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[Alterations in Metabolic and Endocrine Functions]

LIVER CIRRHOSIS
Precipitating Factors:

Predisposing Factor:

- Excessive alcohol - LAENNECS CIRRHOSIS


- Complication of viral, toxic / idiopathic hepatitis
- POSTNECROTIC CIRRHOSIS
- Chronic biliary obstruction and infection - BILIARY CIRRHOSIS
- Severe right-sided heart failure

- Biliary Atresia
- Genetic digestive disorder
- Autoimmune hepatitis

Liver Cell Injury

Increased

Pain

Inflammation

Fatigue
Nausea & Vomiting

Fever
Anorexi

Activation of Hepatic Stellate cells

Expansion of Myofibroblasts-Pool

Fibrosis/Scarring of the Liver

Obstruction of Blood Flow


Increased pressure in the venous and sinusoidal
channels

Portal Hypertension( 10mmHg)

Formation of collateral circulation

pressure to nearest
susceptible organ/s

organs

Splanchnic vascular and Peripheral


arterial vasodilation

Increased circulating
bilirubin

Caput medusae
Jaundice
Hemorrhoids

Esophageal varices

Hypersplenism

Thrombocytopenia

Anemia

Leukopenia

Prolonged bleeding

weakness

infection

Splanchnic Lymph
production

Hepatorenal Syndrome
Effective blood volume decreased

Cardiac output decreased


SNS

Renal Arterial
Vasoconstriction

ADH
RAAS

*Oliguria
*Increased BUN and Creatinine levels - azotemia
*Increased osmolality and urine specific gravity
*Low blood sodium
*Low urine sodium concentration
Renal blood flow

Na+ & Water


Retention

Ascites formation
A

Sources:
Gressner, O., Weiskirchen, R., & Gressner, A. (2007). Medscape Nurses: Evolving Concepts of Liver Fibrogenesis Provide New
Diagnostic and Therapeutic Options. Retrieved March 2015, from http://www.medscape.com/viewarticle/573027.
Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby
Elsevier Inc.
Mayo Foundation for Medical Education and Research. (2015). Cirrhosis. Retrieved March 2015, from
http://www.mayoclinic.org/diseases-conditions/cirrhosis/basics/causes/con-20031617.
Udan, J. (2002). Medical Surgical: Concepts and Clinical Application (First Edition). Philippines: Guiani Prints House.

94

Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from
http://emedicine.medscape.com/article/185856-overview.

[Alterations in Metabolic and Endocrine Functions]


A

Arterial
underfilling

Activation of
vasoconstrictors

Decreased bile in Gastrointestinal


tract and increase urobilinogen

Release of endothelin-1 and


combines to capillary cells

Nitric oxide secreted causing to


vasodilate and increased blood flow

Clay-colored stools
and dark urine

Increased RBC causing insufficient O2 supply and different


pressure d/t different pressure in capillary and alveolus

Hepatic Pulmonary
Syndrome

*Exhaustion
*Fatigue

Poor Vitamin
K absorption

Decreased
emulsification of

Bleeding
tendencies

Hypoglycemia
Malnutrition

Inability to metabolize
ammonia to urea

Ammonia levels
in the blood

Brain edema
Astrocyte swelling
Neurotransmitter and receptor alteration
Altered brain glucose metabolism

Decrease androgen and


estrogen detoxification

Decrease metabolism of
protein and carbohydrates

Osmotic
pressure

* Palmar erythema
* Testicular atrophy
* Gynecomastia
* Spider Angiomas
* Loss of body hair
* Menstrual changes

Ascites

Decrease ADH &


aldosterone detoxification

Edema

Bacterial
Peritonitis

Sepsis

Hepatic Encephalopathy

* Inability to concentrate
* Loss of memory
* Confusion
* Depressed level of consciousness
* Asterixis
* Foul breath
* Respiratory acidosis
* Alteration in sleep

Hepatic Coma

Death

Sources:
Gressner, O., Weiskirchen, R., & Gressner, A. (2007). Medscape Nurses: Evolving Concepts of Liver Fibrogenesis Provide New
Diagnostic and Therapeutic Options. Retrieved March 2015, from http://www.medscape.com/viewarticle/573027.
Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby
Elsevier Inc.
Mayo Foundation for Medical Education and Research. (2015). Cirrhosis. Retrieved March 2015, from
http://www.mayoclinic.org/diseases-conditions/cirrhosis/basics/causes/con-20031617.
Udan, J. (2002). Medical Surgical: Concepts and Clinical Application (First Edition). Philippines: Guiani Prints House.

