Cirrhosis Flashcards
Physical exam findings in Cirrhosis
- jaundice
- spider angiomata
- left lobular enlargement
- caput medusae
- ascites
- muscle wasting
- splenomegaly
Laboratory findings in Cirrhosis
- hypoalbuminemia
- prolonged prothrombin time
- hyperbilirubinemia
- portal hypertension/hypersplenism ==> low platelet count
Radiologic findings in Cirrhosis
- nodular liver
- caudate lobe hypertropy
- ascites
- splenomegaly
- venous collaterals
- hepatocellular carcinoma
Mechanism of Portal Hypertension
- static and dynamic causes of increased intrahepatic vascular resistance
- static = structural <== deposition of fibrous tissue + nodule formation
- dynamic = vascular
- NO (vasodilator) decreased @ endothelium ==> further vasoconstriction
- intrahepatic resistance ==> i_ncreased stress @ splachnic_ ==> increase NO ==> vasodilation ==> increased flow into portal system ==> further hypertension
Site of increased resistance in portal hypertension due to cirrhosis
sinusoidal
Hepatic Venous Pressure gradient in sinusoidal portal hypertension
- Wedged hepatic venous pressure (WHVP) = elevated
- Free HPV = normal
- Gradient (HVPG) = elevated
Mechanism of varices formation
- cirrhosis ==> portal hypertension ==> formation of portal-systemic collaterals
- via dilation of coronary and gastric veins
- collaterals = “gastroesophageal varices”
- associations with variceal growth
- Child B/C cirrhosis
- alcoholic etiology
- red wale marks on endoscopy
Characteristics of variceal hemorrhage
- variceal size predicts variceal hemorrhage
- rupture occurs when expanding force exceed max wall tension
- ==> large or small bleeding ==> hematemesis
Tx for varices
- vasoconstrictors e.g. octreotide
- reduce splanchnic flow into liver ==> slight decrease in portal pressure
- venodilators ==> intrahepatic venous dilation ==> slight decrease in portal pressure
- vasoconstrictors + venodilators
- endoscopic therapy (e.g. banding)
- tx for varices ==> cauterized varice but no change in portal pressure
- TIPS/shunt surgery
- connect portion of portal vein ==> hepatic vein ==> sig. decrease in portal pressure
- complications e.g. encephalopathy and liver failure
Mechanism of ascites formation in cirrhosis
- elevated portal pressure ==> increased NO @ splachnic and systemic circulation
- NO ==>
- splanchnic/systemic vasodilation
- decreased effective arterial blood volume
- activation of renin-angiotensin, aldosterone
- sodium & water retention
Dx of ascites due to spontaneous bacterial peritonitis (SBP)
- sx: fever, jaundice, abdominal pain
- atypical presentation: only encephalopathy and/or renal dysfxn
- diagnostic paracentesis shows:
- PMN count > 250/mm3
- positive culture
Dx of ascites due to cirrhosis
- SAAG = serum-ascites albumin gradient
- = serum albumin - ascitic fluid albumin
- reflection of sinusiodal pressure
- correflates w/HVPG
- SAAG >= 1.1 g/dL ==> ascites due to sinusoidal hypertension
- SAAG < 1.1 ==> source is likely peritoneal
- total ascites protein < 2.5 g/dL
- > 2.5 g/dl = heart fail
Mechanism of hepatic encephalopathy
- HE = neuropsychiatric manifestations of cirrhosis of the liver
- portosystemic shungtin + failure te metabolize neurotoxin substances ==> HE
- ammonia ==> crosses BBB ==> up-regulation of astrocytic benzodiazepine (GABA) receptors ==> cortical depression/HE
Precipitating factors for HE
- high protein load
- GI bleeding
- constipation
- infection
- over-diuresis ==> azotemia and hypokalemia
- narcotics/sedatives can contribute
- can occur in TIPS placement
Pre-hepatic causes of portal HTN
portal or splenic vein thrombosis
Pre-sinusoidal causes of portal HTN
schistosomiasis
Post-sinusoidal causes of portal HTN
veno-occlusive disease
Post-hepatic causes of portal HTN
Budd-Chiari syndrome (Hepatic Vein Thrombosis)
Characteristics of MELD score
- = Model for End-Stage Liver Diseasescore.
- estimate the 3-month mortality in patients with cirrhosis
- used to rank patients on the liver transplant list.
- It is derived from total bilirubin, creatinine, and INR (prothrombin time).
