PATHOPHYSIOLOGY

Risk factors:
● Aging
● Obesity
● Dietary Factors

Causes:
Estrogen and progesterone
stimulation
High cholesterol synthesis /
secretion
High-fat intake

Stasis of Bile Increased

cholesterol into
bile

Bile salts
precipitation Storage of bile in
gallbladder

Cholelithiasis
Distention of
gallbladder with
excess bile
Gallstones in
common bile duct
(obstruction)
Thickened and
edematous
gallbladder wall from
exposure to
concentrated bile

Inflammation of the
gallbladder (Cholecystitis)
If treated If untreated

Pharmacological Manifestations of the ff. signs and symptoms: Possible

treatment: ● Biliary colic ● IndigestionComplications may
● Antimicrobials ● Jaundice ● Vomiting occur such as:
● Narcotic ● Fever ● Ischemia
● Clay-colored stool
Analgesics ● Fatty food intolerance ● dark urine ● Necrosis
● Anticholinergics
● Nausea ● steatorrhea ● Rupture of
● Antiemetics ● Pain ff. eating fatty foods gallbladder
● Gallstone ● Gangrene
solubilizer ● Peritonitis
Surgical Management: DEATH
● Cholecystectomy
● Litotripsy
● Endoscopic
Papillotomy
 Good Prognosis

RECOVERY

PATIENT’S PROFILE

Name: Armando Solis

Address: Blk 11, Lot 2 Silcas Village San Francisco Biñan, Laguna

Age: 28

Gender: Male

Nationality: Filipino

Religion: Roman Catholic

Birth Date: May 03, 1980

Birth Place: Manila

Attending Physician: Dr. Anadol Gonzales

Admitting Physician: Dr. Angelito Geronimo

Date of Admission: January 20, 2008

Time of Admission: 05:00 pm

Chief Complain: abdominal pain

Admission Diagnosis: Calculous Cholecystitis

History of Past Illness:

Two days prior to admission, the patient started to experience abdominal pain

not associated with fever or nausea .Then after a day, the patient still

complained with episodes of epigastric pain. And few hours prior to admission,

epigastric pain was accompanied by vomiting. This prompted consult in Sta.

Rosa Community Hospital where he was advised to be confined after undergoing

a series of examinations. Results of the examinations showed that he has

Calculous Cholecystitis.

SAINT MICHAEL’S COLLEGE OF LAGUNA

Old National Highway, Platero, Biñan
Laguna.

School of Nursing and

Midwifery

In partial Fulfillment in Review of Related Learning Experience

A Case
Study in
Calculous
Cholecystitis
&
 Cholecystecto
my

Submitted by:

Angelique A. Malabo
Airish Nyn M. Manzo
BSN3B / Group 8
Submitted to:

Sir Reigh Tenorio

02Feb2009

MEDICAL MANAGEMENT

A cholecystectomy is the surgical removal of the gallbladder. The two basic types
of this procedure are open cholecystectomy and the laparoscopic approach. The
laparoscopic cholecystectomy involves the insertion of a long narrow cylindrical
tube with a camera on the end, through an approximately 1 cm incision in the
abdomen, which allows visualization of the internal organs and projection of this
image onto a video monitor. Three smaller incisions allow for insertion of other
instruments to perform the surgical procedure. A laser may be used for the
incision and cautery (burning unwanted tissue to stop bleeding), in which case
the procedure may be called laser laparoscopic cholecystectomy.

In a conventional or open cholecystectomy, the gallbladder is removed through a

surgical incision high in the right abdomen, just beneath the ribs. A drain may be
inserted to prevent accumulation of fluid at the surgical site.

Purpose
A cholecystectomy is performed to treat cholelithiasis and cholecystitis. In
cholelithiasis, gallstones of varying shapes and sizes form from the solid
components of bile. The presence of these stones, often referred to as
gallbladder disease, may produce symptoms of excruciating right upper
abdominal pain radiating to the right shoulder. The gallbladder may become the
site of acute infection and inflammation, resulting in symptoms of upper right
abdominal pain, nausea, and vomiting. This condition is referred to as
cholecystitis. The surgical removal of the gallbladder can provide relief of these
symptoms. Cholecystectomy is used to treat both acute and chronic cholecystitis
when there are significant pain symptoms. The typical composition of gallstones
is predominately cholesterol, or a compound called calcium bilirubinate.

An example of Cholecystectomy

Laparoscopic Cholecystectomy

In a laparoscopic cholecystectomy, four small incisions are made in the abdomen

(A). The abdomen is filled with carbon dioxide, and the surgeon views internal
structures with a video monitor (B). The gallbladder is located and cut with
laparoscopic scissors (C). It is then removed through an incision (D).
Intraoperative Cholangiogram

During surgery to remove the gallbladder (cholecystectomy), you may have a

procedure called intraoperative cholangiogram. The doctor places a small tube
called a catheter into the cystic duct, which drains bile from the gallbladder into
the common bile duct. A dye that blocks X-rays is injected into the common bile
duct, and then you will have X-rays taken.

You may have intraoperative cholangiogram to:

• Look for gallstones that may be in the common bile duct.
• Allow the surgeon to see the anatomy of the bile duct system from the
liver to the small intestine. Viewing the bile ducts before removal of the
gallbladder may help ensure that the surgeon does not accidentally cut or
damage the common bile duct.

Complications of intraoperative cholangiogram can include:

• Infection and bleeding.
• Inflammation of the pancreas (pancreatitis).
• Damage to the common bile duct.