95

Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from
http://emedicine.medscape.com/article/185856-overview.

96

[Alterations in Metabolic and Endocrine Functions]

LIVER CIRRHOSIS
Cirrhosis is the final stage attained by various chronic liver diseases after years or
decades of slow progression. The liver cells attempt to regenerate, but the regenerative process is
disorganized, resulting in abnormal blood vessel and bile duct architecture. The overgrowth of
new and fibrous connective tissue distorts the livers normal lobular structure, resulting in
lobules of irregular size and shape with impeded blood flow. Eventually, irregular, disorganized
regeneration; poor cellular nutrition; and hypoxia caused by inadequate blood flow and scar
tissue result in decreased functioning of the liver. Cirrhosis may be having an insidious,
prolonged course.[1]
ETIOLOGY AND RISK FACTORS
Excessive alcohol (Laennecs Cirrhosis) the first change in the liver from excessive
alcohol intake is an accumulation of fat in the liver cells. Uncomplicated fatty changes in the
liver are potentially reversible if the person stops drinking alcohol. If the alcohol abuse
continues, widespread scar formation occurs throughout the liver.
Complication of viral, toxic or idiopathic hepatitis (Postnecrotic Cirrhosis) called as
post necrotic cirrhosis. Chronic biliary obstruction and infection due to gallstones, inflammation
of bile ducts, trauma, biliary strictures (abnormal narrowing of the ducts), cysts, enlarged lymph
nodes, pancreatitis, and injury related to gallbladder or liver surgery, tumors of bile ducts or
pancreas, hepatitis, or parasites. (Biliary Cirrhosis) Severe right-sided heart failure in patients
with corpulmonale, constrictive pericarditis, and tricuspid insufficiency.[2] Biliary Atresia Genetic
digestive disorder Autoimmune hepatitis[3]

Wolf, D. (2014, December 10).Medscape: Cirrhosis. Retrieved March 2015, from


http://emedicine.medscape.com/article/185856-overview

Udan, J. (2002).Medical Surgical: Concepts and Clinical Application (First Edition). Philippines: Guiani Prints House.

97

Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby
Elsevier Inc.

[Alterations in Metabolic and Endocrine Functions]

PATHOPHYSIOLOGY
In cirrhosis, continuous liver damage can result to cell destruction and fibrosis of hepatic
tissues. Fibrosis within the cirrhotic liver obstructs the flow of blood through the liver and to the
liver cells. As a result of the obstruction to the flow of blood through the liver, blood backs-up in
the portal vein, and the pressure in the portal vein increases, a condition called portal
hypertension. Because of the obstruction to flow and high pressures in the portal vein, blood in
the portal vein seeks other veins in which to return to the heart, veins with lower pressures that
bypass the liver. Unfortunately, the liver is unable to add or remove substances from blood that
bypasses it. It is a combination of reduced numbers of liver cells, loss of the normal contact
between blood passing through the liver and the liver cells, and blood bypassing the liver that
leads to many of the manifestations of cirrhosis. In an attempt to reduce the high portal pressure
and to reduce the increased plasma volume and lymphatic flow, collateral circulation develops.
The common area for collateral circulation includes the veins in the esophagus, anterior
abdominal wall, parietal peritoneum and the mesenteric veins in the intestines specifically in the
rectum. Varicosities develop in the collateral areas, resulting to esophageal and gastric varices,
caput medusa and haemorrhoids. These varices can lead to massive haemorrhage if the varices
are being ruptured because of some factors such as acid regurgitation from the stomach,
ingestion of coarse food, swallowing of poorly masticated food, and increased abdominal
pressure.[4]
The spleen normally acts as a filter to remove older red blood cells, white blood cells,
and platelets. The blood that drains from the spleen joins the blood in the portal vein from the
intestines. As the pressure in the portal vein rises in cirrhosis, it increasingly blocks the flow of
blood from the spleen. The blood turns back accumulating in the spleen, and the spleen swells in
size, a condition referred to as hypersplenism.[5] Sometimes, the spleen is so enlarged that it
causes abdominal pain. As the spleen enlarges, it filters out more and more of the blood cells and
platelets until their numbers in the blood are reduced called as thrombocytopenia, leukopenia,
anemia and coagulation disorders. The anemia can cause weakness, the leukopenia can lead to
infections, and the thrombocytopenia can impair the clotting of blood and result in prolonged
bleeding.[6]

Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby
Elsevier Inc.

