Liver Cirrhosis: (Alterations in Metabolic and Endocrine Functions)

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

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
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 cor pulmonale, constrictive pericarditis,
and tricuspid insufficiency.[2]
Biliary Atresia
Genetic digestive disorder
Autoimmune hepatitis[3]

http://emedicine.medscape.com/article/185856-overview
2
Elsevier Inc.
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.[1]
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.[2] 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.[3]
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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.[1]
Rarely, some patients with advanced cirrhosis can develop hepatopulmonary syndrome.
These patients can experience difficulty breathing because certain hormones specifically 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.[2]
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.[3]
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.[5]
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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.[1]
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.[2]
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
6

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
resulting from inability of the liver to synthesize albumin.[3] The hypoalbuminemia results in
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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.[1]
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.[2]
Jaclyn Mae T. Alviola, RN
_____________________________________________________________________________
_
1
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Liver Cirrhosis: (Alterations in Metabolic and Endocrine Functions)

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[Alterations in Metabolic and Endocrine Functions]

- Excessive alcohol - LAENNECS CIRRHOSIS

Liver Cell Injury

Activation of Hepatic Stellate cells

Fibrosis/Scarring of the Liver

Obstruction of Blood Flow

Portal Hypertension ( 10mmHg)

Formation of collateral circulation

Splanchnic vascular and Peripheral

Cardiac output decreased

Na+ & Water

[Alterations in Metabolic and Endocrine Functions]

Decreased bile in Gastrointestinal

Release of endothelin-1 and

Nitric oxide secreted causing to

Increased RBC causing insufficient O2 supply and different

Decrease androgen and

Decrease ADH &

[Alterations in Metabolic and Endocrine Functions]

abuse continues, widespread scar formation occurs throughout the liver.

Genetic digestive disorder

[Alterations in Metabolic and Endocrine Functions]

[Alterations in Metabolic and Endocrine Functions]

memory, confusion, or depressed levels of consciousness, asterixis, foul breath, respiratory

[Alterations in Metabolic and Endocrine Functions]

[Alterations in Metabolic and Endocrine Functions]

decreased colloidal oncotic pressure. Another mechanism is hyperaldosteronism which occurs

Jaclyn Mae T. Alviola, RN

[Alterations in Metabolic and Endocrine Functions]

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