Common Bile Duct Exploration (CBDE)

The CBD is a tube connecting the liver, gallbladder, and pancreas to the small
intestine that helps deliver fluid to aid in digestion.

The CBD exploration is a procedure used to see if a stone or some obstruction is

blocking the flow of bile from your liver and gallbladder to your intestine.

If a stone or obstruction is blocking the CBD, bile can back up into the liver
causing jaundice. Jaundice is when the skin and white of the eyes become
yellow.
The CBD might become infected and require emergency surgery if the stone or
blockage is not removed. This procedure can be done during the removal of the
gall bladder.
An alternative would be an ERCP (Endoscopic retrograde
cholangiopancreatogram) or not having treatment. You should discuss these
options with your doctor.

Preparation for CBD exploration

• Eat light the day before
• Have nothing to eat or drink after midnight
• Take only medicines as instructed the morning of surgery

During the procedure

• General anesthesia relaxes your muscles and puts you into a deep sleep,
so you will feel no pain.
 • The doctor will make a small incision in the abdomen, locate the CBD, and
inject a dye into the duct. Your doctor will then take an X-ray, which will
show where the stone or obstruction is located.
• If stones are found, the doctor will make a cut into the duct and remove
them.
• A tube might be inserted into the duct and out the skin to drain bile into a
bag.
• The bag will remain in place anywhere from seven days to many weeks.
• The doctor might repeat the dye procedure before removing your tube.

Benefits of CBD exploration

The surgery should alleviate your discomfort and will decrease the chance of
infection and jaundice.

Risks
As with any surgery there are risks, although minimal:
• Complications of general anesthesia
• Swelling or scarring of the duct
• Bile leak
• Bleeding
• Infection

Aftercare

Postoperative care for the patient who has had an open cholecystectomy,
as with those who have had any major surgery, involves monitoring of
blood pressure, pulse, respiration, and temperature. Breathing tends to be
shallow because of the effect of anesthesia, and the patient's reluctance
to breathe deeply due to the pain caused by the proximity of the incision
to the muscles used for respiration. The patient is shown how to support
the operative site when breathing deeply and coughing and is given pain
medication as necessary. Fluid intake and output is measured, and the
operative site is observed for color and amount of wound drainage. Fluids
are given intravenously for 24–48 hours, until the patient's diet is
gradually advanced as bowel activity resumes. The patient is generally
encouraged to walk eight hours after surgery and discharged from the
hospital within three to five days, with return to work approximately four
to six weeks after the procedure.
Care received immediately after laparoscopic cholecystectomy is similar
to that of any patient undergoing surgery with general anesthesia. A
unique postoperative pain may be experienced in the right shoulder
related to pressure from carbon dioxide used in the laparoscopic tubes.
This pain may be relieved by lying down on the left side with right knee
and thigh drawn up to the chest. Walking will also help increase the
body's reabsorption of the gas. The patient is usually discharged the day
after surgery and allowed to shower on the second postoperative day. The
patient is advised to gradually resume normal activities over a three-day
period, while avoiding heavy lifting for about 10 days.

Risks

Potential problems associated with open cholecystectomy include

respiratory problems related to location of the incision, wound infection,
or abscess formation. Possible complications of laparoscopic
cholecystectomy include accidental puncture of the bowel or bladder and
uncontrolled bleeding. Incomplete reabsorption of the carbon dioxide gas
could irritate the muscles used in respiration and cause respiratory
distress. While most patients with acute cholecystitis respond well to the
laparoscopic technique, about 5–20% of these patients require a
conversion to the open technique because of complications.

Normal Results

The prognosis for cholecystitis and cholelithaisis patients who receive

cholecystectomy is generally good. Overall, cholecystectomy relieves
symptoms in about 95% of cases.

Alternatives

Acute cholecystitis usually improves following conservative therapy in

most patients. This conservative therapy involves the withholding of oral
feedings, the use of intravenous feedings, and the administration of
antibiotics and analgesics. This is only a short-term alternative in
hospitalized patients. Most of these patients should receive
cholecystectomy within a few days to prevent recurrent attacks. In the
short-term, patients often receive narcotic analgesics such as meperidine
to relieve the intense pain associated with this condition. Patients who
have evidence of gallbladder perforation or gangrene need to have an
immediate cholecystectomy.

In patients with cholelithasis who are deemed unfit for surgery, alternative
treatments are sometimes effective. These individuals often have
symptom improvement after lifestyle changes and medical therapy.
Lifestyle changes include dietary avoidance of foods high in
polyunsaturated fats and gradual weight loss in obese individuals. Medical
therapy includes the administration of oral bile salts. Patients with three
or fewer gallstones of cholesterol composition and with a gallstone
diameter less than 0.6 in (15 mm) are more likely to receive medical
therapy and have positive results. The primary requirements for receiving
medical therapy include the presence of a functioning gallbladder and the
absence of calcification on computed tomography (CT) scans. Other non-
surgical alternatives include using a solvent to dissolve the stones and
using sound waves to breakup small stones. A major drawback to medical
therapy is the high recurrence rate of stones in those treated.

INTRODUCTION

Several disorders affect the biliary system and interfere with normal
drainage of the bile into the duodenum. The disorders include
inflammation of the biliary system and carcinoma that obstruct the biliary
tree. Gallbladder disease with gallstones is the most common disorder of
the biliary system. Although not all occurrences of gallbladder
inflammation (cholecystitis) are related to gallstones (cholelithiasis), more
than 90% of patients with acute cholecystitis have gallstones.