98

Mayo Foundation for Medical Education and Research. (2015). Cirrhosis. Retrieved March 2015, from
http://www.mayoclinic.org/diseases-conditions/cirrhosis/basics/causes/con-20031617.

Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from
http://emedicine.medscape.com/article/185856-overview.

[Alterations in Metabolic and Endocrine Functions]

Some of the protein in food that escapes digestion and absorption is used by bacteria that
are normally present in the intestine. While using the protein for their own purposes, the bacteria
make substances that they release into the intestine. These substances then can be absorbed into
the body. Some of these substances, for example, ammonia, can have toxic effects on the brain.
Ordinarily, these toxic substances are carried from the intestine in the portal vein to the liver
where they are removed from the blood and detoxified. When cirrhosis is present, blood are not
detoxified and ammonia and other substances are present in the systemic circulation. When the
toxic substances accumulate sufficiently in the blood, the function of the brain is impaired, a
condition called hepatic encephalopathy. Symptoms include irritability, inability to concentrate
or perform calculations, loss of memory, confusion, or depressed levels of consciousness,
asterixis, foul breath, respiratory acidosis, and alteration in sleep. Hepatic encephalopathy will
further complicate to hepatic coma if not well managed that will lead to death.[7]
Rarely, some patients with advanced cirrhosis can develop hepatopulmonary syndrome.
These patients can experience difficulty breathing because certain hormonesspecifically the
endothelin-1, a portent vasoconstrictor, released in advanced cirrhosis cause the lungs to function
abnormally. The basic problem in the lung is that not enough blood flows through the small
blood vessels in the lungs that are in contact with the alveoli of the lungs. Blood flowing through
the lungs is shunted around the alveoli and cannot pick up enough oxygen from the air in the
alveoli. As a result the patient experiences shortness of breath, particularly with exertion.[8]
In uncontrolled multiplication of liver cells for recovery of lost cells, cancer of the liver
develops. The most common symptoms and signs of primary liver cancer are abdominal pain and
swelling, hepatomegaly, weight loss, and fever.[9]
The liver cells and the channels through which bile flows are also affected in cirrhosis.
Bile is a fluid produced by liver cells that has two important functions: to aid in digestion and to
remove and eliminate toxic substances from the body. The bile that is produced by liver cells is
secreted into very tiny channels that run between the liver cells that line the sinusoids, called
canaliculi. The canaliculi empty into small ducts which then join together to common bile duct.
[10]

Gressner, O., Weiskirchen, R., & Gressner, A. (2007).Medscape Nurses: Evolving Concepts of Liver Fibrogenesis Provide New
Diagnostic and Therapeutic Options. Retrieved March 2015, from http://www.medscape.com/viewarticle/573027.

99

Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby
Elsevier Inc.

Mayo Foundation for Medical Education and Research. (2015). Cirrhosis. Retrieved March 2015, from
http://www.mayoclinic.org/diseases-conditions/cirrhosis/basics/causes/con-20031617.

10

Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from
http://emedicine.medscape.com/article/185856-overview.

[Alterations in Metabolic and Endocrine Functions]

Ultimately, all of the ducts combine into one duct that enters the small intestine. In this way, bile
gets to the intestine where it can help with the digestion of food. At the same time, toxic
substances contained in the bile enter the intestine and then are eliminated in the stool. In
cirrhosis, the canaliculi are abnormal and the relationship between liver cells and canaliculi is
destroyed, just like the relationship between the liver cells and blood in the sinusoids. As a result,
obstructive jaundice may also occur and is usually accompanied by pruritus, an accumulation of
bile salts underneath the skin. The liver is not able to eliminate toxic substances normally, and
they can accumulate in the body. To a minor extent, digestion in the intestine also is reduced.
Jaundice occurs as a result of decreased ability to conjugate and excrete bilirubin. If obstruction
of the biliary tracts occurs,obstructive jaundice may also occur and is usually accompanied by
pruritus, an accumulation of bile salts underneath the skin.[11]
Patients with worsening cirrhosis can develop hepatorenal syndrome. This syndrome is a
serious complication in which the function of the kidneys is reduced. It is a functional problem
in the kidneys, meaning there is no physical damage to the kidneys. Instead, the reduced function
is due to changes in the way the blood flows through the kidneys themselves. Due to the portal
hypertension along with liver decompensation results in splanchnic and systemic vasodilation
and decreased arterial blood volume, renal vasoconstriction occurs and renal failures occur.This
syndrome consists of progressive oliguria and azotemia in the absence of structural damage to
the kidney. There will be an increase BUN and Creatinine levels in the urinalysis result. There
will be also an increase osmolality and urine specific gravity, low blood sodium and low urine
sodium concentration due to sodium reabsorption.[12]
As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt and
water in the body. The excess salt and water first accumulates in the tissue beneath the skin of
the ankles and legs because of the effect of gravity when standing or sitting. This accumulation
of fluid is called edema or pitting edema. Fluid also may accumulate in the abdominal cavity
between the abdominal wall and the abdominal organs. This accumulation of fluid, called ascites
causes swelling of the abdomen, abdominal discomfort, and increased weight. When BP is
elevated in the liver, proteins move from the blood vessels via the large pores of sinusoids into
the lymph space. When the lymphatic system is unable to carry off the excess proteins and water,
they leak through the liver capsule into the peritoneal cavity. The osmotic pressure of the
proteins pulls additional fluid into the peritoneal cavity. Another mechanism is hypoalbuminemia
100

