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CIRRHOSIS AND PORTAL HYPERTENSION
CIRRHOSIS AND PORTAL HYPERTENSIONASDN 228ADULT MED-SURG
I.
 
DEFINITIONA. End stage of chronic liver disease. Progressive, irreversible disorder ,eventually leading to liver failureB.
 
PathophysiologyFunctional liver tissue is destroyed and replaced by fibrous scartissueMetabolic functions of the liver are lostBile statsis occurs due to constrictive bandsBlood does not flow freely through the liver to inferior vena cavaIncreased pressure in portal venous system - congested veins result II.
 
CAUSESA.
 
Alcoholic cirrhosis – most common cause1.
 
Alcohol causes metabolic changes in liver2.
 
Fatty infiltration of hepatocytes3.
 
Inflammatory cells infiltrate the liver causing necrosis, fibrosisand destruction of functional liver tissue4.
 
Liver shrinks and develops a nodular appearance5.
 
Malnutrition commonly accompanies alcoholic cirrhosisB.
 
Billary Cirrhosis1.
 
Obstructed bile damages and destroys liver cells2.
 
Leads to inflammation, fibrosis and formation of regenerative nodulesC.
 
Posthepatic Cirrhosis1.
 
Results from chronic hepatitis B or C or unknown cause2.
 
Liver is shrunken and nodular with cell loss and fibrosis III.
 
SIGNS AND SYMPTOMSA.
 
Early – few symptoms1.
 
Liver is usually enlarged and may be tender2.
 
Dull ach in RUQ3.
 
Weight loss, weakness and anorexia4.
 
Bowel changes with diarrhea or constipationB.
 
Late – related to liver cell failure and portal hypertension1.
 
Malnutrition, muscle wastingImpaired nutrient metabolismImpaired fat absorption2.
 
Bleeding problems/bruisingDecreased clotting factor synthesisIncreased platelet destruction by enlarged spleenImpaired vitamin K absorption and storage3.
 
Ascites/edemaImpaired plasma protein synthesisIncreased pressure in portal venous system4.
 
JaundiceImpaired bilirubin metabolism and excretion
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CIRRHOSIS AND PORTAL HYPERTENSION
5.
 
Neurologic changes/encephalopathyAccumulated metabolic toxinsImpaired ammonia metabolism and excretion
MULTISYSTEM EFFECTS OF CIRRHOSIS
 Neurologic SystemAgitation leading to lethargy, stupor, comaAsterixis (liver flap) flapping tremor of hands whenarms are extendedEndocrine systemGynecomastia in males, possible diabetesRespiratory systemDyspneaCardiovascular systemBounding pulses, pulmonary hypertension,dysrhythmiasHepatic systemSplenomegaly, possible liver cancerGastrointestinal SystemAbdominal pain, anorexia, Nauses, Clay-coloredstools, peptic ulcers, GI bleeding, hemorrhoidsHematologic Systemthrombocytopenia, anemiaReproductive SystemOligomenorrhea (female)(testicular atrophy (male)Integumentary SystemJaundice, erythemai of palsm, spider angioma,decreased body hair, pruritis, ecchymoses, caputmedusae (dilated veins around the umbilicus)Immune Systemleukocytopenia, increased susceptibility to infection IV.
 
COMPLICATIONSA.
 
Portal hypertension1.
 
Normal blood flow returning to the heart from the abdominalorgans collects in the portal veins and travels through the liver2.
 
Pressure increases in the portal vein due to restricted flow3.
 
Collateral channels develop between the portal and systemic veinsthat supply the lower rectum and esophagus and the umbilical veins4.
 
Results in hemorrhoids, esophageal varices and caput medusae (dilatedveins around the umbilicus)B.
 
Splenomegaly1.
 
Spleen enlarges due to portal hypertension and shunting of blood into splenicvein2.
 
Increased destruction of red and white blood cells and platelets3.
 
Leads to anemia, leukopenia and thrombocytopeniaC.
 
Ascites1.
 
Accumulation of fluid in abdominal cavity2.
 
Hypoalbuminemia – low serum albumin levelsD.
 
Esophageal Varices1.
 
Enlarged, thin-walled veins in the esophagus due to portal hypertension2.
 
May bleed, rupture causing massive hemorrhageE.
 
Hepatic Encephalopathy1.
 
Accumulation of neurotoxins in the blood2.
 
Ammonia accumulation – destroys brain cells
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CIRRHOSIS AND PORTAL HYPERTENSION
F.
 
Hepatorenal Syndrome1.
 
Renal failure with azotemia2.
 
Sodium retention, oliguria, hypotension V.
 
TREATMENTA.
 
Medications1.Avoid known hepatotoxic drugs and alcohol (barbiturates, sedatives, hypnotics, and acetaminophen)2. Diuretics – reduce fluid retention and ascitesSpironolactone – lasix3.Reduce nitrogenous load and lower serum ammonia levelsLactulose and neomycin. Reduce the number of ammonia forming organismsin the bowel and ammonium is excreted in the feces4. Lower hepatic venous pressure- prevent rebleeding of esophageal varicesCorgard, Imdur, Monoket5.
 
Ferrous sulfate and folic acid – treat anemia6.
 
Vitamin K – reduce risk of bleeding7.
 
Antacids are prescribed as indicated8.
 
Serax a benzodiazepine antianxiety/sedative drug, not metabolized by liverto treat acute agitationB.
 
Dietary and fluid management1.
 
Sodium intake is restricted to under 2 g/day2.
 
Fluids are limited to 1500mL/day3.
 
Adequate calories 75-100g of protein per day4.
 
With encephalopathy is present, 60-80 g/day5.
 
Vitamins and mineral supplements. Particularly B-complex6.
 
Magnesium deficiency common in alcohol-induced cirrhosis7.
 
TPN (total parenteral nutrition) may be initiated through a Central lineContains carbohydrates high concentration of dextrose), protein, e-lytesvitamins, minerals and fat emulsion.New containers every 24 hours – procedure for checking similar to bloodchecks.Solutions are mixed specifically for patient based on lab valueAlways infused with pumpBlood glucose levels carefully monitored and insulin may be administeredas needed. e-lytes also closely monitored and formula adjusted as neededHigh risk for infection due to disruption of skin barrier and highglucose solution. Monitor closely for S&S of infectionC.
 
Paracentesis1.
 
Aspiration of fluid from peritoneal cavity to relieve respiratory distress2.
 
Moderate withdrawal 500ml to 1L to reduce risk of fluid and electrolyteimbalances3.
 
4-6L of fluid may be done Albumin intravenously during largevolume paracentesis4.
 
Nursing care :Informed consentWeight prior to paracentesisVital signs for baseline
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