It is an acute inflammation (cholecystitis) of the gallbladder causes

pain, tenderness, and rigidity of the upper abdomen that may radiate to
the midsternal area or right shoulder and is associated with nausea,
vomiting, and the urinal signs of an acute inflammation. In empyema of
the gallbladder develops if the gallbladder becomes filled with purulent
fluid (pus).

Calculous cholecystitis is the cause of more than 90% of cases of

acute cholecystitis. In calculous cholecystitis, a gallbladder stone
obstructs bile outflow. Bile remaining in the gallbladder initiates a
chemical reaction; autolysis and edema occur, and the blood vessels in
the gallbladder are compressed, compromising its vascular supply.
Gangrene of the gallbladder with perforation may result. Bacteria play a
minor role in acute cholecystitis; however, secondary infection of bile with
Escherichia coli (60%), klebsiella species (22%), or streptococcus (18%) is
identified with cultures obtained during surgery in a small percentage of
surgical treated patients.

Acalculous cholecystitis describes acute inflammation in the

absence of obstructions by gallstones. Acalculous cholecystitis occurs
after major surgical procedures, severe trauma or burns. Other factors
associated with this type of cholecystitis include torsion, cystic duct
obstruction, primary bacterial infection of the gallbladder and multiple
blood transfusions. It is speculated that acalculous cholecystitis is caused
by alterations in fluids and electrolytes and alterations in regional blood
flow in the visceral circulation. Bile stasis (lack of gallbladder contraction)
and increase viscosity of the bile are also thought to play a role.

A typical attack of cholecystitis usually lasts two to three days. The

following are the most common symptoms of gallstones. However, each
individual may experience symptoms differently. Symptoms may include;
pain in the upper right part of the abdomen, pain (often worse with deep
breaths and extends to lower part of right shoulder blade) , nausea,
vomiting , rigid abdominal muscles on right side , and slight fever .

The symptoms of cholecystitis may resemble other conditions or

medical problems. Consult a physician for diagnosis.
ANATOMY AND PHYSIOLOGY
 The liver, gallbladder, and pancreas share intimate anatomical and
physiological codependence and therefore, will be discussed together in this
section. The liver lies just below the diaphragm occupying the entire right
hypochondrium, epigastrium, and a portion of the left side of the abdomen.
Although it lies below the diaphragm it is attached to it moving up and down
with ventilations. Under the cover of the 5th to 10th ribs it is easily injured by rib
fractures resulting from high impact trauma. The liver is the largest organ and
gland in the body weighing approximately 1500-1700 grams. Its surface
anatomy consists of four lobes that can be plainly seen at dissection. Only two
major lobes, the right and left lobes, which are separated by the falciform
ligament, are seen on the anterior surface. The falciform ligament is a remnant
of the umbilical vein; it attaches the liver to the anterior abdominal wall and
diaphragm. Posteriorly the liver presents the left lobe and the right lobe that is
divided into three lobes: the right lobe proper, and two minor lobes, the caudate
and quadrate lobes. Frequently seen in women is a normal variation of the right
lobe that gives the appearance of an additional lobe that has become known as
the Riedel lobe. The liver’s diaphragmatic surface is dome shaped conforming to
the shape of the inferior surface of the diaphragm. The gallbladder usually lies in
a shallow surface on the posterior aspect of the right lobe.

Liver lobes are composed of cells called hepatocytes that are arranged
into lobules. Liver cells perform over 100 known functions among which are
forming blood cells, detoxifying poisons (alcohol and drugs), and metabolizes
foodstuff (carbohydrates, fats, proteins). The liver also stores fat soluble vitamins
A, D, E, K, and B12 but no water-soluble vitamins like vitamin C. Special cells
called Kuppfler cells are found within the liver’s parenchyma. They engulf spent
red blood cells (phagocytosis) and recycle hemoglobin in the form of bilirubin
making it available for newly formed red blood cells. All hepatocytes make bile
from substrates like bilirubin and cholesterol. The liver also makes many
essential blood proteins products like albumin and fibrinogen for clotting blood.
Urea excreted in urine comes from protein metabolism in the liver, and the liver
can even make glucose when blood sugar becomes low. With so many functions
it is easy to see why any process that diminishes the liver’s functions will be felt
systemically. This remarkable organ can maintain the body’s physiological needs
even when up to 70% of it is removed. It also has remarkable regenerative
properties to replace hepatocytes lost due to liver resection, which is something
other organs cannot do.

Deep fissures on the posterior surface form an “H-shaped” groove further

dividing the liver into four lobes. The crossbar of the H is called the porta
hepatis; it separates the caudate and quadrate lobes. This area is important to
radiologists, surgeons, and to imaging professions because it contains the portal
vein, hepatic artery, and hepatic ducts. Though it is only about 5 cm in length it
is very compact with anatomical structures that include nerves and lymphatics.

