Cirrhosis of the Liver

by krzystjl
Last updated 8 years ago

No category
No topic

Toggle fullscreen Print glog
Cirrhosis of the Liver

Cirrhosis of the Liver

*Permanently damage liver cells *Become non-functioning connective scar tissue; *Nodules form irregularly around scarred areas as liver regenerates;*Impedes blood flow --leading to portal hypertension *Liver hard, lumpy & large in early stages; *Later shrinks & is covered with gray connective tissue. *Function becomes impaired as disease progresses= chronic liver failure.

Physiologic Affects:

*interruption in digestion & metabolism*Altered blood coagulation*Fluid & Electrolyte imbalances*Altered ability to metabolize hormones/ detoxify chemicals.


Lannec’s (Alcoholic) Cirrhosis:**Linked to malnutrition; also low chronic chemical poisoning; ingesting heptotoxic drugs such as Tylenol.*necrotic liver cells replaced with scar tissue--progresses to not damaged cells than functioning.*can take 30 yrs or more to develop.

Postnecrotic Cirrhosis:*Damage occurs as a result of infection such as Hepatitis; metabolic liver disease; hepatotoxins; industrial chemicals.

Biliary Cirrhosis:*Scarring occurs around bile ducts usually d/t chronic biliary obstruction and infection; *Inflammatory process destroys small intrahepatic biliary ducts preventing bile from flowing into small intestine. *End result is cirrhosis & liver failure.

Timby, B.K., & Smith, N.E. (2010) Introductory Medical Surgical Nursing, (10th Ed). Philadelphia, PA: Lippincott.


Portal Hypertension:*Blood flow blocked in the portal vein causing a back up into the portal system causing increased pressure (portal hypertension).*Collateral veins become distended- esophagus (varices), rectum (hemorrhoids), & caput medusae (abdominal surface)

Esophageal Varices:*D/T portal hypertension*Veins in the esophagus become distended & dilate. *Very easy to bleed- due to location at the surface of the mucosa*Can be irritated by rough food or chemicals.*High risk for bleeding--can bleed out quickly--is emergent.

Ascites:*Develops d/t PH which leads to hepatorenal syndrome which alters fluid distribution & impedes fluid excretion. Therefore, fluid collects in the peritoneal cavity. *Proteins in the peritoneal cavity draw plasma from circulating blood through osmosis. *Renal response: renin-angiotensin- aldosterone system activates, conserves Na+, adding more fluid retention, ADH suppressed.

Hepatic Encephalopathy:*Ammonia levels increase d/t liver unable to convert it to urea for excretion. *Crosses blood-brain barrier interfering with brain metabolism causing neurological symptoms: confusion, disorientation, memory loss, + Babinski.*Symptoms intensify with consumption of high-protein meal or active GI bleed (digested blood cells) increase ammonia in the intestine.

MANAGEMENT:*Healthy diet, vitamin & nutritional supplements.*Vitamin K*No alcohol consumption*Lactulose to decrease ammonia levels with encephalopathy.*Administer Platelet or packed RBCs PRN*Restrict Sodium & diuretics to control fluid retention. (K+ sparing)*Beta-adrenergic blocker to <BP & <pressure in portal system*Liver Transplant*Soft diet & no aspirin or anything irritating to esophagus.*Antitussives & stool softeners*Sclerotherapy for varices- solidifies varices*Variceal banding *Abd paracentesis*Low-protein diet

Nursing ManagementMonitor vital signs, weight, intake, output, and abdominal girth; Small mealsClient response to drug therapy: Change in mental status; Signs of GI bleedClient teaching: Liver disorder; Support groups; Treatment regimen; Home care




    There are no comments for this Glog.