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LIVER
CIRRHOSIS
By,
Ms. Ekta S Patel
AP.
Liver cirrhosis
✢ Introduction
✢ It is a chronic disease in which
there has been diffuse destruction
and fibrotic regeneration of hepatic
cells.
Liver cirrhosis
✢ As necrotic tissue is replaced by fibrotic
tissue, normal liver structure and
vasculature is altered , impairing blood
and lymph flow.
✢ It results in hepatic insufficiency and
portal hypertension.
✢ Definition
✢ Cirrhosis of liver is a chronic,
progressive disease characterized
by widespread fibrosis(scarring)
and nodule formation.
✢ The development of cirrhosis is
an insidious, prolonged course,
usually after decades of chronic
liver disease.
✢ Cirrhosis is a consequence of
chronic liver disease,
characterized by replacement of
liver tissue by fibrosis, scar tissue
and regenerative nodules leading
to loss of liver function.
✢ Incidence:
✢ Cirrhosis is the 8th leading
cause of death in United states.
✢ Around 20% of patients with
Chronic HCV and 10%-20% of
patients with chronic HBV
develop cirrhosis.
✢ Classification:
Alcoholic Post nectrotic
Biliary Cardiac
Classification:
Alcoholic Cirrhosis
✢ Laennec’s cirrhosis, micronodular, portal
cirrhosis.
✢ Men are more likely to have alcoholic
cirrhosis.
✢ Fibrosisoccurs mainly around central veins
and portal areas.
✢ It is associated with chronic alcoholic abuse.
✢ Small nodules form as result of some
offending agent.
Post nectrotic
✢ Macronodular cirrhosis toxin-induced
cirrhosis
✢ Most common worldwide form.
✢ Broad bands of scar tissue.
✢ Caused by postacute viral B, C hepatitis,
Postintoxication with industrial chemicals.
✢ More common in women.
Biliary cirrhosis
✢ Scaring around bile ducts and lobes of the
liver.
✢ It results from chronic biliary injury and
obstruction of the intrahepatic or
extrahepatic biliary system.
✢ Primary biliary cirrhosis and Primary
Sclerosing Cholangitis are biliary causes
of cirrhosis.
Cardiogenic
Cirrhosis
✢ It is rare.
✢ It is chronic liver disease associated
with long term severe right sided heart
failure.
✢ It is caused by AV valve disease,
constrictive pericarditis
✢ Etiology and risk factors:
✢ chronic (long-term) viral infections
of the liver (hepatitis types B and
C),
✢ fatty liver associated with obesity
and diabetes,
✢ alcohol abuse.
✢ Primary biliary cirrhosis
✢ Primary Sclerosing Cholangitis
✢ Biliary atresia
✢ Cystic fibrosis
✢ Hemochromatosis (iron overload)
✢ Wilson’s disease (copper diposition)
✢ Budd cherry syndrome. (occlusion of
hepatic vein )
✢ Galactosemia or
glycogen storage disease
(elevated level of galctose)
✢ Autoimmune hepatitis
✢ Medication suchas
methotrexate, acetaminophen.
✢ Alagille syndrome.
✢ Infection such as syphilis
✢ Amyloidosis (deposition of
amyloid protein)
✢ Pathophysiology :
Due to etiological factor
Diffuse destruction and regeneration of liver
cell
Formation of fibrous tissue
Destroyed liver cell are replaced gradually
by scar tissues necrotic tissue yield fibrosis,
cirrhosis damage liver tissue
Obstruction of blood, lymph and bile flow
Hepatic insufficiency
✢ Stages of Liver Damage
Liver cirrhosis
✢ Clinical Manifestation :
✢ EARLY MENIFESTATIONS:
✢ The onset of cirrhosis is insidious.
Early symptom is fatigue.
✢ LATER MENIFESTATIONS:
✢ Later symptom may be severe and result
from liver failure and portal hypertension.
✢ Jaundice, ascites, peripheral edema
develop gradually. Other late symptoms
include skin lesions, hematological
disorders, endocrine disturbances,
peripheral neuropathies etc.
Systemic clinical
manifestation
Liver cirrhosis
Neurological
✢ Hepatic encephalopathy
✢ Peripheral encephalopathy
✢ Asterixis
Liver cirrhosis
GI
✢ Anorexia
✢ Dyspepsia
✢ Nausea, vomiting
✢ Change in bowel habits
✢ Dull abdominal pain
✢ Gastritis
✢ Hematemesis
✢ Fetor hepaticus
✢ Esophageal and gastric verices.
✢ Hemorrhoidal verices
✢ Fetor hepaticus occurs when your breath has a
strong, musty smell.
✢ It’s a sign that your liver is having trouble doing
its job of filtering out toxic substances, usually
due to severe liver disease.
✢ As a result, sulfur substances end up in
your bloodstream and can make their way
to your lungs.