The liver performs several important roles in the digestive system. One is
the removal of toxins and bacteria that enter the blood during absorption of raw
foods (lipids, carbohydrates, and proteins) through the gut mucosa. Purification
of nutrients occurs before they are released into the systemic circulation and
made available to the body’s cells. The liver is therefore a defense organ of the
body’s immune system protecting it against microorganism invasion. The
importance here is in the absorption of nutrients to supply the energy needs of
the body. This function is dependent on a good blood supply, which the liver has.
Moreover, the liver is special in that it receives a double blood supply. The portal
vein supplies most of the blood (70%) and the hepatic artery gives the
remainder (30%); this duel supply is important to the unique metabolic needs of
the liver. The portal vein is formed just posterior to the neck of the pancreas by
the union of the superior mesenteric and splenic veins. The portal vein carries
nutrients it receives from the gut (via the superior mesenteric vein) to the liver
for detoxification.
 Hepatocytes require lots of energy and oxygen when detoxifying nutrients
received from the portal vein. The hepatic artery brings oxygenated blood that
mixes with deoxygenated blood from the portal vein to supply the additional
oxygen hepatocytes need for detoxification. This happens within the sinusoids of
the liver parenchyma where the hepatocytes are bathed with unidirectional
blood flow. The hepatic artery is a distal branch of the hepatic artery proper that
branches from the celiac trunk on the anterior surface of the aorta. Hepatocytes
are stacked hexagonally to form the architecture of the sinusoids. The apposing
membranes of hepatocytes form channels for bile to flow called canaliculi. The
functional unit is the lobule where detoxification and bile secretion occurs in a
counter current type flow, an arrangement that maximizes cellular contact with
blood. These rich vascular beds perfuse the liver allowing hepatocytes to
perform metabolic functions like detoxification of nutrients. Once these foods are
“cleaned” they leave the liver via hepatic veins. The hepatic veins join the
inferior vena cava, which carries blood to the right atrium of the heart.

Blood in the sinusoids travel towards the hepatic veins, while bile moves
in the opposite direction within the hepatic plates, so blood and bile never mix in
the liver lobules. Bidirectional flow allows for what is called enterohepatic
circulation. As blood moves along in the sinusoids hepatocytes absorb and
secrete a variety of exogenous compounds. Many medications used to treat
illnesses are removed from the liver by this mechanism too. The removal of
drugs from the blood by the liver is called the first-pass effect, or first-pass
metabolism. During first-pass metabolism an ingested drug is absorbed through
the bowel mucosa into the blood. The superior mesenteric vein takes the drug to
the liver via the portal vein where some, but not all of it is absorbed by
hepatocytes and secreted into the bile. This accounts for the low bioavailability
of many drugs. Drugs administered by intravenous, intramuscular, or
sublinguinal routes can avoid the first-pass effect. What is interesting about the
liver is that hepatocytes can recognize sugars, proteins, amino acids, and lipids
and do not filter food vital to the body for energy production. Bile is released into
the gut through the duodenum returning drugs to the gut to be reabsorbed and a
portion released in stool.

All hepatocytes synthesize and secrete bile into small ducts called
canaliculi, which lie between the hepatic plates. These canaliculi anastomose to
form networks throughout the liver parenchyma. Bile canaliculi have no structure
of their own; the membranes of adjacent hepatocytes form channels that are the
bile canaliculi. These many small microscopic intrahepatic bile canaliculi form a
network of ducts that become progressively larger becoming the hepatic ducts
that drain the liver. A normal liver will secrete between 700 and 1200 ml of bile
into these ducts daily. Bile is collected from both main lobes of the liver into the
large right and left hepatic ducts that come together to form the extrahepatic
common hepatic duct. The biliary tree is formed by the right and left hepatic
ducts, common hepatic duct, cystic duct, common bile duct, the ampula of Vater.
The biliary duct system shunts bile to the gallbladder to be concentrated and
stored, and ultimately to the duodenum.

The gallbladder is a pear-shaped sac that lies in a shallow fossa on the

posterior inferior surface of the gallbladder. Only a small portion (the fundus) can
be seen from the anterior surface. The gallbladder’s surface anatomy is quite
simple consisting of three parts: fundus, body, and neck. The neck of the
gallbladder is continuous with the cystic duct that receives and empties bile from
the common bile duct. The mucosa of the cystic duct is thrown into rugae that
form spiral tracts called the spiral valve of Heister. The valve performs like a
sphincter to regulate substances entering and leaving the gallbladder. Some
individuals have a prominent pouch just posterior to the neck of the gallbladder
called a Hartmann pouch. This is a prime site for gallstones to lodge possibly
obstructing the gallbladder. A Hartmann pouch can best be seen with ultrasound
when imaging the gallbladder.
 The function of the gallbladder is to concentrate and store bile. The liver
produces up to 20 times more bile than the capacity of the gallbladder. The cells
of the gallbladder absorb water returning it to surrounding capillaries. Water,
sodium, chloride and most electrolytes are absorbed from bile concentrating bile
salts, cholesterol, lecithin, and bilirubin. Bile in the gallbladder is concentrated
by a factor of 12 to 18 fold its liver secretion. The capacity of the gallbladder is
between 30 and 60 ml. The mucosa of the gallbladder is formed into rugae that
expand as it receives bile. Within its wall is a smooth muscle layer called the
muscularis, which contracts when stimulated providing the force to eject bile.
Contractions of the gallbladder eject concentrated bile into the biliary tree. This
is coordinated with relaxation of the sphincter of Oddi to allow bile to pass into
the duodenum without resistance.

