones are produced by the
adrenal cortex throughout life in relatively small amounts;
although the bulk of sex hormones produced by the innermost
cortex layer are androgens (male sex hormones), some
estrogens (female sex hormones), are also formed.
Hormones of the Adrenal Medulla
The adrenal medulla, like the posterior pituitary, develops from a
knot of nervous tissue.
• When the medulla is stimulated by sympathetic nervous system
neurons, its cells release two similar hormones, epinephrine, also
called adrenaline, and norepinephrine (noradrenaline), into
the bloodstream; collectively, these hormones are referred to
as catecholamines.
• Function. Basically, the Catecholamines increase heart rate,
blood pressure, and blood glucose levels and dilate the small
passageways of the lungs; the catecholamines of the adrenal
medulla prepare the body to cope with a brief or short-term
stressful situation and cause the so-called alarm stage of the
stress response.
Pancreatic Islets
The pancreas, located close to the stomach in the abdominal
cavity, is a mixed gland.
• The islets of Langerhans also called pancreatic islets, are little
masses of hormone-producing tissue that are scattered among
the enzyme-producing acinar tissue of the pancreas.
• Two important hormones produced by the islet cells are insulin
and glucagon.
• Islet cells act as fuel sensors, secreting insulin and glucagon
appropriately during fed and fasting states.
• High levels of glucose in the blood stimulate the release of
insulin from the beta cells of the islets.
• Glucagon’s release by the alpha cells of the islets is stimulated
by low blood glucose levels.
• Insulin acts on just about all the body cells and increases their
ability to transport glucose across their plasma membranes;
because insulin sweeps glucose out of the blood, its effect is
said to be hypoglycemic.
• Glucagon acts as an antagonist of insulin; that is, it helps to
regulate blood glucose levels but in a way opposite that of
insulin; its action is basically hyperglycemic and its primary
target organ is the liver, which it stimulates to break down
stored glycogen into glucose and release the glucose into the
blood.
Pineal Gland
The pineal gland, also called the pineal body, is a small cone-
shaped gland.
• Location. The pineal gland hangs from the roof of the third
ventricle of the brain.
37 | 41
• Melatonin is the only hormone that appears to be secreted in
substantial amounts by the pineal gland; the levels of
melatonin rise and fall during the course of the day and night;
peak levels occur at night and make us drowsy as melatonin is
believed to be the “sleep trigger” that plays an important role
in establishing the body’s day-night cycle.
Thymus Gland
The thymus gland is large in infants and children and decreases in
size throughout adulthood.
• Location. The thymus gland is located in the upper thorax,
posterior to the sternum.
• The thymus produces a hormone called thymosin and others
that appear to be essential for normal development of a
special group of white blood cells (T-lymphocytes, or T cells)
and the immune response.
Gonads
The female and male gonads produce sex hormones that are
identical to those produced by adrenal cortex cells; the major
difference are the source and relative amount produced.
Hormones of the Ovaries
The female gonads or ovaries are a pair of almond-sized organs.
• Location. The female gonads are located in the pelvic cavity.
• Steroid hormones. Besides producing female sex cells, ovaries
produce two groups of steroid hormones, estrogen, and
progesterone.
• Alone, the estrogens are responsible for the development of
sex characteristics in women at puberty; acting with
progesterone, estrogens promote breast development and
cyclic changes in the uterine lining (menstrual cycle).
• Progesterone acts with estrogen to bring about the menstrual
cycle; during pregnancy, it quiets the muscles of the uterus so
that an implanted embryo will not be aborted and helps
prepare breast tissue for lactation.
Hormones of the Testes
The testes of the male are paired oval organs in a sac.
• Location. The testes are suspended in a sac, the scrotum,
outside the pelvic cavity.
• In addition to male sex cells, or sperm, the testes also produce
male sex hormones, or androgens, of which testosterone is the
most important.
• At puberty, testosterone promotes the growth and maturation
of the reproductive system organs to prepare the young man
for reproduction; it also causes the male’s secondary sex
characteristics to appear & stimulates male sex drive; It is also
necessary for the continuous production of sperm.
Other Hormone-Producing Tissues and Organs
Besides the major endocrine organs, pockets of hormone-
producing cells are found in fatty tissue and in the walls of the small
intestine, stomach, kidneys, and heart-organs whose chief functions
have little to do with hormone production.
Placenta
The placenta is a remarkable organ formed temporarily in the uterus
of pregnant women.