✢ When you exhale, these substances give
your breath a distinct smell.
✢ You might also hear fetor hepaticus
referred to as “breath of the dead.” This is
due to its association with severe liver
disease, which can be fatal.
Reproductive
✢ Amenorrhea( Younger women)
✢ Testicular atrophy
✢ Gynecomastia
✢ Impotence with loss of libido
(sexual desire)
✢ Loss of axillary and pubic hair
✢ Vaginal bleeding( Older women)
Intengumentory
✢ Jaundice
✢ Spider angioma
✢ Palmar erythema
✢ Purpura
✢ Petechiae
✢ Caput medusae
Purpura
✢ Blood spots/ skin hemorrhage
✢ Purple spots due to low
platelets.
Jaundice
Spider Angioma
✢ Also known as
spider nevus.
Common in people
with alcoholic
cirrhosis. It is the
enlarged blood vessel
in skin due to high
estrogen level.
Palmar Erhythema
✢ Also called
liver palms .
Reddening of
both of the
palms due to
excess
estrogen.
caput medusae
✢ These are large
visible distended,
engorged
paraumbilacal veins
due to severe portal
hypertension.
Metabolic
✢ Hypokalemia
✢ Hyponatremia
✢ Hypoalbuminemia
Hematologic
✢ Anemia
✢ Thrombocytopenia
✢ Leukopenia
✢ Coagulation disorders
✢ Splenomegaly
Cardiovascular
✢ Fluid retention
✢ Peripheral edema
✢ Ascites
✢ Diagnostic evaluation :
✢ History collection
✢ Physical examination
✢ Elevatedliver enzymes such as
AST, ALT, GGT, ALP.
✢ Increased serum bilirubin.
✢ Liver ultrasound to assess
the severity of cirrhosis.
✢ Liver biopsy to identify liver
cell changes & alterations in the lobular
structure.
✢ Prolonged prothrombin time (11-12sec)
✢ Complete blood count.
✢ Serum electrolytes.
✢ Esophagogastroduodenoscopy also
known as upper endoscopy.
✢ CT scan
✢ Decreased cholesterol level due to
abnormal fat metabolism.
✢ Paracentesis to examine ascitic fluid for
cell, protein, bacterial counts.
✢ PTC (Percutaneous transhepatic
cholangiography)
✢ Management
✢ Minimize further deterioration of liver
function through the withdrawal of toxic
substances, alcohol, and drugs.
✢ Correction of nutritional deficiencies with
vitamins and nutritional supplements and
a high-calorie and moderate- to high-
protein diet.
✢ Treatment of ascites and fluid and
electrolyte imbalances.
○ Restrict sodium and water intake,
depending on amount of fluid retention.
○ Bed rest to aid in diuresis.
○ Diuretic therapy, frequently with
spironolactone (Aldactone), a potassium-
sparing diuretic that inhibits the action of
aldosterone on the kidneys.
○ Furosemide (Lasix), a loop diuretic, may
also be used in conjunction with
spironolactone to help balance potassium
depletion.
○ Abdominal paracentesis to remove fluid
and relieve symptoms
○ ascitic fluid may be ultrafiltrated and
reinfused through a central venous access.
○ Administration of albumin to maintain
osmotic pressure.
✢ Transjugular intrahepatic portosystemic
shunt (TIPS), an interventional radiologic
procedure, may be performed in patients
whose ascites are resistant to other forms of
treatment. TIPS is a percutaneously created
connection within the liver between the
portal and systemic circulations. A shunt is
placed to reduce the portal pressure in
patients with complications related to portal
hypertension.
Liver cirrhosis
✢ Symptomatic relief measures, such as
pain medication and antiemetics.
✢ Treatment of other problems associated
with liver failure. Administration of
lactulose (Cephulac) or neomycin
(Myciguent) for hepatic encephalopathy.
✢ Orthotopic liver transplantation may be
necessary.
Liver cirrhosis
✢ Complications
✢ Hyponatremia and water retention.
✢ Bleeding esophageal varices.
✢ Coagulopathies.
✢ Spontaneous bacterial peritonitis.
✢ Hepatic encephalopathy, which may
be precipitated by the use of sedatives,
high-protein diet, sepsis, or electrolyte
imbalance.
✢ Nursing Assessment
✢ Obtain history of precipitating factors,
such as alcohol abuse, hepatitis, or biliary
disease. Establish present pattern of
alcohol intake.
✢ Assess mental status through interview
and interaction with the patient.
✢ Perform abdominal examination,
assessing for ascites
✢ Observe for bleeding.
✢ Assess daily weight and
abdominal girth measurements.
