LIVER CIRRHOSIS

[Alterations in Metabolic and Endocrine Functions]LIVER CIRRHOSIS

Precipitating Factors:Predisposing Factor:

- Excessive alcohol - LAENNECS CIRRHOSIS - Biliary Atresia- Complication of viral, toxic / idiopathic hepatitis - Genetic digestive disorder- POSTNECROTIC CIRRHOSIS- Chronic biliary obstruction and infection - BILIARY CIRRHOSIS - Autoimmune hepatitis- Severe right-sided heart failure

PainLiver Cell Injury

Increased WBCs

FeverFatigueInflammation

Nausea & VomitingActivation of Hepatic Stellate cellsAnorexia

Expansion of Myofibroblasts-Pool

Fibrosis/Scarring of the Liver

Obstruction of Blood FlowIncreased pressure in the venous and sinusoidal channels

Portal Hypertension ( 10mmHg)

Increased circulating bilirubinSplanchnic vascular and Peripheral arterial vasodilationFormation of collateral circulation

Caput medusae

pressure to nearest susceptible organ/sorgans

Jaundice

Hemorrhoids

Esophageal varices

Hypersplenism

Splanchnic Lymph production

LeukopeniaAnemiaThrombocytopenia

Prolonged bleeding infectionweakness

Hepatorenal Syndrome

Effective blood volume decreased

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

Cardiac output decreased

SNS

Renal Arterial Vasoconstriction

Renal blood flowADH

Na+ & WaterRetention

Ascites formationRAAS

A BSOURCES:

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 B

Activation of vasoconstrictorsArterial underfilling

Release of endothelin-1 and combines to capillary cells

Decreased bile in Gastrointestinal tract and increase urobilinogen

Clay-colored stools and dark urineNitric oxide secreted causing to vasodilate and increased blood flow

Increased RBC causing insufficient O2 supply and different pressure d/t different pressure in capillary and alveolus

Hepatic Pulmonary Syndrome

*Exhaustion*Fatigue

Decrease ADH & aldosterone detoxificationDecrease androgen and estrogen detoxificationDecrease metabolism of protein and carbohydratesDecreased emulsification of fatsPoor Vitamin K absorption

Edema* Palmar erythema* Testicular atrophy* Gynecomastia* Spider Angiomas* Loss of body hair* Menstrual changesHypoglycemiaMalnutritionOsmotic pressureBleeding tendencies

Inability to metabolize ammonia to urea

Ascites

Ammonia levels in the bloodBacterial Peritonitis

SepsisBrain edemaAstrocyte swelling Neurotransmitter and receptor alterationAltered brain glucose metabolism

Hepatic Encephalopathy

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

DeathHepatic Coma

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.

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]

1Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from http://emedicine.medscape.com/article/185856-overview 2Udan, J. (2002). Medical Surgical: Concepts and Clinical Application (First Edition). Philippines: Guiani Prints House.3Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby Elsevier Inc.

PATHOPHYSIOLOGYIn 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 calledportal 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 manyof 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]

1Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby Elsevier Inc.2Mayo Foundation for Medical Education and Research. (2015). Cirrhosis. Retrieved March 2015, from http://www.mayoclinic.org/diseases-conditions/cirrhosis/basics/causes/con-20031617.3Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from http://emedicine.medscape.com/article/185856-overview.

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 thatnot 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]

1Gressner, 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/573027.2Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby Elsevier Inc.3Mayo Foundation for Medical Education and Research. (2015). Cirrhosis. Retrieved March 2015, from http://www.mayoclinic.org/diseases-conditions/cirrhosis/basics/causes/con-20031617.4Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from http://emedicine.medscape.com/article/185856-overview.

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. Thisaccumulation 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 resulting from inability of the liver to synthesize albumin.[3] The hypoalbuminemia results in

1Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from http://emedicine.medscape.com/article/185856-overview.2Gressner, 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/573027.3Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby Elsevier Inc.

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

______________________________________________________________________________1Lewis, S. and et.al. (2008). Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby Elsevier Inc.2Wolf, D. (2014, December 10). Medscape: Cirrhosis. Retrieved March 2015, from http://emedicine.medscape.com/article/185856-overview.

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