• Function. In addition to its roles as the respiratory, excretory,
and nutrition delivery systems for the fetus, it also produces
several proteins and steroid hormones that help to maintain the
pregnancy and pave the way for delivery of the baby.
• During very early pregnancy, a hormone called human
chorionic gonadotropin (hCG) is produced by the developing
embryo and then by the fetal part of the placenta; hCG
stimulates the ovaries to continue producing estrogen and
progesterone so that the lining of the uterus is not sloughed off
in the menses.
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• Human placental lactogen (hPL) works cooperatively with
estrogen and progesterone in preparing the breasts for
lactation.
• Relaxin, another placental hormone, causes the mother’s
pelvic ligaments and the pubic symphysis to relax and become
more flexible, which eases birth passage.
Physiology of the Endocrine System
Although hormones have widespread effects, the major processes
they control are reproduction, growth, and development;
mobilizing the body’s defenses against stressors; maintaining
electrolyte, water, and nutrient balance of the blood; and
regulating cellular metabolism and energy balance.
The Chemistry of Hormones
The key to the incredible power of the endocrine glands is the
hormones they produce and secrete.
• Hormones may be defined as chemical substances that are
secreted by endocrine cells into the extracellular fluids and
regulate the metabolic activity of other cells in the body.
• Classification. Although many different hormones are
produced, nearly all of them can be classified chemically as
either amino acid-based molecules (including proteins,
peptides, and amines) or steroids.
• Steroid hormones (made from cholesterol) include the sex
hormones made by the gonads and hormones produced by
the adrenal cortex.
• Amino acid-based hormones. All the others are nonsteroidal
amino acid derivatives.
Mechanisms of Hormone Action
Although the blood-borne hormones circulate to all the organs of
the body, a given hormone affects only certain tissue cells or organs.
• For a target cell to respond to the hormone, specific protein
receptors must be present on its plasma membrane or in its
interior to which that hormone can attach; only when this
binding occurs can the hormone influence the workings of
cells.
• Function of hormones. The hormones bring about their effects
on, the body cells primarily by altering cellular activity- that is,
by increasing or decreasing the rate of a normal, or usual,
metabolic process rather than stimulating a new one.
• Changes in hormone binding. The precise changes that follow
hormone binding depend on the specific hormone and the
target cell type, but typically one or more of the following
occurs:
o Changes in plasma membrane permeability or electrical
state.
o Synthesis of protein or certain regulatory molecules (such
as enzymes) in the cell.’
o Activation or inactivation of enzymes.
o Stimulation of mitosis.
o Promotion of secretory activity.
Control of Hormone Release
What prompts the endocrine glands to release or not release their
hormones?
• Negative feedback mechanisms are the chief means of
regulating blood levels of nearly all hormones.
• Endocrine gland stimuli. The stimuli that activate the endocrine
organs fall into three major categories:
o The most common stimulus is a hormonal stimulus, in which
the endocrine organs are prodded into action by other
hormones; for example, hypothalamic hormones stimulate
the anterior pituitary gland to secrete its hormones, and
many anterior pituitary hormones stimulate other
endocrine organs to release their hormones into the blood.
o Changing blood levels of certain ions and nutrients may
also stimulate hormone release, and this is referred to as
38 | 41
humoral stimuli; for example, the release of parathyroid
hormone (PTH) by cells of the parathyroid glands is
prompted by decreasing blood calcium levels.
o In isolated cases, nerve fibers stimulate hormone release,
and the target cells are said to respond to neural stimuli; a
classic example is sympathetic nervous system stimulation
of the adrenal medulla to release norepinephrine and
epinephrine during periods of stress.
I. Hyperpituitarism
• Chronic, progressive hyper-function of the anterior pituitary
resulting in over secretion of one or more of the anterior pituitary
hormones.
• Acromegaly is a rare disorder of excessive bone and soft tissue
growth due to elevated levels of growth hormone. In young
children, prior the completed fusion and growth of bones,
excessive growth hormone can cause a similar condition
called gigantism (proportional overgrowth of all body tissues
with remarkable height).
Etiologic factors
• Tumor and hyperplasia (Benign pituitary adenoma, hyperplasia
of pituitary tissue)
• Prolactinomas (prolactin-secreting tumors) account for 60 to
80% of all pituitary tumors.