resulting from inability of the liver to synthesize albumin.[13] The hypoalbuminemia results in

11

Wolf, D. (2014, December 10).Medscape: Cirrhosis. Retrieved March 2015, from


http://emedicine.medscape.com/article/185856-overview.
12
Gressner, O., Weiskirchen, R., & Gressner, A. (2007).Medscape Nurses: Evolving Concepts of Liver Fibrogenesis Provide New
Diagnostic and Therapeutic Options. Retrieved March 2015, from http://www.medscape.com/viewarticle/573027.
13
Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby
Elsevier Inc.

[Alterations in Metabolic and Endocrine Functions]

decreased colloidal oncotic pressure. Another mechanism is hyperaldosteronism which occurs


when aldosterone is not metabolized by damaged hepatocytes. The increased level of aldosterone
causes increased sodium reabsorption by the renal tubules. This retention of sodium as well as
the increased in antidiuretic hormone, causes additional water retention. When this ascites will
rupture, usually at the abdominal part, this may lead to bacterial peritonitis, sepsis and may
progress and lead to death.[14]
Several signs and symptoms relating to the metabolism and inactivation of adrenocortical
hormones, estrogen and testosterone occur in cirrhosis. When the liver is unable to metabolize
the hormones, various manifestations occur. In men, gynecomastia, loss of axillary and pubic
hair, testicular atrophy, and impotence with loss of libido may occur as a result of increased
estrogen levels. In younger women, amenorrhea may occur, and in older women there may be
vaginal bleeding. The liver fails to metabolize aldosterone adequately, resulting in
hyperaldosteronism with subsequent sodium and water retention and potassium loss.[15]

Jaclyn Mae T. Alviola, RN


MSN Student

101

14

Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby
Elsevier Inc.
15
Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from
http://emedicine.medscape.com/article/185856-overview.

102

[Alterations in Metabolic and Endocrine Functions]

CHOLECYSTITIS
Precipitating factors:

Predisposing factor:

- Pregnancy
- Diabetes
- Tumor surrounding the Gallbladder
- Hyperlipidemia
- Losing weight rapidly and diet
- Obesity
- Gallstones
- Oral contraceptives

- Female (estrogen levels)


- Pregnancy
- Hormone therapy
- Family History
- Ethnicity

Decreased contractility of Bile

Bile stasis

Contraction of substances present in bile

Precipitation of bile substances

Bile substances will increase in size

Stones migrate to gallbladder

Kinking/compression of common bile duct/pancreatic duct

Obstruction to gallbladder

Obstruction of flow of bile

Stimulates smooth
muscle contraction

Increase intraluminal pressure

RUQ abdominal
pain

Increase tension
to duodenum

Gallbladder distention

Pain radiates to
lower back

Presence of bile in the


circulation
Wall edema
Impaired Hepatic
uptake of bilirubin

Collection of soluble
bilirubin in the urine

No bile reaches
the GIT

Vascular compromise

Ischemia to
Cholesterol salts
in the skin

Jaundice

No bile in small intestine


for fat digestion
Escape of
bilirubin to GUT

Presence of bile in
the urine

Dark yellow
urine
Sources:

Decrease bile in
the duodenum

Decreased
sterobilin
Emulsification
of fats

Nausea and
Vomiting

Necrosis to Gallbladder

Invasion of bacteria

Realease of toxic metabolites into


Clay-colored
stool

Shock
Pulmonary Insufficiency
Acute renal failure
Dissemenated Intravascular
Coagulation

Intuit and Docstoc. (2014). Cholecystitis Pathophysiology. Retrieved March 2015, from
http://img.docstoccdn.com/thumb/orig/113462569.png.
Mayo Foundation for Medical Educationand Research. (2015). Cholecystitis. Retrieved March 2015, from

103

http://www.mayoclinic.org/diseases-conditions/cholecystitis/basics/symptoms/con-20034277.
Nursing Crib. (2015). Pathophysiology of Cholelithiasis/Cholecystitis. Retrieved March 2015, from http://nursing
crib.com/pathophysiology/pathophysiology-of-cholelithiasischoleccsytitis/.

