liver Cirrhosis

Cirrhosis of the LiverPrepared by: Dr. ahlam Said.

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Description

• A chronic, progressive disease of the liver– Extensive parenchymal cell

degeneration– Destruction of parenchymal cells

Description

• Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis

Description

• Normal lobular structure distorted by fibrotic connective tissue

• Lobules are irregular in size and shape with impaired vascular flow

• Insidious, prolonged course

Statistics

• > 50% of liver disease in the US is directly related to alcohol consumption

• Of the estimated 15 million alcoholics in the USA 10-20% have or will develop cirrhosis

Statistics

• Growing number of cases related to chronic hepatitis C

• 4th leading cause of death in people between 35 and 54 years of age

Statistics

• Direct correlation between alcohol consumption in any geographic area and the death rate from cirrhosis in that area

Etiology and Pathophysiology

• Cell necrosis occurs• Destroyed liver cells are replaced by

scar tissue• Normal architecture becomes nodular

Etiology and Pathophysiology• Four types of cirrhosis:

– Alcoholic (Laennec’s) cirrhosis– Postnecrotic cirrhosis– Biliary cirrhosis– Cardiac cirrhosis


• Alcoholic (Laennec’s) Cirrhosis– Associated with alcohol abuse– Preceded by a theoretically reversible

fatty infiltration of the liver cells– Widespread scar formation

Etiology and Pathophysiology• Postnecrotic Cirrhosis

– Complication of toxic or viral hepatitis– Accounts for 20% of the cases of

cirrhosis– Broad bands of scar tissue form within

the liver


• Biliary Cirrhosis – Associated with chronic biliary

obstruction and infection– Accounts for 15% of all cases of

cirrhosis


• Cardiac Cirrhosis – Results from longstanding severe

right-sided heart failure

Manifestations of Liver Cirrhosis

Fig. 42-5

Clinical ManifestationsEarly Manifestations

• Onset usually insidious• GI disturbances:

– Anorexia – Dyspepsia – Flatulence – N-V, change in bowel habits

Clinical ManifestationsEarly Manifestations

• Abdominal pain• Fever• Lassitude• Weight loss• Enlarged liver or spleen

Clinical ManifestationsLate Manifestations

• Two causative mechanisms– Hepatocellular failure– Portal hypertension

Clinical ManifestationsJaundice

• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue

Clinical ManifestationsJaundice

• Intermittent jaundice is characteristic of biliary cirrhosis

• Late stages of cirrhosis the patient will usually be jaundiced

Clinical ManifestationsSkin

• Spider angiomas (telangiectasia, spider nevi)

• Palmar erythema

Clinical Manifestations Endocrine Disturbances

• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

Clinical Manifestations Endocrine Disturbances

• Alteration in hair distribution– Decreased amount of pubic hair– Axillary and pectoral alopecia

Clinical Manifestations Hematologic Disorders

• Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)

Clinical Manifestations Hematologic Disorders

• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

Clinical Manifestations Peripheral Neuropathy

• Dietary deficiencies of thiamine, folic acid, and vitamin B12

Complications

• Portal hypertension and esophageal varices

• Peripheral edema and ascites• Hepatic encephalopathy• Fetor hepaticus

Complications Portal Hypertension

• Characterized by:– Increased venous pressure in portal

circulation– Splenomegaly– Esophageal varices– Systemic hypertension


• Primary mechanism is the increased resistance to blood flow through the liver


Splenomegaly

• Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the splenic vein

Complications Portal Hypertension Esophageal Varices

• Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices

Complications Portal Hypertension Esophageal Varices

• Varices have fragile vessel walls which bleed easily


Internal Hemorrhoids

• Occurs because of the dilation of the mesenteric veins and rectal veins


Caput Medusae

• Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

Complications Peripheral Edema and Ascites

• Ascites:- - Intraperitoneal accumulation of

watery fluid containing small amounts of protein

Complications Peripheral Edema and Ascites

• Factors involved in the pathogenesis of ascites:- Hypoalbuminemia Levels of aldosterone Portal hypertension

Complications Hepatic Encephalopathy

• Liver damage causes blood to enter systemic circulation without liver detoxification

Complications Hepatic Encephalopathy

• Main pathogenic toxin is NH3 although other etiological factors have been identified

• Frequently a terminal complication

Complications Fetor Hepaticus

• Musty, sweetish odor detected on the patient’s breath

• From accumulation of digested by-products

Development of Ascites

Fig. 42-6

Diagnostic Studies

• Liver function tests• Liver biopsy• Liver scan• Liver ultrasound

Diagnostic Studies

• Esophagogastroduodenoscopy• Prothrombin time• Testing of stool for occult blood

Collaborative Care

• Rest• Avoidance of alcohol and anticoagulants• Management of ascites

Collaborative Care

• Prevention and management of esophageal variceal bleeding

• Management of encephalopathy

Collaborative Care Ascites

• High carbohydrate, low protein, low Na+ diet

• Diuretics• Paracentesis

Collaborative Care Ascites

• Peritoneovenous shunt– Provides for continuous reinfusion of

ascitic fluid from the abdomen to the vena cava

Peritoneovenous Shunt

Fig. 42-8

Collaborative Care Esophageal Varices

• Avoid alcohol, aspirin, and irritating foods

• If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)

Collaborative Care Esophageal Varices

• Endoscopic sclerotherapy or ligation• Balloon tamponade• Surgical shunting procedures (e.g.,

portacaval shunt, TIPS)

Sengstaken-Blakemore Tube

Fig. 42-9

Portosystemic Shunts

Fig. 42-11

Collaborative Care Hepatic Encephalopathy

• Goal: reduce NH3 formation– Protein restriction (0-40g/day)– Sterilization of GI tract with antibiotics (e.g.,

neomycin)– lactulose (Cephulac) – traps NH3 in gut– levodopa

Drug Therapy

• There is no specific drug therapy for cirrhosis

• Drugs are used to treat symptoms and complications of advanced liver disease

Nutritional Therapy

• Diet for patient without complications:– High in calories CHO– Moderate to low fat– Amount of protein varies with degree

of liver damage

Nutritional Therapy

• Patient with hepatic encephalopathy– Very low to no-protein diet

• Low sodium diet for patient with ascites and edema

Nursing ManagementNursing Assessment

• Past health history• Medications • Chronic alcoholism• Weight loss

Nursing ManagementNursing Diagnoses

• Imbalanced nutrition: less than body requirements

• Impaired skin integrity• Ineffective breathing pattern• Risk for injury

Nursing ManagementPlanning

• Overall goals:– Relief of discomfort– Minimal to no complications– Return to as normal a lifestyle as

possible

Nursing ManagementNursing Implementation

• Health Promotion– Treat alcoholism– Identify hepatitis early and treat– Identify biliary disease early and treat


• Acute Intervention– Rest– Edema and ascites– Paracentesis– Skin care– Dyspnea– Nutrition


• Acute Intervention– Bleeding problems– Balloon tamponade– Altered body image– Hepatic encephalopathy


• Ambulatory and Home Care– Symptoms of complications– When to seek medical attention– Remission maintenance– Abstinence from alcohol

Nursing ManagementEvaluation

• Maintenance of normal body weight• Maintenance of skin integrity• Effective breathing pattern• No injury• No signs of infection

Health & Medicine

liver Cirrhosis