Cirrhosis Flashcards
- Describe how to diagnose cirrhosis based on physical exam, laboratory and radiographic findings.
spider angiomata, palmar erythema, petichiae, purpura, testicular atrophy, splenomegaly, gynecomastia, muscle wasting, edema, white nails, clubbing, caput medusa, jaundice
lab testing (LFT’s) low albumin (due to portal HTN), low platelt counts, prolonged INR, High bilirubin
radiologic testing, unrelated procedure (cholecystectomy
acites, encephalopathy, variceal hemorrhage, nodular
suspect any patient with chronic liver disease
-chronic abnormal aminotransferases and or alk phos
- Describe the mechanism of portal hypertension in cirrhosis and how it leads to varices and ascites formation.
P=RxF
- increase intrahepatic resistance to portal flow
- initial mechanism. the sponge (sinusoidal) of the liver becomes cirrhotic and is more like a brick–>more pressure in the hose—>splenomegaly
- increase in portal venous inflow
- due to splanchnic vasodilation from wall stress and increased NO
as radius gets bigger tension gets bigger on wall
- Recognize the components of the Model for End-Stage Liver Disease (MELD score) and describe its use in ranking patients on the transplant list.
good for patients undergoing TIPS, and just finding risk of dying normal score is 6
- INR
- serum cresatinine
- serum total bilirubin
fulminant hepatic failure has highest priority
Meld score determines priority in cirrhosis
complications of cirrhosis
portal HTN
- ascites
- sponaneous bacterial hemmorhage
- hepatorenal syndrome - variceal hemmorhage
liver insufficiency
- encephalopathy
- jaundice
is liver biopsy neccesary to dx cirrhosis?
no, only if they dont have signs
5 types of portal HTN
pre hepatic-portal vein thrombosis
pre sinusoidal- shistisomiasis
sinusoidal- cirrhosis
post sinusoidal- post siunsoidal obstructive syndrome
- small hepatic veins are obstructed - complication of bone marrow transplant regimen - RUQ pain, ascites, hepatomegaly, jaundice
post hepatic- budd chiari syndrome
what plays a role in regulating intrahepatic resistance?
NO. NO is reduced in cirrhosis
how does splanchnic vasodilation increase portal HTN
portal hypertension increased wall stress on splanchnic vasculature—> NO relaease–> increases portal flow–>increases wall stress on splanchnic vasculture andd so on
ascites and infection will make feedback loop worse
WHVP
shows level of portal HTN
catheter in hepatic vein, and catheter in siunusoid, if there is large differnce then…
in heart failure–> high free hepatic vein pressure
TIPS shunt
bypasses liver portal vein to hepatic vein
reduces pressure, reduces pressure in esophageal veins to get below 12
***octreotide
causes splanchnic vasoconstriction
use for temporary pressure droppage of portal system
common causes of ascites
cirrhosis- 80% peritoneal malignancy Heart Failure peritoneal TB other
Portal HTN-> shear stress-> NO release-> vasodilation-> drops SVR-> RAAS activation–> Na and water retention
ascites workup
look at PMN's protein and albumin levels glucose and LDH--secondary infection amylase--pancreatic ascites cytology -->malignant ascites
diagnostic paracentesis
indications- new onset ascites
- admission to hospital
- signs and symptoms of SBP
- renal dysfunction
- unexplained encephalopathy
contraindications
none
*** serum ascites albumin gradient
serum albumin - ascites albumin
SAAG gradient
value of 1.1 or greater–> high SAAG cirrhosis and HF
value below 1.1–> low SAAG–> malignancy
protein- low in cirrhosis, high in HF