[Alterations in Metabolic and Endocrine Functions]

CHOLECYSTITIS
Cholecystitis is inflammation of the gallbladder, a small organ near the liver that plays a
part in digesting food. It is usually associated with cholelithiasis. Normally, fluid called bile
passes out of the gallbladder on its way to the small intestine. If the flow of bile is blocked, it
builds up inside the gallbladder, causing swelling, pain, and possible infection. Cholecystitis
may be acute or chronic. These conditions usually occur together.[1]
ETIOLOGY AND RISK FACTORS
Cholecystitis occurs when gallbladder becomes inflamed. Gallbladder inflammation can
be caused by gallstones, the result of hard particles that develop in gallbladder from imbalances
in the substances in bile such as cholesterol and bile salts. Gallstones can block the cystic duct,
the tube through which bile flows when it leaves the gallbladder, causing the bile to build up and
resulting in inflammation. Also, it is caused by tumor that may prevent bile from draining out of
the gallbladder properly, causing the buildup that can lead to cholecystitis. Kinking or scarring of
the bile ducts can cause also blockages that lead to cholecystitis.[2]
Risk factors in developing cholecystitis include increasing age, female gender, obesity
and rapid weight loss, using hormonal therapies, pregnancy, having diabetes and being Native
American or Hispanic.[3]
Sometimes the bile duct becomes blocked temporarily. When this occurs repeatedly, it
can lead to chronic cholecystitis. This is swelling and irritation that continues over time.
Eventually, the gallbladder becomes thick and hard. It also does not store and release bile as
well.[4]
PATHOPHYSIOLOGY
The initial event in acute cholecystitis (ACC) is believed to be obstruction to
gallbladder drainage. This causes an increase in intraluminal pressure, gallbladder distention, and
wall edema that may progress to venous and lymphatic obstruction, ischemia, and necrosis. A
number of potential mediators have been identified including cholesterol-supersaturated bile,
lysolecithin,phospholipase A, and prostaglandins. Enhanced production of prostaglandins is

104

Mayo Clinic Health Letter-Online Edition. (2014, August 28). Disease and Conditions: Cholecsytitis. Retrieved March 2015,
from http://www.mayoclinic.org/diseases-conditions/cholecystitis/basics/symptoms/con-20034277.
2
Mayo Foundation for Medical Educationand Research. (2015). Cholecystitis. Retrieved March 2015, from
http://www.mayoclinic.org/diseases-conditions/cholecystitis/basics/symptoms/con-20034277.
3
Udan, J. Medical Surgical: Concepts and Clinical Application (First Edition). Philippines: Guiani Prints House. (2002).
4
Black, J.M., & Hawks, J.H. Medical-Surgical Nursing Clinical Management for Positive Outcomes. Philippines: Elsevier.
(2005).

[Alterations in Metabolic and Endocrine Functions]

believed to play a key role in mediating inflammation, and agents that reduce prostaglandin
production have been shown to block the inflammatory response and reduce the pain of
cholecystitis. Bile is sterile in the early stages of acute cholecystitis and infection is believed to
be a secondary event. Indeed, although ACC is often considered an infection. The organisms
most commonly cultured are enteric bacteria including Escherichia coli, Klebsiella, and
Enterococcus.[5]
Cholelithiasis develops when the balance that keeps cholesterol, bile salts, and calcium
in solution is altered so that precipitation of these substances occurs. Conditions that upset this
balance include infection and disturbances in the metabolism of cholesterol. It is known that in
patients with cholethiasis, the bile secreted by the liver is supersaturated with cholesterol. The
bile in the gallbladder also becomes supersaturated with cholesterol. When bile is supersaturated
with cholesterol, precipitation of cholesterol will occur.[6]
The main symptom is pain in the upper right side or upper middle of your belly that
usually lasts at least 30 minutes. You may feel: Sharp, cramping, or dull pain, steady pain, pain
that spreads to your back or below your right shoulder blade. Other symptoms that may occur
include: clay-colored stools, steatorrhea, fever, nausea and vomiting, yellowing of skin and
whites of the eyes (jaundice), and hronic diarrhea (4 - 10 bowel movements every day for at least
3 months) may be a common symptom of gallbladder dysfunction.[7]

Jaclyn Mae T. Alviola, RN


MSN Student

105

Mayo Clinic Health Letter-Online Edition. (2014, August 28). Disease and Conditions: Cholecsytitis. Retrieved March 2015,
from http://www.mayoclinic.org/diseases-conditions/cholecystitis/basics/symptoms/con-20034277.
6
Black, J.M., & Hawks, J.H. Medical-Surgical Nursing Clinical Management for Positive Outcomes. Philippines: Elsevier.
(2005).
7
Lewis, S. and et.al. Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby Elsevier
Inc. . (2008).