It is important for radiographers to understand the role of bile salts. There

are two main functions of bile salts (bile acids), emulsification of fats and
facilitating absorption of lipids and fat-soluble vitamins. Bile is composed of bile
salts, bile pigments, cholesterol, bilirubin, inorganic ions (sodium, potassium,
chloride, and calcium), and substances that give alkalinity to bile. Bile salts are
made from cholesterol that is either supplied in the diet or is synthesized in the
liver. Cholesterol is converted in the liver to two bile salts: cholic acid and
chenodeoxycholic acid. Bacteria in the gut convert a portion of these primary
bile acids to secondary bile acid: deoxycolic and lithocholic acids. Bile salts
cannot perform their function of emulsifying fat in the intestine until they are
conjugated to either glycine or to taurine (amino acids) to form glycol-
conjugated bile acids or taurine-conjugated bile acids. Conjugation of bile acids
takes place in the liver. Calcium or potassium is added to conjugated bile acids
to form a bile salt. Conjugated bile salts when secreted from the liver are able to
emulsify lipids. The emulsification action of bile on lipids has been called the
detergent function of bile. This is because bile breaks lipids apart causing them
to foam when agitated by peristalsis. Emulsified lipids look a lot like soapy foam
produced by dishwashing liquid. At the molecular level, we would see small
structures called micelles formed in the emulsification process. Micelles are
small “bubbles” of lipids that have cholesterol and fat inside and bile acids on
the outside. This arrangement gives lipids solubility in water; otherwise lipids are
insoluble and float on water. This arrangement also facilitates the transport of
lipids to the gut mucosa and causes them to stick to it. This is an effective and
efficient method of absorption of fats from the diet.

As you can see bile plays an important role in providing nutrients to the
body. Here are a few other important reasons bile salts must be available in the
gut to aid in digesting lipids. Without bile salts about 40% of lipids are lost in the
stool creating a deficit of essential lipids. Essential lipids are those needed by the
body for normal bodily functions, but cannot be endogenously synthesized by
the body. Linoleate and linolenate are the two essential fatty acids that must be
taken in through the diet. Fat-soluble vitamins A, D, E, and K are absorbed with
lipids from the gut; excess fat-soluble vitamins are also stored in the liver. Of
these, only vitamin K is not stored in sufficient quantity by the liver. In just a few
days vitamin K deficiency will develop if insufficient amount is not absorbed from
the diet. Vitamin K is a necessary nutrient for the liver to synthesize blood
clotting agents. In just a few days without vitamin K, prothrombin, and
coagulation factors VII, IX, and X become deficient. Therefore, bile formation and
flow are very important for homeostasis of the blood coagulation system.

Bile salts are physiologically conserved; approximately 95% of bile salts

are reabsorbed in the small intestine terminal ileum. Only a small amount of bile
is newly synthesized daily, approximately about 0.2-0.5 grams per day. The
circulating bile pool is roughly 2-3 grams, which recycles in enterohepatic
circulation at a rate of twice per meal, or 6 times a day. In the liver bile is
reabsorbed by hepatocytes almost 100% in the first pass and secreted into the
bile canaliculi. It is estimated that bile salts circulate some 18 times in the
enterohepatic cycle before being excreted in feces. The small quantity of bile
salts (less than 5 %) that is lost in feces is replaced with newly synthesized bile
salts by hepatocytes. Any impairment of enterohepatic bile circulation, such as
obstruction of the biliary ducts by cholelith or chronic cirrhosis of the liver is a
significant medical problem.

Enterohepatic circulation is defined as the recurrent cycle in which bile

salts and other substances excreted by the liver pass through the intestinal
mucosa and become reabsorbed by the hepatic cells and re-excreted. Any
impairment of enterohepatic bile circulation, such as obstruction of the biliary
ducts by cholelith or chronic cirrhosis of the liver is a significant medical
problem.

The pancreas is positioned horizontally along the posterior abdominal wall

adjacent to lesser curvature of the stomach. It is a retroperitoneal organ located
mainly in the epigastrium. It consists of a head, neck, body, and tail. The head is
the expanded part found within the C-loop of the duodenum. Inferiorly the head
constricts forming an uncinate process before tapering slightly forming the neck.
The head and neck lie anterior to the inferior vena cava. The body is the longest
part lying transversely across the posterior abdominal wall. The tail tapers along
its course ending in or near the hilum of the spleen. It is a soft spongy organ
about 12 cm long and 2.5 cm thick. The pancreas is both an endocrine and
exocrine gland. Clusters of cells called the pancreatic islets (a.k.a. islets of
Langerhans) carry out endocrine functions. The pancreatic islets produce insulin
and glucagons. Both insulin and glucagon are secreted into the blood directly
and are distributed systemically by the superior mesenteric vein to the portal
vein. Because these hormones are secreted into the blood they are not affected
by biliary duct obstruction. These hormones participate in carbohydrate
metabolism and help regulate blood glucose level. Special exocrine cells called
alpha 2 and beta cells comprise about 2% of the pancreas parenchyma. Alpha 2
cells secrete glucagons, and beta cells of the islets produce insulin. Endocrine
cells comprise about 2% of the pancreas and exocrine cells make up about 98%
of the pancreas. The biliary system consists of the liver, gallbladder and biliary
ducts. The pancreas is not considered part of the biliary system based on its role
of secreting inactive digestive juices into the duodenum. Inability to secrete
digestive juices into the duodenum due to biliary obstruction can adversely
affect the pancreas.

