Exam 4 Flashcards by Kelly Cecil

unconjugated/free/indirect bilirubin

traveling in the blood - not in liver yet

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direct/conjugated bilirubin

in the liver

excreted as part of bile

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Jaundice

d/t elevated bilirubin in the blood

1.2 normal level of bilirubin

2.5-3 = jaundice

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hemolytic/pre-hepatic jaundice

unconjugated bilirubin traveling to the liver

reasons occur BEFORE the liver - it’s no really liver disease

an increase destruction of RBCs - too much for the liver to handle

causes:

hemolytic anemia

autoimmune or tranfusion hemolysis

hemolytic processes caused by sickle cell diease or thalassemia

septicemia

newborns

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lab test for pre-hepatic jaundice results

total bilirubin is elevated

increase in indirect/unconjugated bilirubin

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heptocellula or intrahepatic jaundice

problem within the liver - liver disease

cirrohsis, hepatitis, cancer, durgs

liver is either unable to:

take in the increased bilirubin from the blood OR

in unable to conjugated or excrete the bilirubin once it enters the liver

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intrahepatic jaundice lab test

increase in total bilirubin

increase in direct bilirubin

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post-hepatic or obstruction jaundice

liver is okay, there is some obstruction of bile flow to gallbladder

ex. cholelithiasis, bilary tract tumors, cancer of gall bladder, pancreatitis

will cause clay/light colored stool

bilirubin cannot leave the liver

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post hepatic lab tests

increased total bilirubin

increase in direct bilirubin

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clinical manifestation of jaundice

will depend on underlying cause

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collaborative care of jaundice

treate causes and complications

hematlytic anemia - administer iron or blood transfusions

cirrhosis

gall stones - cholecystectomy

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Cirrhosis etiology

alcholic, biliary, post-hepatic

connective tissue forms conective bands that disrupt blood and bile flow

restrictive blood flow causes portal hypertension

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alcoholic cirrhosis

alcohol causes metabolic changes

inflammatory cells infiltrate liver and cause:

necrosis
fibrosis
destruction of functional liver tissue

final stage: nodules form on liver

triglyceride and fatt acid synthesis increases - fatty liver

MAY be reversable if ETOH consmption stops before fibrosis

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Post Hepatic cirrhosis

advanced and progressive liver disease D/T:

chronic HEP B or C

ischemic hepatitis from R sided heart failure

from unknown causes

liver size shrinks and becomes nodular with fibrosis and loss of liver cells

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biliary cirrhosis

d/t chronic bile flow obstruction

stones, tumor, infection

retained bile damages and destroys liver cells causing: inflamation, fibrosis, formation of nodules

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risk factors for cirrhosis

excessive alcohol

IV drug use

clinical manifestations cirrhosis

early: mild to none

enlarged or tender liver

dull, aching pain in RUQ

weight loss

weakness

anorexia

bowel function diruption: diarrhea or constipation

Other conditions caused by cirrhosis include

portal HTN

splenomegaly

ascites

esophogeal varices

encephalopathy

portal HTN

normal pressure 5-10 mMHG

scar tissue blocks blood flow - blood is redirected to lower pressure veins so blood from pancreas, spleen, intestines, stomach that usually drain to the portal vein reroute to:

esophagus
rectum
abdomen

clinical manifestations of portal HTN

veins become congested and engorged with blood

ascites

GI bleeding

esophagus varices

abdoment pain, anorexia, nausea

hemorrhoids

splenomegaly

d/t portal HTN

d/t backup of blood to splenic vein

enlarged spleen

increase rate of blood removal:

anemia, leukopenia, thrombocytopenia

ascites

d/t portal htn

increased hydrostatic pressure in protal venous system

deceased serum protein & albumin holds fluid

increase in aldosterone secretion - hypovolemia and retaining fluid

fluid builds up and leaks into abdominal tissue

esophogeal varices

d/t portal HTN

veins dilate and weaken in the esophagus D/T backed up pressure from portal vein

very susceptible to bleeding - medical emergency

thrombocytepenia puts pt at risk of hemorrhage

physical assessment of cirrhosis of the liver

malnourised

ascites

color - icteric *yellow)

enlarged liver

percuss hepatomegaly

ascites- fluid shifts with positioning, measure abdominal girth, ewight gain, abdomen becomes fibrotic

additional manifestations of cirrhosis

imparied clotting factors - bleeding increased pressure in protal veins - varices enlarged veins in GI tract - gastritis, esophagitis, anorexia, diarrhea impaired metaboism - malnutrition, muscle wasting accumulating toxins - asterixis (flapping of hands) encephalopathy

hepatic encephalopathy

d/t increased ammonia levels in blood from cerebral edema mild confusion to deep coma, anxiety, restlessness, euphoria, irritability, agitation, slurred speech, personality changes asterixis - muscle termors "liver flap" paraesthesia leading cause of death from end stage liver disease: cerebral eema, cerebral hypoxis

heptatorenal sydnrome

cause unclear renal failure w/ azotemia sodium retention oliguria hypotension d/t inadequate blood flow to the kidney (prerenal) in patient with advanced cirrosis

labs for liver disease

LFT (ALT/AST) - elevation may not correlate with extent of liver disease alanine aminotransferase aspartate aminotransferase elevated AST/ALT bilirubin (total, direct, indirect) amonia levels elevated d/t liver cannot convert ammonia to urea serum protein - albumin - low low electrolytes, serum cholestrol and glucose low, clotting fators prolonged, CBC platelet decrease

diagnostic liver disease

hepatobiary US, CT, MRI nuclear imaging EGC liver biopsy

treatment of ascites

paracentesis, diruetics, albumin to increase osmotic pressure, TIPS (shunt)

esophageal varices treatment

beta blockers - nadolol ocrtretide acetate - sandostratin IV to reduce bleeding ant prtal HTN esophogogastroduodenoscopy - banding, scleorsing balloon temponade - stop bleeding

bleeding, bruising treatment

ferrous sulfate, folic acid vitamin K platelets, FFP, PRBC

gastritis, anorexia, diarrhea treatment

stop alcohol nutritional therapy protein restrictions in acute pareteneral nutrition

nutritional therapy cirrhosis

restrict sodium and fluids reduce ascities protein - 60-80 g daily if ammonia levels re elevated must trestrict protein

impaired ammonia treatemtn

lactulose, neomycin side effects: bloating, discomfort, several soft stools ,flatulence metabolic acidosis

hepatic failure

medical emergency. diagnostics: LFT, coag studies

medications for cirrhosis and liver failure

lower hepatic venous pressure: betablockers (nadolol), nitrate (isosobide) treat anemia (ferrous sulfate, folic acid) reduce r/o bleeding (vitamin K, FFP or platelets, bleeding precautions) RBCs antianxiety - oxazepam

liver transplant

contraindiciations: malignancy alcohol use high surgical risk MODS