106

[Alterations in Metabolic and Endocrine Functions]

PANCREATITIS

ctors:
e
pertensives, diuretics, antimicrobials, immunosuppresives, oral contraceptives)
ction
a
ridemia
auma

Predisposing factors:
- Genetic/ Family History
- Anatomical variants

Damage to pancreatic cells


Elastase
Inflammation of the parenchyma
Necrosis of blood vessels and ductal fibers
Edema of the pancreas and pancreatic duct
Hemorrhage
Phospholipase A

Fat necrosis
Cell membrane disruption

Activation of pancreatic enzymes inside pancreas


Acute Pancreatitis
Autodigestion of the pancreas

Further inflammation of pancreas

Lipase

Fat Necrosis

Obstruction to the flow of pancreaticChronic


enzymePancreatitis

Kalikrein

Edema
Vascular permeability
Smooth muscle contraction
Vasodilation

Hypoperfusion

Necrosis
Invasion of bacteria
Infected necrotic pancreas or abscess

Peripancreatic exudation or pancreatic ductal


leakage

Pseudocyst

Compresses nearby organs

Constant pain or deep ache in the


abdomen which felt in the back

Realease of toxic metabolites into peritoneal space


Ruptured due to trauma to the sac
Realease of toxic metabolites into blood
Hemorrhage
DEATH

Shock
Pulmonary Insufficiency
Acute renal failure
Dissemenated Intravascular
Coagulation

Hypovolemia

107

Sources:
Fisher, T. & Raton, B. (2015, March 16). MedlinePlus: Pancreatic Pseudocyst. Retrieved March 20, 2015, from
http://www.nlm.nih.gov/medlineplus/ency/article/000272.htm.
Freedman, S. (2013, October).The Merck Manual: Acute Pancreatitis. Retrieved March 2015, from
http://www.merckmanuals.com/professional/gastrointestinal_disorders/pancreatitis/acute_pancreatitis.html.
Gardner, T. (2014, December 8). Medscape: Acute Pancreatitis. Retrieved March 2015, from
http://emedicine.medscape.com/article/181364-overview.
Pancreatitis. (2015). In Encyclopdia Britannica.Retrieved from
http://www.britannica.com/EBchecked/topic/441022/pancreatitis.

108

[Alterations in Metabolic and Endocrine Functions]

PANCREATITIS

Pancreatitis is a disease in which the pancreas becomes inflamed. Pancreatic damage


happens when the digestive enzymes are activated before they are released into the small
intestine and begin attacking the pancreas.[1]
There are two forms of pancreatitis: acute and chronic.
Acute pancreatitis.
Acute pancreatitis is a sudden inflammation that lasts for a short time. It may range from
mild discomfort to a severe, life-threatening illness. Most people with acute pancreatitis recover
completely after getting the right treatment. In severe cases, acute pancreatitis can result in
bleeding into the gland, serious tissue damage, infection, and cyst formation. Severe pancreatitis
can also harm other vital organs such as the heart, lungs, and kidneys.[2]
Chronic pancreatitis.
Chronic pancreatitis is long-lasting inflammation of the pancreas. It most often happens
after an episode of acute pancreatitis. Heavy alcohol drinking is another big cause. Damage to
the pancreas from heavy alcohol use may not cause symptoms for many years, but then the
person may suddenly develop severe pancreatitis symptoms.[3]
ETIOLOGY AND RISK FACTORS
Acute pancreatitis has many causes, such as alcohol abuse, cholelithiasis, abdominal
trauma, virus infection, drugs, and metabolic factors. The mechanisms by which these conditions
trigger pancreatic inflammation have not been identified.[4]
Acute pancreatitis is thought to result from inappropriate intrapancreatic activation of
proteases, which causes autodigestion of the pancreas. Exactly how this occurs is unknown. [5]It is
thought that alcohol-induced pancreatitis may include a physiochemical alteration of protein that
results in plugs that

Pancreatitis. (2015).In Encyclopdia Britannica.Retrieved from


http://www.britannica.com/EBchecked/topic/441022/pancreatitis..
2
Freedman, S. (2013, October).The Merck Manual: Acute Pancreatitis. Retrieved March 2015, from
http://www.merckmanuals.com/professional/gastrointestinal_disorders/pancreatitis/acute_pancreatitis.html.
3
Lewis, S. and et.al. Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby Elsevier
Inc. . (2008).