• GH-producing adenomas
Causes
• In most cases, acromegaly is caused by over-secretion of
growth hormone (GH) produced by a benign tumor of the
pituitary gland. The pituitary gland is a small gland located at
the base of the brain that produces many hormones. In a small
number of cases, malignant tumors of other organs (pancreas,
adrenal, lung) may be the source of excess GH.
Risk Factors
• Some rare cases of acromegaly are hereditary.
• The average age of diagnosis is 40-45 years old.
Symptoms
• Symptoms usually develop very slowly over time.
• Acromegaly – gradual, marked enlargement of the bones of
the face, jaw, hands and feet. There can be diaphoresis,
hyperglycemia, oily skin and hirsutism. It can cause serious
complications and premature death if not treated.
• Gigantism
• Neurologic manifestations
o Headache
o Somnolence, Behavioral changes, seizures
o Signs and symptoms of increased ICP
o Disturbance in appetite, sleep, temperature regulation
and emotional balance due to hypothalamic involvement
o Visual disturbances due to the compression of the optic
chiasm above the pituitary gland:
o Hemianopsia or scotomas or blindness
o Scotoma “blindspot in vision”
• In children, excess GH production causes elongation of the
bones and associated soft tissue swelling. If not treated,
children with this disorder can grow ta height of 7-8 feet.
• Symptoms and complications in adults may include the
following:
o Abnormally large growth and deformity of the:
◦ Hands (rings no longer fit)
◦ Feet (need a bigger size shoe)
◦ Face (protrusion of brow and lower jaw)
◦ Jaw (teeth do not line up correctly when the mouth is
closed)
◦ Lips
◦ Tongue
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o Carpal tunnel syndrome
o Skin changes, such as:
◦ Thickened, oily, and sometimes darkened skin
◦ Severe acne
◦ Excessive sweating and offensive body order due
enlargement of the sweat glands
o Deepening voice due enlarged sinuses, vocal cords, and
soft tissues of the throat
o Fatigue and weakness in legs and arms
o Sleep apnea
o Arthritis and other joint problems especially in the jaw
o Hypothyroidism
o Enlargement of the liver, kidneys, spleen, heart, and/or
other internal organs, which can lead to:
◦ Diabetes
◦ High blood pressure
◦ Cardiovascular disease
• In women:
o Irregular menstrual cycles
o Galactorrhea (abnormal production of breast milk) in 50%
of cases
• In men:
o In about 50% of cases, impotence
Diagnosis
• Blood tests will be done measure the level of insulin-like growth
factor (IGF-I), growth hormone releasing hormone (GHRH), and
other pituitary hormones.
• A glucose tolerance test may also give to see if the GH level
drops—it will not drop in cases of acromegaly.
• If these tests confirm acromegaly, the following may be done
to locate the tumor that is causing the disorder:
o Head CT scan—a type of x-ray that uses a computer to
make pictures of the inside of the brain and surrounding
structures
o MRI Scan
• Plasma GH levels determination: increased
o Adult male – 4-10ng/ml
o Female – 1-14ng/ml
o Child – 10-50ng/ml
Nursing Diagnosis
• Disturbed Body Image related to anxiety over thickened skin
and enlargement of face, hands, and feet.
• Ineffective Coping related to change in appearance.
• Disturbed Sensory Perception
• Disturbed Sleeping Pattern related to soft tissue swelling
• Fluid Volume Deficit
• Anxiety related to change in appearance
• Knowledge Deficit
Treatment
• Reduce production of GH to normal levels
• Stop & reverse the symptoms caused by over-secretion of GH
• Correct other endocrine abnormalities (thyroid, adrenal, sex
organs)
• Reduce the tumor size
Treatment may include:
• Surgical removal of the pituitary tumor, or other tumor, that is
believed to be causing acromegaly may be done. In most
cases, this is the preferred treatment.
• Transsphenoidal hypophysectomy
• Radiosurgery is the use of highly focused external beams of
radiation to shrink the tumor. It is used most often in patients
who not respond to conventional surgery or medications.
• Radiation therapy is used in combination with either medical
and/or surgical treatment.
39 | 41
• Medication: Drugs may be given to reduce the level of GH
secretion from the pituitary gland. These include:
o Cabergoline (Dostinex) – given orally
o Pergolide (Permax) – given orally
o Octreotide (Sandostatin) – given by injections
o Pegvisomant – given by injections for patients not
responding to other forms of treatment
o Bromocriptine (Parlodel) – may be given before surgery to
shrink tumor. Also used to treat amenorrhea, a condition in
which the menstrual period does not occur; infertility
(inability to get pregnant) in women; abnormal discharge
of milk from the breast; Hypogonadism; Parkinson's
disease; and inhibit the synthesis of GH & prolactin
• Medications must often be combined with other therapies to
treat larger tumors affecting surrounding structures.