What we are concerned with in this module is the exocrine functions of the
pancreas, which produces digestive enzymes. Pancreatic juice contains enzymes
to digest all three major foods: proteins, carbohydrates, and lipids. The pancreas
also secretes sodium bicarbonate at a concentration of nearly 5 times that in
serum. Strong digestive juices produced by the pancreas are capable of
digesting it so these enzymes are secreted into ducts. Pancreatic enzymes are
produced in an inactive form called a zymogen. Once they enter the protected
mucosa of the duodenum they become activated and can digest proteins, lipids,
and carbohydrates. Pancreatic enzymes are secreted into two main ducts of the
pancreas. The main pancreatic duct called Wirsung’s duct runs transversely from
the head to the tail of the pancreas. It joins the common duct that partially
passes through the head of the pancreas as it transports bile to the duodenum. A
minor accessory duct is seen in about 15% of the population; it drains the head
of the pancreas into a minor duodenal papilla. Pancreatic enzymes are necessary
to help digest food for absorption across the bowel mucosa. Pancreatic enzymes
are alkaline so that when they are secreted into the duodenum acidic chyme is
neutralized. Neutralization of acids from the stomach protects the rest of the gut
from self-digestion. Enzymes from the pancreas include amylase to metabolize
sugars, lipase to digests lipids, and trypsin, which digest proteins. These
enzymes are inactive until they enter the duodenum where catalytic
enterokinase activates them. This protects the pancreas and biliary ducts for
self-digestion. Acute pancreatitis can be caused by reflux of active pancreatic
enzymes from the duodenum back into the pancreatic duct. Enzymatic necrosis
is a type of inflammation that is unique to the pancreas and is seen in acute
pancreatitis. Active pancreatic digestive enzymes’ entering the main pancreatic
duct digesting the pancreas causes this condition.

The biliary system consists of the organs and ducts (bile ducts, gallbladder,
and associated structures) that are involved in the production and transportation
of bile. The transportation of bile follows this sequence:

1. When the liver cells secrete bile, it is collected by a system of ducts that
flow from the liver through the right and left hepatic ducts.
2. These ducts ultimately drain into the common hepatic duct.
3. The common hepatic duct then joins with the cystic duct from the
gallbladder to form the common bile duct, which runs from the liver to the
duodenum (the first section of the small intestine).
4. However, not all bile runs directly into the duodenum. About 50 percent of
the bile produced by the liver is first stored in the gallbladder, a pear-
shaped organ located directly below the liver.
5. Then, when food is eaten, the gallbladder contracts and releases stored
bile into the duodenum to help break down the fats.

The organs and ducts by which bile is formed, concentrated, and carried from
the liver to the duodenum (the first part of the small intestine). Bile removes
waste products from the liver and carries bile salts, necessary for the breakdown
and absorption of fat, to the intestine.

Bile is secreted by the liver cells and collected by a system of tubes that
mirrors the blood supply to the organ. This network of bile-drainage channels
carries the bile out of the liver by way of the hepatic ducts, which join together
to form a common duct that opens into the duodenum at a controlled orifice
called the ampulla of Vater. Bile does not pass directly into the duodenum but is
first concentrated and then stored until needed in the gall bladder, a pear-
shaped reservoir lying in a hollow under the liver, to which it gains access by
way of the cystic duct.

When food is eaten, the presence of fat in the duodenum causes the
secretion of a hormone, which opens the ampulla of Vater and causes the gall
bladder to contract, squeezing stored bile via the cystic and common bile ducts
into the duodenum. In the duodenum, bile salts emulsify the fat, breaking it
down to a kind of milk of microscopic globules.

Functions of the biliary system:

The biliary system's main function includes the following:

• to drain waste products from the liver into the duodenum

• to help in digestion with the controlled release of bile

Bile is the greenish-yellow fluid (consisting of waste products, cholesterol, and

bile salts) that is secreted by the liver cells to perform two primary functions,
including the following:

• to carry away waste

• to break down fats during digestion

Bile salt is the actual component which helps break down and absorb fats.
Bile, which is excreted from the body in the form of feces, is what gives feces its
dark brown color.

The biliary tree conducts bile and pancreatic digestive enzymes to the
duodenum. The gross anatomy of the biliary tree begins with the right and left
hepatic ducts that drain bile from the two halves of the liver. These become the
common hepatic duct that is joined by the cystic duct from the gallbladder. The
union of the common hepatic and cystic ducts form the common bile duct. The
common bile duct is about 7.5 cm long. It passes posterior and often through the
pancreas to join the main pancreatic duct (duct of Wirsung). The union of the
main pancreatic duct and common bile duct form a short ampula called the
hepatopancreatic ampula (a.k.a. ampula of Vater). The ampula inserts on the
major duodenal papilla, which is guarded by the hepatopancreatic sphincter
(a.k.a. sphincter of Oddi). A minor accessory duct called Santorini’s duct, when
present may drain a portion of the pancreatic head into the minor duodenal
papilla. The accessory duct is not present in most individuals.

The physiology of the biliary tract causes bile to be concentrated in the

gallbladder in the absence of fat in the diet. Likewise, bile is released when fat
and some proteins are present in the diet. The mechanism for bile concentration,
storage and release is controlled primarily by the hormone cholecystokinin
(CCK); other hormones gastrin and secretin along with vagal stimulation play
minor roles. When the sphincter of Oddi is closed, hydrostatic pressure forces
bile through the cystic duct into the gallbladder (retrograde filling). When chyme-
containing fat reaches the duodenum, cells in the duodenum secrete CCK into
the blood. Cholecystokinin is a hormone that when it reaches the gallbladder it
causes it to contract. The action of CCK on the duodenal sphincter is to relax
allowing muscular contractions of the gallbladder moves bile without resistance.
The time from ingestion of lipids to stimulation of the gallbladder to contract is
roughly 30 minutes. Complete emptying of the gallbladder takes about 1 hour.
The hormones CCK, gastrin and secretin are cholesecretagogues. A
secretagogue is a substance that stimulates secretion. Cholesecretagogues
stimulate secretion of bile by the gallbladder.

