Flashcards in Portal HTN Deck (32)
How do patients with obstruction or biliary disease usually initially present as opposed to patients with parenchymal disease?
pruritis or jaundice
complication of portal HTN
What pressures are considered abnormal and portal hypertension?
portal or splenic pressures >15 mm Hg or portal pressure >5 mm above IVC pressure
How does blood exit the liver?
hepatic veins to IVC to right atrium
no valves - portal venous pressure approximates systemic venous pressure
Where are the major components of resistance to portal blood flow that cause portal HTN?
pre-capillary or pre-sinusoidal
virtually no resistance through sinusoids
What are the three main types of portal HTN?
post-hepatic (hepatic vein)
intra-hepatic - post-sinusoidal, sinusoidal, pre-sinusoidal
pre-hepatic (portal vein)
What are causes of post-hepatic portal HTN?
What are intra-hepatic causes of portal HTN?
post-sinusoidal: veno-occlusive dz (thrombosis)
sinusoidal: alcoholic cirrhosis (pericellular fibrosis)
pre-sinusoidal: schisto (granulomas)
What are pre-hepatic causes of portal HTN?
splenic vein thrombosis
portal vein thrombosis
What are the complications of portal HTN?
Which types of portal HTN have varices as a complication?
pre-hepatic or intra-hepatic
What is the relative frequency of hemorrhage with different sites of collaterals?
Umbilical: not seen
retroperitoneal: very rare
What findings can congestive splenomegaly be associated with?
decreased RBC survival (splenic hemolysis)
What are some signs and symptoms of someone with ruptured gastro-esophageal varices?
What is the threshold in most patients for variceal hemorrhage?
portal vein-IVC pressure gradient >12
What can be done to treat variceal hemorrhage at the time of diagnosis?
band ligation during endoscopy
How does sinusoidal portal HTN cause ascites?
leads to increased levels of extra-hepatic NO causing vasodilation including splanchnics --> increases portal blood flow further increasing portal pressures
vasodilation --> decreased EABV --> renal compensation --> increased hydrostatic pressure in splanchnic capillaries --> fluid flow to interstitial space
What are the two major forces contributing to portal hypertensive ascites?
increased capillary hydrostatic pressure from systemic or portal venous HTN
decreased capillary oncotic pressure from hypoalbuminemia
What are the two sources of ascitic fluid?
What is the non-portal way of getting ascites?
peritonitis - intra-abdominal inf or ascitic fluid from portal HTN getting inf
What is spontaneous bacterial peritonitis (SBP) as opposed to secondary peritonitis?
secondary has source of direct spread like perf or abscess
What types of patients more likely get SBP?
pts with low ascitic protein levels (total usually <2.5) - inadequate opsonization
Which types of patients present with ascites and which don't?
sinusoidal or post sinusoidal (inc post hepatic) obstruction of portal blood flow do
pre-sinusoidal rarely develop
What circulatory changes are seen in a patient with ascites?
hyperdynamic systemic circulation - decreased peripheral vascular resistance, increased CO, diminished mean arterial pressure
How do ascitic protein levels help determine cause of ascites?
post-sinusoidal (RHF) - high >2.5
secondary to cirrhosis - low 2.5
nephrosis - low <2.5
How can the serum-ascites albumin gradient differentiate between etiologies of ascites?
portal HTN - >1.1 difference
other causes <= 1.1 difference
What are portal hypertensive causes of ascites?
hepatic vein thrombosis
What are non-portal hypertensive causes of ascites?
pancreatic duct extravasation
What is the management of portal hypertensive ascites?
dietary sodium restriction (<4 g/d)
diuretic therapy (aldo antagonists - spironolactone)
possibly thiazide or furosemide
What is the management of diuretic resistance ascites?
What is the pathogenesis of hepatic encephalopathy due to portal HTN and shunting?
shunt causes decreased hepatic metabolism and clearance of ammonia
portal collaterals bypass liver completely
What are precipitants of hepatic encephalopathy?
(GI) bleeding, inf, fluid or electrolyte abnormalities (excess dietary protein and hypokalemic alkalosis)
not seen first in those who've had therapeutic shunts created