Nursing Management: Surgery
• Pre-operatively: Health Teaching
o Explain to the patient that this surgery will remove the
tumor from the pituitary gland
o A nasal catheter and nasal packing are expected in the
nasal cavity for a day
o Indwelling catheter will be inserted (to monitor UO) –
Diabetes Insipidus can be a complication of the surgery
o Review all patient’s medication regimen and provide
routine pre-op care
• Post-operatively:
o Strictly keep the patient on BED rest for 24° and encourage
ambulation on day 2
o Position the patient fowler’s to avoid tension on the suture
line and to avoid increased intracranial pressure
o Remind the patient NOT to sneeze, forcefully cough, bend
over and blow the nose for several days to avoid disturbing
the suture lines
o Mild analgesic can be given for headache
o Anticipate the patient to manifest signs and symptoms of
DI after surgery
◦ Be alert for increase thirst and increase UO w/ low SG
◦ Replace fluids and administer IV vasopressin as
ordered. DI should resolve in 72°
◦ Report outputs above 900 ml / 2 hours or specific
gravity below 1.004 (D. Insipidus)
o Arrange for a visual field testing because progressive visual
field defects may indicate bleeding
o Be alert for potential leakage of CSF from the operative
site
o If rhinorrhea is present, test the discharge for glucose and
if positive, report to the physician of the CSF leakage
Nursing Management
• Provide emotional support to help patient cope with an altered
body image
• Perform range of motion exercises to promote maximum joint
mobility and prevent injury due to muscle weakness
• Keep skin dry and avoid using oily lotion
• Provide safety measures because pituitary tumor can cause
visual disturbances. Approach the patient to the unaffected
side if he has hemianopsia.
• Deal with the mood swings appropriately
• Home teaching include: emphasizing that hormone
replacement is needed lifetime, wear an ID, have regular
follow-up
• Home care instruction
o Explain the need to take the medication as prescribed
o Report progressive visual changes, excessive urination
o Advise patient NOT to brush the teeth for 2 weeks to avoid
injury to the suture lines
o Find alternative measures for oral care like mouthwash
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Prevention • Vasopressin deficiency: polyuria, polydipsia, dehydration,

• There are guidelines for preventing acromegaly. unable to concentrate urine.
• Early diagnosis and treatment, however, will help prevent
Diagnostic Tests
serious complications, some of which are irreversible.
• Skull x-ray, CT scan, MRI (reveal pituitary tumor)
II. Hypopituitarism • Blood examination: decrease plasma hormone levels
• Hypofunction of the pituitary gland (hypopituitarism) can occur (depending on specific hormones under-secreted)
due to diseases of the gland or the hypothalamus.
Physical Examination
• Hypopituitarism refers to the state of the anterior pituitary
secretion of several hormones, which is very low. 1. Physical examination
• Hypopituitarism is hypersecretion of one or more anterior - Inspection: Observe the shape and size of the body,
pituitary hormones. measuring weight and height, observe the shape and size
• Hypopituitarism is a condition that arises as a result of pituitary of the breast, axillary and pubic hair growth in male clients,
hypofunction. Definition of anterior pituitary hormones may observe also the growth of facial hair (beard and
occur from 3 pathways: mustache).
o Abnormalities in the gland that can damage the secretory - Palpation: Palpation of the skin, the woman usually
cells. becomes dry and rough. Depending on the cause
o Abnormalities within or adjacent to the pituitary stalk which hypopituitary, other data should also be assessed as a
can lead to termination of the spread of the factors that concomitant of data as if the cause is a tumor, it is
originate from the hypothalamus. necessary to check the function of the cerebrum and
o Abnormalities in the hypothalamus which may impair the cranial nerve function and the presence of headaches.
release of the regulator on the front hypofyse. 2. Assess the physical changes also impact on the ability of clients
to meet their basic needs.