LABORATORY AND DIAGNOSTIC EXAMS

 NURSING CARE PLAN

Assessment Nursing Scientific Planning Interventions Rationale Evaluation

Diagnosis Explanation
S: “lagi na lang Risk for Impaired Immobility, which Patient’s skin  establish rapport  to facilitate NPI Patient’s skin
akong nakahiga” Skin Integrity r/t leads to pressure, remains intact,  place the pt in a  to prevent remained intact,
shear, and friction, comfortable position backaches or
as verbalized by prolonged bed is the factor most
as evidenced by as evidenced by
 take and record muscle aches.
the patient. rest 20 post- likely to put an no redness over vital signs  to note any
no redness over
operative individual at risk for bony significant changes bony
O: procedure altered skin prominences and that may be brought prominences and
integrity. Advanced absence of skin about by the absence of skin
 Conscious and  Assess general
age; the normal loss condition of skin. disease
coherent of elasticity; breakdown breakdown
 Healthy skin
 c body inadequate varies from
weakness nutrition; individual to
environmental
 restless individual, but
moisture, especially should have good
 c limited ROM from incontinence; turgor, feel warm
 ambulatory c and vascular and dry to the
assistance insufficiency touch, be free of
 Specifically assess
potentiate the impairment, and
 V/S taken as skin over bony
effects of pressure have quick capillary
follows: prominences
and hasten the refill (<6 seconds).
T: 37.4 development of skin  Areas where skin
P: 86 breakdown. Groups is stretched tautly
R: 18 of persons with the over bony
BP: 120/70 highest risk for prominences are at
altered skin higher risk for
integrity are the breakdown because
spinal cord injured, the possibility of
those who are
 Assess patient’s ischemia to skin is
confined to bed or
ability to move. high as a result of
wheelchair for compression of skin
prolonged periods of
 Reassess skin capillaries between
time, those with
often and whenever a hard surface and
edema, and those
the patient’s the bone.
 who have altered condition or  Immobility is the
sensation that treatment plan greatest risk factor
triggers the normal results in an in skin breakdown.
protective weight increased number of  The incidence and
shifting. Pressure risk factors. onset of skin
relief and pressure  encourage change breakdown is
reduction devices of position in a directly related to
for the prevention of regular basis the number of risk
skin breakdown factors present.
include a wide  provide adequate
range of surfaces, clothing/covers;  to prevent
specialty beds and protect from drafts pressure to certain
mattresses, and  emphasize parts of the body
other devices. importance of  to prevent
Preventive adequate nutritional/ vasoconstriction
measures are fluid intake
usually not  recommend  to maintain
reimbursable, even keeping nails short general good health
though costs related and skin turgor
to treatment once  recommend  to reduce risk of
breakdown occurs elevation of lower dermal injury when
are greater. extremities when severe itching is
sitting present
 encourage  to enhance
ambulation as venous return and
tolerated reduce edema
formation
 to enhance
circulation
 Assessment Nursing Diagnosis Scientific Planning Interventions Rationale Evaluation
Explanation
S: “Hindi ko alam Knowledge deficient Knowledge After 8 hours Independent: After 8hours of
ang gagawin sa regarding deficit is a of nursing  Review disease  Provides nursing
sugat ko” as process, surgical knowledge
condition and self nursing interventions interventions,
verbalized by the procedure or base on which
care r/t information diagnosis that the patient will prognosis. patient can make the patient was
patient.
misinterpretation. addresses a verbalize informed able
O:
client problem understanding  Demonstrate choices. verbalize
or potential of therapeutic care  Promotes understanding of
 Statement of of incisions or Independence in
misinterpretation
problem needs. therapeutic
dressing or drains. care and reduces
resulting from a risk of needs.
 Request for
information lack of  Emphasize complications.
knowledge or importance of  During initial 6
 V/S taken as
follows: psychomotor maintaining low fat months after
skill. The diet, eating small surgery, low fat
T: 37.3 frequent diet limits need
P: 80 evolutionary meals, gradual for bile and
R: 19 view of analysis reintroduction of reduces
BP: 120/80 acknowledges foods or fluids discomfort
that contextual containing fats associated with
and temporal over 4 to 6 month inadequate
period. digestion of fats.
influences
 Discuss avoiding
affect concepts. or limiting use of
Because the alcoholic  Minimizes the
contextual beverages. risk of pancreatic
attributes of a  Inform patient involvement.
concept change that loose stools  Intestines
may occur for require time to
over time, several months. adjust to stimulus
either by of
convention or  Identify signs continuous output
purposeful and of bile.
redefinition, the symptoms  Indicators of
requiring obstruction of bile
continued notification of flow or altered
development of healthcare digestion,
knowledge provider like dark requiring further
urine, jaundiced evaluation and
depends on its color of eyes or intervention.
reevaluation skin, clay colored
and refinement. stools.  Resumption of
 Review activity usual activities is
limitations normally
depending on Accomplished
individual within 4-5 weeks.
situation.
 Assessment Nursing Scientific Planning Interventions Rationale Evaluation
Diagnosis Explanation
S: “Masakit yung Acute pain Pain has 4 stages; After 8 hours Independent: After 8 hours of
tahi ko” as r/t disruption of the first one is the of nursing  Evaluate pain  Provides Nursing
transduction, it regularly noting information about
verbalized by skin, tissue, and occurs when a
interventions, interventions,
characteristics, need for or
the patient. muscle integrity. stimulus, such as the patient’s patient’s pain
location, intensity effectiveness of
pressure, thermal pain will be was relieved
(0-10 scale). interventions.
O: energy, or chemical relieved or and controlled.
irritation, is  Identify specific  Prevents undue
 Facial mask of controlled activity limitations. strain on
converted into a
pain. nerve signal. This operative site.
 Guarding occurs at the ends  Recommend  Promotes
behavior. of sensory nerve planned or return of normal
cells whose progressive function and
 Narrowed terminals are exercise. enhances feelings
focus. sensitive to this of
 V/S taken as type of activation. general well
follows: These cells, known
 Schedule being.
T: 37.3 as nociceptors, are
distributed adequate rest  Prevents fatigue
P: 80 throughout the periods. and conserves
R: 18 body. Second is the  Review energy for
Bp: 110/90 transmission, it is importance of healing.
the process of nutritious diets  Provides
transferring pain and adequate fluid elements
information from intake. necessary for
the peripheral to  Reposition as tissue
the central nervous regeneration or
indicated.
system. Signals are
healing.
transmitted along
the axons of  Provide  May relieve
nociceptors. additional pain and enhance
From here, comfort measures circulation.
projection neurons like back rub.  Improves
carry information to circulation,
the brainstem, reduces muscle
thalamus, and  Encourage use tension and
hypothalamus as of anxiety associated
well as to reflex arcs with pain.
relaxation
 to mediate an technique like  Relieves
avoidance response. deep breathing muscle and
The third stage is exercises. emotional
the pain modulation tension.
wherein there is
Collaborative:
transmission of pain
signals through the  Administer
analgesics or non  To relieve mild
dorsal horn. The
current view is that steroidal anti- or moderate pain.
signals originating inflammatory
in the brain can drugs as
both inhibit and prescribed.
facilitate pain signal
transmission. And
the last stage is the
perception; it is the
awareness of pain
associated with a
specific area of the
body. It depends on
the transmission of
pain signals through
the thalamus to the
cortex and limbic
system.