109

Gardner, T. (2014, December 8). Medscape: Acute Pancreatitis. Retrieved March 2015, from
http://emedicine.medscape.com/article/181364-overview.

110

[Alterations in Metabolic and Endocrine Functions]

block the small pancreatic ductules. Biliary pancreatitis occurs when edema or an obstruction
blocks
the ampulla of Vater, resulting in reflux of bile into pancreatic ducts or direct injury to the acinar
cells.
Other causes include the following: hyperlipidemia, which may occur secondary to nephritis,
castration, or exogenous estrogen administration, or as hereditary hyperlipidemia, hypercalcemia
arising as a result of hyperparathyroidism, cholecystitis and cholelithiasis, familial cases with no
definite mechanism defined, pancreatic tumor, pancreatic trauma or pancreatic duct obstruction,
such as penetrating or blunt external trauma, intraoperative manipulation, or ampullar
manipulation,

and

pancreatic

ductal

overdistention

during

endoscopic

retrograde

cholangiopancreatography (ERCP), pancreatic ischemia during episodes of hypotensive shock,


cardiopulmonary bypass, visceral atheroembolism, or vasculitis, drugs; although azathioprine
and estrogens have been directly linked with the disease, many other drugs are believed to have
an association (e.g., antibiotics, anticonvulsants, thiazide diuretics, sulfonamides, valproic acid),
and ther general causes, such as pancreatic duct obstruction, obesity, duodenal obstruction, viral
infection (e.g., mumps), carcinoma, scorpion venom, ERCP, peritoneal dialysis, and factors still
to be determined.[5]
PATHOPHYSIOLOGY
Pancreatitis occurs when digestive enzymes produced in your pancreas become activated
while inside the pancreas, causing damage to the organ.[6]
During normal digestion, the inactivated pancreatic enzymes move through ducts in your
pancreas and travel to the small intestine, where the enzymes become activated and help with
digestion.[7]

Pancreatitis. (2015).In Encyclopdia Britannica. Retrieved from


http://www.britannica.com/EBchecked/topic/441022/pancreatitis.

111

6
7

Udan, J. (2002).Medical Surgical: Concepts and Clinical Application (First Edition). Philippines: Guiani Prints House.
Ibid

[Alterations in Metabolic and Endocrine Functions]

In pancreatitis, the enzymes become activated while still in the pancreas. This causes the
pancreas to undergo the process of inflammation. It is thought that alcohol increases the
production of digestive enzymes in the pancreas and/or increases the sensitivity to the hormone
cholecystokinin (CKK). CCK stimulates the production of pancreatic enzymes. Other and most
common pathologic mechanism is autodigestion of the pancreas that may lead to further damage
to thepancreas. One possible cause is the reflux of the bile acids into the pancreatic ducts through
an open or distended sphincter of Oddi. This causes the enzymes to irritate the cells of your
pancreas, causing inflammation and the signs and symptoms associated with pancreatitis.[8]
Regardless of the etiology, pancreatic enzymes (including trypsin, phospholipase A2, and
elastase) become activated within the gland itself. The enzymes can damage tissue and activate
the complement system and the inflammatory cascade, producing cytokines. This process causes
inflammation, edema, and sometimes necrosis. In mild pancreatitis, inflammation is confined to
the pancreas. In severe pancreatitis, there is significant inflammation, with necrosis and
hemorrhage of the gland and a systemic inflammatory response. After 5 to 7 days, necrotic
pancreatic tissue may become infected by enteric bacteria.[9]
Activated enzymes and cytokines that enter the peritoneal cavity cause a chemical burn
and third spacing of fluid; those that enter the systemic circulation cause a systemic
inflammatory response that can result in acute respiratory distress syndrome and renal failure.
The systemic effects are mainly the result of increased capillary permeability and decreased
vascular tone, which result from the released cytokines and chemokines. Phospholipase A2 is
thought to injure alveolar membranes of the lungs.[10]
In about 40% of patients, collections of enzyme-rich pancreatic fluid and tissue debris
form in and around the pancreas. In about half, the collections resolve spontaneously. In others,
the collections become infected or form pseudocysts. Pseudocysts have a fibrous capsule without
an epithelial lining. Pseudocysts may hemorrhage, rupture, or become infected.[11]