Etiology 3. Supporting data of the diagnostic workup such as:
Hypopituitarism may occur due to a malfunction of the pituitary - X-ray of cranium to see the dilation and erosion of the sella
gland or hypothalamus. Cause concerns: turcica or
• Trauma, vascular lesion, surgery/radiation of pituitary gland, - Examination of blood serum: LH and FSH GH, prolactin,
congenital aldosterone, testosterone, cortisol, androgens, which
• Infection or inflammation by: fungal, pyogenic bacteria. include test stimulation of insulin tolerance test and thyroid
• Autoimmune diseases (autoimmune lymphoid pituitary) releasing hormone stimulation.
• Tumors, for example of a type of hormone-producing cells that
can interfere with the formation of one or another hormone Complication
arbitrarily. • Cardiovascular.
• Feedback from the target organ experiencing malfunctions. o Hypertension.
For example, there will be a decrease in the secretion of TSH o Thrombophlebitis.
from the pituitary gland when the thyroid is diseased secrete o Thromboembolism.
excessive levels of HT. o Acceleration atherosclerosis.
• Hypoxic necrotic (death due to lack of O2) pituitary or • Immunology.
oxygenation can damage some or all of the hormone- o Increased risk of infection and disguise any signs of
producing cells. One of them can syndrome, which occurs infection.
after maternal hemorrhage. • Changes in the eye.
o Glaucoma.
Clinical Manifestations o Corneal lesions.
• Observed when 75% of the pituitary gland is dysfunctional • Musculoskeletal.
• Metabolic dysfunction, sexual immaturity, growth retardation o Muscle wasting.
• Headache and Hemianopsia / visual disturbances or signs of o Poor wound healing.
increased intracranial pressure. o Osteoporosis with vertebral compression fractures, long
• Weight loss, emaciation, varying signs of hormonal bone pathologic fractures, aseptic necrosis of the femoral
disturbances depending on which hormones are being under- head.
secreted: menstrual dysfunction, hypometabolism, adrenal • Metabolic. Changes in glucose metabolism of steroid
insufficiency, growth retardation withdrawal syndrome.
• Overview of the production of growth hormone excess include • Changes in appearance.
acromegaly (large hands and feet as well as the tongue and o Such as moon face (moon face).
jaw), profuse sweating, hypertension and arthralgia (joint pain). o Weight gain.
• Hyperprolactinemia: amenorrhea or oligomenorrhea, o Acne.
galactorrhea (30 %), infertility in women, impotence in men.
Collaborative Management
• Cushing syndrome: central obesity, hirsutism, striae,
hypertension, diabetes mellitus, osteoporosis. • Specific treatment depends on cause
• Growth hormone deficiency: (growth hormone = GH) growth o Tumor: surgical removal or irradiation of the gland
disorders in children. o Regardless of cause, treatment will include replacement
• Gonadotropin deficiency: impotence, decreased libido, body of deficient hormones (HRT):
hair loss in men, amenorrhea in women. ◦ Corticosteroids
• TSH deficiency: fatigue, constipation, dry skin laboratory picture ◦ Thyroid hormone
of hyperthyroidism. ◦ Sex hormones, gonadotropins
• Corticotropin Deficiency: malaise, anorexia, fatigue is real,
Nursing Diagnosis for Hypopituitarism
pale, the symptoms are very severe for ordinary mild systemic
disease, laboratory overview of the decline in adrenal function. 1. Disturbed Body Image related to changes in body structure
and function of the body due to deficiency of gonadotropin
and growth hormone deficiency.

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2. Ineffective individual coping related to the chronicity of the
disease condition.
3. Low Self-Esteem related to changes in body appearance.
4. Disturbed Sensory perception (visual) related to impaired
transmission of impulses as a result of suppression of tumor on
the optic nerve.
5. Anxiety related to threat or change in health status.
6. Self-care deficit related to the decrease in muscle strength.
7. Risk for impaired skin integrity (drought) related to declining
hormonal levels.
TERMINOLOGIES
1. Acidosis: too much acid in the body. For a person with
diabetes, ketoacidosis is a type of acidosis.
2. Adult-onset diabetes: former term for type 2 diabetes, also
formerly called noninsulin-dependent diabetes.
3. Albuminuria: more than normal amounts of a protein called
albumin in the urine. Albuminuria may be a sign of kidney
disease.
4. Blood urea nitrogen (BUN): waste product of the kidneys.
Increased BUN levels may indicate early kidney damage.
5. Dawn phenomenon: a sudden rise in blood glucose levels in the
early morning hours. This is more common in people with type 1
diabetes than type 2 diabetes.
