Exam 4 Flashcards

1
Q

unconjugated/free/indirect bilirubin

A

traveling in the blood - not in liver yet

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2
Q

direct/conjugated bilirubin

A

in the liver

excreted as part of bile

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3
Q

Jaundice

A

d/t elevated bilirubin in the blood

1.2 normal level of bilirubin

2.5-3 = jaundice

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4
Q

hemolytic/pre-hepatic jaundice

A

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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5
Q

lab test for pre-hepatic jaundice results

A

total bilirubin is elevated

increase in indirect/unconjugated bilirubin

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6
Q

heptocellula or intrahepatic jaundice

A

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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7
Q

intrahepatic jaundice lab test

A

increase in total bilirubin

increase in direct bilirubin

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8
Q

post-hepatic or obstruction jaundice

A

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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9
Q

post hepatic lab tests

A

increased total bilirubin

increase in direct bilirubin

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10
Q

clinical manifestation of jaundice

A

will depend on underlying cause

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11
Q

collaborative care of jaundice

A

treate causes and complications

hematlytic anemia - administer iron or blood transfusions

cirrhosis

gall stones - cholecystectomy

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12
Q

Cirrhosis etiology

A

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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13
Q

alcoholic cirrhosis

A

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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14
Q

Post Hepatic cirrhosis

A

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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15
Q

biliary cirrhosis

A

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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16
Q

risk factors for cirrhosis

A

excessive alcohol

IV drug use

17
Q

clinical manifestations cirrhosis

A

early: mild to none

enlarged or tender liver

dull, aching pain in RUQ

weight loss

weakness

anorexia

bowel function diruption: diarrhea or constipation

18
Q

Other conditions caused by cirrhosis include

A

portal HTN

splenomegaly

ascites

esophogeal varices

encephalopathy

19
Q

portal HTN

A

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

20
Q

clinical manifestations of portal HTN

A

veins become congested and engorged with blood

ascites

GI bleeding

esophagus varices

abdoment pain, anorexia, nausea

hemorrhoids

21
Q

splenomegaly

A

d/t portal HTN

d/t backup of blood to splenic vein

enlarged spleen

increase rate of blood removal:

anemia, leukopenia, thrombocytopenia

22
Q

ascites

A

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

23
Q

esophogeal varices

A

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

24
Q

physical assessment of cirrhosis of the liver

A

malnourised

ascites

color - icteric *yellow)

enlarged liver

percuss hepatomegaly

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

25
Q

additional manifestations of cirrhosis

A

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

26
Q

hepatic encephalopathy

A

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

27
Q

heptatorenal sydnrome

A

cause unclear

renal failure w/ azotemia
sodium retention
oliguria
hypotension

d/t inadequate blood flow to the kidney (prerenal) in patient with advanced cirrosis

28
Q

labs for liver disease

A

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

29
Q

diagnostic liver disease

A

hepatobiary US, CT, MRI

nuclear imaging

EGC

liver biopsy

30
Q

treatment of ascites

A

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

31
Q

esophageal varices treatment

A

beta blockers - nadolol
ocrtretide acetate - sandostratin IV to reduce bleeding ant prtal HTN

esophogogastroduodenoscopy - banding, scleorsing

balloon temponade - stop bleeding

32
Q

bleeding, bruising treatment

A

ferrous sulfate, folic acid

vitamin K

platelets, FFP, PRBC

33
Q

gastritis, anorexia, diarrhea treatment

A

stop alcohol

nutritional therapy

protein restrictions in acute

pareteneral nutrition

34
Q

nutritional therapy cirrhosis

A

restrict sodium and fluids

reduce ascities

protein - 60-80 g daily

if ammonia levels re elevated must trestrict protein

35
Q

impaired ammonia treatemtn

A

lactulose, neomycin

side effects: bloating, discomfort, several soft stools ,flatulence

metabolic acidosis

36
Q

hepatic failure

A

medical emergency.

diagnostics: LFT, coag studies

37
Q

medications for cirrhosis and liver failure

A

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

38
Q

liver transplant

A

contraindiciations:

malignancy
alcohol use
high surgical risk
MODS