Pancreatitis. (2015).In Encyclopdia Britannica.Retrieved from


http://www.britannica.com/EBchecked/topic/441022/pancreatitis..
9
Freedman, S. (2013, October).The Merck Manual: Acute Pancreatitis. Retrieved March 2015, from
http://www.merckmanuals.com/professional/gastrointestinal_disorders/pancreatitis/acute_pancreatitis.html.
10
Gardner, T. (2014, December 8). Medscape: Acute Pancreatitis. Retrieved March 2015, from
http://emedicine.medscape.com/article/181364-overview.

112

11

Fisher, T. & Raton, B. (2015, March 16). MedlinePlus: Pancreatic Pseudocyst. Retrieved March 20, 2015, from
http://www.nlm.nih.gov/medlineplus/ency/article/000272.htm.

[Alterations in Metabolic and Endocrine Functions]

With repeated bouts of acute pancreatitis, damage to the pancreas can occur and lead to
chronic pancreatitis. Scar tissue may form in the pancreas, causing loss of function. A poorly
functioning pancreas can cause digestion problems and diabetes.[12]
Signs and symptoms of pancreatitis may vary, depending on which type you experience.
Acute pancreatitis signs and symptoms include: upper abdominal pain, abdominal pain that
radiates to your back Abdominal pain that feels worse after eating, nausea and vomiting,
tenderness when touching the abdomen. Chronic pancreatitis signs and symptoms include: upper
abdominal pain, losing weight without trying, oily, smelly stools (steatorrhea)
The following uncommon physical findings are associated with severe necrotizing
pancreatitis: cullen sign (bluish discoloration around the umbilicus resulting from
hemoperitoneum), Grey-Turner sign (reddish-brown discoloration along the flanks resulting
from retroperitoneal blood dissecting along tissue planes); more commonly patients may have a
ruddy erythema in the flanks secondary to extravasated pancreatic exudates, and erythematous
skin nodules, usually no longer than 1 cm and typically located on extensor skin surfaces;
polyarthritis.[13]
Pancreatitis can cause serious complications, including: Infection. Acute pancreatitis can
make your pancreas vulnerable to bacteria and infection. Pancreatic infections are serious and
require intensive treatment, such as surgery to remove the infected tissue. [14] Pseudocyst. Acute
pancreatitis can cause fluid and debris to collect in cyst-like pockets in your pancreas. A large
pseudocyst that ruptures can cause complications such as internal bleeding and infection, [15]
reathing problems. Acute pancreatitis can cause chemical changes in your body that affect your
lung function, causing the level of oxygen in your blood to fall to dangerously low levels. [16]
Diabetes. Damage to insulin-producing cells in your pancreas from chronic pancreatitis can lead
to diabetes, a disease that affects the way your body uses blood sugar. [17] Kidney failure. Acute
pancreatitis may cause kidney failure, which can be treated with dialysis if the kidney failure is
severe and persistent.[18]

12

Gardner, T. (2015, April 1). Medscape: Acute Pancreatitis. Retrieved April 15, 2015, from
http://emedicine.medscape.com/article/181364-overview.
13
Ibid
14
Ibid
15
Fisher, T. & Raton, B. (2015, March 16). MedlinePlus: Pancreatic Pseudocyst. Retrieved March 20, 2015, from
http://www.nlm.nih.gov/medlineplus/ency/article/000272.htm.

113

16

Freedman, S. (2013, October).The Merck Manual: Acute Pancreatitis. Retrieved March 2015, from
http://www.merckmanuals.com/professional/gastrointestinal_disorders/pancreatitis/acute_pancreatitis.html.
17
Ibid
18
Ibid

Malnutrition. Both acute and chronic pancreatitis can cause your pancreas to produce fewer
of the enzymes that are needed to break down and process nutrients from the food you eat.
This can lead to malnutrition, diarrhea and weight loss, even though you may be eating the
same foods or the same amount of food.[19] Pancreatic cancer. Long-standing inflammation
in your pancreas caused by chronic pancreatitis is a risk factor for developing pancreatic
cancer.[20]

Jaclyn Mae T. Alviola


MSN Student

114

19

Gardner, T. (2014, December 8). Medscape: Acute Pancreatitis. Retrieved March 2015, from
http://emedicine.medscape.com/article/181364-overview.
20
Ibid

115