6. Diabetic ketoacidosis (DKA): severe, untreated hyperglycemia
(high blood sugar) that needs emergency treatment. DKA
happens when there is not enough insulin. Ketoacidosis can
lead to coma and even death.
7. Fasting plasma glucose test: a lab test that measures a person’s
blood glucose level after fasting or not eating anything for 10
to 12 hours. Normal fasting blood glucose is less than 100 mg/dl
for people who do not have diabetes. A diagnosis of diabetes
is made when two blood tests show that your fasting blood
glucose level is greater than or equal to 126 mg/dl.
8. Fats: substances that help the body use some vitamins and
keep the skin healthy. They are also the major way the body
stores energy. In food, there are two types of fats; saturated
and unsaturated.
9. Gestational diabetes mellitus: a high blood glucose level that is
discovered during pregnancy. As pregnancy progresses, there
is an increased need for glucose for the developing baby.
Additionally, hormone changes during pregnancy affect the
action of insulin, resulting in high blood glucose levels. Usually,
blood glucose levels return to normal after childbirth. However,
women who have had gestational diabetes are at increased
risk of developing type 2 diabetes later in life.
10. Glaucoma: an eye disease associated with increased pressure
within the eye. Glaucoma can damage the optic nerve and
cause impaired vision and blindness.
11. Glucagon: a hormone that raises the level of glucose (sugar) in
the blood. Glucagon is sometimes injected when a person has
lost consciousness (passed out) from a low blood sugar
reaction. The injected glucagon helps raise the level of glucose
in the blood.
12. Glucose: a simple sugar found in the blood. It is the body’s main
source of energy; also known as dextrose.
13. Glucose tolerance test: a test that can be used to determine if
a person has diabetes. The test is done in a lab or doctor’s
office in the morning before the person has eaten. First a
sample of blood is taken. Then the person drinks a liquid that
has glucose (sugar) in it. Periodically, another sample of blood
is taken to see how the body processes the glucose in the
blood.
14. Human insulin: bio-engineered insulin that is very similar to
insulin made by your own body.
15. Hyperglycemia: high blood sugar. Many things can cause
hyperglycemia. It occurs when the body does not have
enough insulin or cannot use the insulin it does have.
41 | 41
16. Hypoglycemia: low blood glucose. Hypoglycemia in people
with diabetes is often caused by an imbalance in diabetes
medications, food intake, and/or activity levels.
17. Injection site rotation: changing the areas on the body where
a person injects insulin. If the same injection site is used over and
over again, hardened areas, lumps or indentations can
develop under the skin which keep the insulin from being used
properly. These lumps or indentations are called
lipodystrophies.
18. Injection sites: recommended places on the body where
people can inject insulin. These sites include the back of the
upper arm, the abdomen, the thighs and the buttocks.
19. Insulin: a hormone that helps the body use glucose for energy.
The beta cells of the pancreas make insulin.
20. Insulin dependent diabetes: former term used for type 1
diabetes, also formerly called juvenile diabetes.
21. Insulin pump: a small, computerized device that is worn on a
belt, in a pocket, or under clothes. Most insulin pumps deliver
insulin through a small, flexible tube inserted under the skin. It
delivers a steady flow of insulin 24 hours a day, and on-demand
doses programmed by the user for food or high blood sugar.
22. Insulin receptors: areas on the outer part of a cell that allow
insulin in the blood to join or bind with the cell. When the cell
and insulin bind together, the cell can take glucose from the
blood and use it for energy.
23. Insulin resistance: when a person’s body will not allow insulin to
work properly in the body. This condition can occur when a
person is overweight, and it often improves when the person
loses weight.
24. Insulin shock: loss of consciousness as a result of severe
hypoglycemia (low blood sugar).
25. Lancet: a fine, sharp pointed needle for pricking the skin. Used
in blood glucose monitoring.
26. Polydipsia: excessive thirst that lasts for long periods of time;
may be a sign of diabetes.
27. Polyphagia: excessive hunger and eating; may be a sign of
diabetes. People with polyphagia as a result of diabetes often
lose weight even though they are eating more than normal.
28. Polyunsaturated fat: a type of fat that comes from vegetables.
29. uced is either not enough or doesn’t work properly in the body.
As a result, glucose cannot get into the body’s cells for use as
energy. This causes blood glucose to rise.
30. Unit of insulin: the basic measure of insulin. U-100 is the most
common concentration of insulin. U-100 means that there are
100 units of insulin per milliliter (ml) of liquid.
I. BAISA