✢ Nursing Diagnoses
✢ Activity Intolerance related to fatigue, general
debility, and discomfort
✢ Imbalanced Nutrition: Less Than Body
Requirements related to anorexia and GI
disturbances
✢ Impaired Skin Integrity related to edema,
jaundice, and compromised immunologic
status
✢ Risk for Injury related to altered clotting
mechanisms
✢ Disturbed Thought Processes related to
deterioration of liver function and increased
serum ammonia level

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Liver cirrhosis

  • 4. ✢ It is a chronic disease in which there has been diffuse destruction and fibrotic regeneration of hepatic cells.
  • 6. ✢ As necrotic tissue is replaced by fibrotic tissue, normal liver structure and vasculature is altered , impairing blood and lymph flow. ✢ It results in hepatic insufficiency and portal hypertension.
  • 8. ✢ Cirrhosis of liver is a chronic, progressive disease characterized by widespread fibrosis(scarring) and nodule formation.
  • 9. ✢ The development of cirrhosis is an insidious, prolonged course, usually after decades of chronic liver disease.
  • 10. ✢ Cirrhosis is a consequence of chronic liver disease, characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules leading to loss of liver function.
  • 12. ✢ Cirrhosis is the 8th leading cause of death in United states. ✢ Around 20% of patients with Chronic HCV and 10%-20% of patients with chronic HBV develop cirrhosis.
  • 14. Alcoholic Post nectrotic Biliary Cardiac Classification:
  • 15. Alcoholic Cirrhosis ✢ Laennec’s cirrhosis, micronodular, portal cirrhosis. ✢ Men are more likely to have alcoholic cirrhosis. ✢ Fibrosisoccurs mainly around central veins and portal areas. ✢ It is associated with chronic alcoholic abuse. ✢ Small nodules form as result of some offending agent.
  • 16. Post nectrotic ✢ Macronodular cirrhosis toxin-induced cirrhosis ✢ Most common worldwide form. ✢ Broad bands of scar tissue. ✢ Caused by postacute viral B, C hepatitis, Postintoxication with industrial chemicals. ✢ More common in women.
  • 17. Biliary cirrhosis ✢ Scaring around bile ducts and lobes of the liver. ✢ It results from chronic biliary injury and obstruction of the intrahepatic or extrahepatic biliary system. ✢ Primary biliary cirrhosis and Primary Sclerosing Cholangitis are biliary causes of cirrhosis.
  • 18. Cardiogenic Cirrhosis ✢ It is rare. ✢ It is chronic liver disease associated with long term severe right sided heart failure. ✢ It is caused by AV valve disease, constrictive pericarditis
  • 19. ✢ Etiology and risk factors:
  • 20. ✢ chronic (long-term) viral infections of the liver (hepatitis types B and C), ✢ fatty liver associated with obesity and diabetes, ✢ alcohol abuse.
  • 21. ✢ Primary biliary cirrhosis ✢ Primary Sclerosing Cholangitis ✢ Biliary atresia ✢ Cystic fibrosis ✢ Hemochromatosis (iron overload) ✢ Wilson’s disease (copper diposition) ✢ Budd cherry syndrome. (occlusion of hepatic vein )
  • 22. ✢ Galactosemia or glycogen storage disease (elevated level of galctose) ✢ Autoimmune hepatitis ✢ Medication suchas methotrexate, acetaminophen. ✢ Alagille syndrome. ✢ Infection such as syphilis ✢ Amyloidosis (deposition of amyloid protein)
  • 24. Due to etiological factor Diffuse destruction and regeneration of liver cell Formation of fibrous tissue Destroyed liver cell are replaced gradually by scar tissues necrotic tissue yield fibrosis, cirrhosis damage liver tissue Obstruction of blood, lymph and bile flow Hepatic insufficiency
  • 25. ✢ Stages of Liver Damage
  • 28. ✢ EARLY MENIFESTATIONS: ✢ The onset of cirrhosis is insidious. Early symptom is fatigue.
  • 29. ✢ LATER MENIFESTATIONS: ✢ Later symptom may be severe and result from liver failure and portal hypertension. ✢ Jaundice, ascites, peripheral edema develop gradually. Other late symptoms include skin lesions, hematological disorders, endocrine disturbances, peripheral neuropathies etc.
  • 32. Neurological ✢ Hepatic encephalopathy ✢ Peripheral encephalopathy ✢ Asterixis
  • 34. GI ✢ Anorexia ✢ Dyspepsia ✢ Nausea, vomiting ✢ Change in bowel habits ✢ Dull abdominal pain ✢ Gastritis ✢ Hematemesis ✢ Fetor hepaticus ✢ Esophageal and gastric verices. ✢ Hemorrhoidal verices
  • 35. ✢ Fetor hepaticus occurs when your breath has a strong, musty smell. ✢ It’s a sign that your liver is having trouble doing its job of filtering out toxic substances, usually due to severe liver disease.