DRUG STUDY

Narcotic analgesics – relieves pain of inflammation and infection

GENERIC BRAND ACTION INDICATION CONTRA-INDICATION ADVERSE NURSING

NAME NAME REACTION CONSIDERATION
Meperdine Demerol Narcotic - moderate Hypersensitivity. - respiratory and - Assess level,
 analgesic. to sever circulatory duration and
They attach pain depression frequency of
to specific - pre- - Respiratory and pain.
receptor operative circulatory - Assess renal
located in the
medication arrest. function before
CNS to
produce
- Shock initiating therapy.
alteration of - Lightheadednes - Assess
both s respiration
perception - Sedation - Monitor allergic
and - Nausea reactions.
emotional - Vomiting - Monitor for
response to - sweating possible drug
pain. It induced adverse
involves reaction.
decreased
permeability
of the cell
membrane to
sodium,
which result
to diminished
transmission
of pain
impulse.

An
ticholinergics – used to relieved spasm of the gallbladder by inhibiting the action of acetylcholine on the postganglionic
parasympathetic muscarinic receptors, local anesthetic action and decreasing GI motility.

GENERIC BRAND ACTION INDICATION CONTRA- ADVERSE NURSING

NAME NAME INDICATION REACTION CONSIDERATION
Dicyclomine Bentyl Acts on the Treatment of - Obstructive - dry mouth - Assess for signs of
muscle in the functional uropathy - nausea toxicity to other
wall of the gut bowel/irritable - Obstructive - vomiting drugs.
and also the bowel syndrome. disease of the - constipation - Monitor I and O
urinary gastrointestinal - bloated ratio.
bladder. It tract feeling - Monitor for
relaxes the - Severe - abdominal possible drug
muscle and ulcerative pain induced adverse
prevents colitis - taste loss reaction
spasms from - Reflux - anorexia
occurring. It esophagitis
also can - Unstable
slightly reduce cardiovascular
the production status in acute
of stomach hemorrhage
acid. - Glaucoma
- Myasthenia
gravis

Anti-emetics – used to reduce nausea and vomiting by depressing the chemoreceptor trigger zone or by inhibiting serotonin

receptors to block nausea response.

 GENERIC BRAND NAME ACTION INDICATION CONTRA- ADVERSE NURSING
NAME INDICATION REACTION CONSIDERATION
Dimenhydrinate -- Inhibits - treatment -- - drowsiness - assess for signs of
vestibular for nausea - GI toxicity to other
stimulation - vomiting disturbances drugs.
which may - dizziness or - monitor v/s; BP
prevent motion vertigo - monitor I and O
sickness. ratio.

Gallstone solubilizer – used for dissolving gallstones that are less than 20mm diameter by suppression of liver synthesis and
secretion of cholesterol and inhibition of intestinal absorption of cholesterol.

GENERIC NAME BRAND ACTION INDICATION CONTRA- ADVERSE NURSING

NAME INDICATION REACTION CONSIDERATION
Ursodeoxychlolic ursofalk Suppresses the Dissolution of - Inflammatory Rarely, doughy - obtain patients
acid ((urosodiol) synthesis and cholesterol bile duct stools. history: lifestyle,
secretion of gallstones disease. hypersensitivity and
cholesterol by - acute medication.
- perform Complete
the liver and cholecystitis
blood test; cholesterol
inhibits - obstructive level.
intestinal hepatobiliary - perform liver function
absorption of disease test.
cholesterol. Assess for tenderness
in the RUQ.
- Assess for radiating
pain to the right left
scapula
- Perform ultrasound.