Cirrhosis Flashcards
Cirrhosis
Normal Lobular structure of the liver is distorted by fibrotic connective tissue. Scarred tissue presses hepatic cells between them.
Lobules are irregular in size and shape with impaired vascular flow
Insidious, prolonged course
Cirrhosis Patho
Some offending agent such as alcohol intake over many years causes cell necrosis
Destroyed liver cells are replaced by scar tissue
Normal architecture becomes nodular
Alcoholic Cirrhosis
Associated with alcohol abuse
Preceded by a potentially reversible fatty infiltration of liver cells
Widespread scar formation
Post-necrotic cirrhosis
Complication of toxic or viral hepatitis
~20% of cases
Broad bands of scar tissue form within liver
Biliary Cirrhosis
Associated with chronic obstruction and infection of bile ducts, bile can’t move well out of liver so it stagnates and causes inflammation
~15% all cases
Cardiac Cirrhosis
Secondary to longstanding severe right sided heart failure
Caused by the transmission of elevated right atrial pressure to the liver via inferior vena cava and hepatic veins
Treatment is often aimed at underlying heart failure
Lab studies
Protein-decreased albumin level
Increased alkaline phosphate, AST/SGOT, ALT/SGPT
Prolonged PT, PTT
Increased total bili
Increased ammonia level (byproduct of protein metabolism which liver processes by turning to urea)
Physical Manifestations of Cirrhosis
Onset usually insidious GI disturbances Anorexia Dyspepsia Flatulence N&V, change in bowel habits Abdominal pain Fever Weight loss Enlarged liver or spleen
Hematologic Manifestations of Cirrhosis
Jaundice: occurs because insiffucient conjugation of bili by the liver cells and local obstruction of biliary ducts by scarring and regenerating tissue
Hematologic disorders (blood cells don’t form quite right)
Bleeding tendencies as result of decreased production of clotting factors
Anemia, leukopenia, thrombocytopenia resulting from enlarged spleen
Dietary deficiencies of thiamine, folic acid, B12
Portal HTN
Peripheral edema and Ascites: intraperitoneal accumulation of watery fluid containing small amounts of protein
Due to hypoalbumenia, elevated aldosterone and ADH, and portal HTN
Portal Hypertension
Primary mechanism is the increased resistance to blood flow through the liver
Characterized by: splenomegaly, esophageal varices, increased venous pressure in the portal circulation, systemic HTN, Caput Medusae: collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus
Splenomegaly
back pressure caused by portal HTN 🡪 chronic passive congestion as a result of increased pressure in the splenic vein
Esophageal varices
blood flow backs up through portal system resulting in dilation and enlargement of plexus veins of esophagus and produces varices; can impair swallowing and are susceptible to bleeding
Management of Esophageal Varices
Avoid alcohol, aspirin, and irritating food
Control coughing
Non-selective beta blockers to reduce risk of bleeding
If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)
Prepare Pt with Esophageal Varices For:
Endoscopic sclerotherapy or ligation
Balloon tamponade – used when patient is bleeding
Shunting procedures (portacaval shunt, TIPS)
Tips – Transjugular Intrahepatic Portosystemic Shunt: tunnel through the liver connect portal vein to one of the hepatic veins to decrease pressure and in 90% of cases reduces variceal bleeding
Sengstaken-Blakemore tube
Hepatic Encephalopathy
Liver damage cause blood to enter the systemic circulation without liver detox
Main pathogenic toxin is Ammonia (NH3) although other etiologic factors have been identified
Frequently results in coma and death