  • 36. ✢ As a result, sulfur substances end up in your bloodstream and can make their way to your lungs. ✢ When you exhale, these substances give your breath a distinct smell. ✢ You might also hear fetor hepaticus referred to as “breath of the dead.” This is due to its association with severe liver disease, which can be fatal.
  • 37. Reproductive ✢ Amenorrhea( Younger women) ✢ Testicular atrophy ✢ Gynecomastia ✢ Impotence with loss of libido (sexual desire) ✢ Loss of axillary and pubic hair ✢ Vaginal bleeding( Older women)
  • 38. Intengumentory ✢ Jaundice ✢ Spider angioma ✢ Palmar erythema ✢ Purpura ✢ Petechiae ✢ Caput medusae
  • 39. Purpura ✢ Blood spots/ skin hemorrhage ✢ Purple spots due to low platelets.
  • 41. Spider Angioma ✢ Also known as spider nevus. Common in people with alcoholic cirrhosis. It is the enlarged blood vessel in skin due to high estrogen level.
  • 42. Palmar Erhythema ✢ Also called liver palms . Reddening of both of the palms due to excess estrogen.
  • 43. caput medusae ✢ These are large visible distended, engorged paraumbilacal veins due to severe portal hypertension.
  • 45. Hematologic ✢ Anemia ✢ Thrombocytopenia ✢ Leukopenia ✢ Coagulation disorders ✢ Splenomegaly
  • 46. Cardiovascular ✢ Fluid retention ✢ Peripheral edema ✢ Ascites
  • 48. ✢ History collection ✢ Physical examination ✢ Elevatedliver enzymes such as AST, ALT, GGT, ALP. ✢ Increased serum bilirubin. ✢ Liver ultrasound to assess the severity of cirrhosis. ✢ Liver biopsy to identify liver cell changes & alterations in the lobular structure. ✢ Prolonged prothrombin time (11-12sec)
  • 49. ✢ Complete blood count. ✢ Serum electrolytes. ✢ Esophagogastroduodenoscopy also known as upper endoscopy. ✢ CT scan ✢ Decreased cholesterol level due to abnormal fat metabolism. ✢ Paracentesis to examine ascitic fluid for cell, protein, bacterial counts. ✢ PTC (Percutaneous transhepatic cholangiography)
  • 51. ✢ Minimize further deterioration of liver function through the withdrawal of toxic substances, alcohol, and drugs. ✢ Correction of nutritional deficiencies with vitamins and nutritional supplements and a high-calorie and moderate- to high- protein diet.
  • 52. ✢ Treatment of ascites and fluid and electrolyte imbalances. ○ Restrict sodium and water intake, depending on amount of fluid retention. ○ Bed rest to aid in diuresis. ○ Diuretic therapy, frequently with spironolactone (Aldactone), a potassium- sparing diuretic that inhibits the action of aldosterone on the kidneys.
  • 53. ○ Furosemide (Lasix), a loop diuretic, may also be used in conjunction with spironolactone to help balance potassium depletion. ○ Abdominal paracentesis to remove fluid and relieve symptoms ○ ascitic fluid may be ultrafiltrated and reinfused through a central venous access. ○ Administration of albumin to maintain osmotic pressure.
  • 54. ✢ Transjugular intrahepatic portosystemic shunt (TIPS), an interventional radiologic procedure, may be performed in patients whose ascites are resistant to other forms of treatment. TIPS is a percutaneously created connection within the liver between the portal and systemic circulations. A shunt is placed to reduce the portal pressure in patients with complications related to portal hypertension.
  • 56. ✢ Symptomatic relief measures, such as pain medication and antiemetics. ✢ Treatment of other problems associated with liver failure. Administration of lactulose (Cephulac) or neomycin (Myciguent) for hepatic encephalopathy. ✢ Orthotopic liver transplantation may be necessary.
  • 59. ✢ Hyponatremia and water retention. ✢ Bleeding esophageal varices. ✢ Coagulopathies. ✢ Spontaneous bacterial peritonitis. ✢ Hepatic encephalopathy, which may be precipitated by the use of sedatives, high-protein diet, sepsis, or electrolyte imbalance.
  • 61. ✢ Obtain history of precipitating factors, such as alcohol abuse, hepatitis, or biliary disease. Establish present pattern of alcohol intake. ✢ Assess mental status through interview and interaction with the patient. ✢ Perform abdominal examination, assessing for ascites
  • 62. ✢ Observe for bleeding. ✢ Assess daily weight and abdominal girth measurements.
  • 64. ✢ Activity Intolerance related to fatigue, general debility, and discomfort ✢ Imbalanced Nutrition: Less Than Body Requirements related to anorexia and GI disturbances ✢ Impaired Skin Integrity related to edema, jaundice, and compromised immunologic status ✢ Risk for Injury related to altered clotting mechanisms ✢ Disturbed Thought Processes related to deterioration of liver function and increased serum ammonia level