AI generated- Hepatic Portal hypertension, ascites, coagulopathy Flashcards
What is portal hypertension, and how is it classified?
○ PH occurs when blood flow through the liver is obstructed, leading to
increased pressure in the portal vein.
○ Classified as pre-hepatic, hepatic (pre-sinusoidal, sinusoidal, post-
sinusoidal), or post-hepatic.
What causes sinusoidal portal hypertension?
○ the most Common form of PH in inflammatory/fibrotic hepatopathies.
○ Caused by changes to sinusoidal endothelium, leading to imbalance of
vasodilatory and vasoconstrictive substance ( endothelin 1, Ag II)
What happens to splanchnic arteries in portal hypertension?
Splanchnic arteries dilate due to local release of vasodilators,
increasing portal and splanchnic flow and exacerbating portal
hypertension.
What leads to the development of ascites in PH?
Caused by increased hydrostatic pressure from PH and/or decreased
oncotic pressure from hypoalbuminemia.
What does the presence of ascites indicate in liver disease?
In both chronic and acute liver disease, ascites presence is a poor
prognostic indicator.
How does RAAS contribute to intrahepatic portal hypertension and
ascites?
○ Activation of RAAS increases renin and aldosterone levels, contributing
to PH pathophysiology.
○ Suggests spironolactone can treat ascites and suppress intrahepatic
PH.
: Is there benefit in managing portal hypertension before overt clinical signs
in dogs or cats?
No information on benefits of managing PH prior to overt clinical signs.
but should consider as spironolactone experimentally mitigate hepatic
fibrosis and sinusoidal capillarization. Also, renin and aldosterone from
the activation of RAAS contribute to the pathophysiology of PH.
Q: How are diuretics used in managing portal hypertension and ascites?
○ Spironolactone counters RAAS effects, requiring 1-2 weeks for full
effect.
○ Furosemide may be added if response to spironolactone is insufficient,
or too slow.
○ Goal: reduce body weight by 0.5-1.5% per day.
What is done for refractory ascites with abdominal tension?
Therapeutic drainage combined with diuretic use can provide relief.
What additional benefits does spironolactone have in PH management?
○ Besides countering RAAS effects, experimentally shown to mitigate
hepatic fibrosis and sinusoidal capillarization.
How do vasodilators affect portal hypertension?
○ Local release of vasodilators in splanchnic arteries increases flow,
exacerbating hypertension.
How do liver diseases affect portal hypertension?
Alter hepatic resistance and capacitance, leading to types of PH
depending on the location of obstruction.
What role do angiogenic mediators play in portal hypertension?
Vascular endothelial growth factor opens and develops acquired
portosystemic shunts (aPSSs), allowing portal blood to enter the
systemic circulation directly.
Why might spironolactone be used early in the disease process before
ascites develops?
○ To prevent worsening of PH by mitigating hepatic fibrosis and
sinusoidal capillarization. and decrease renin and aldosterone that play
a role in the pathophysiology of PH
How do RAAS and ADH activation contribute to ascites development?
Lead to the expansion of the systemic blood volume, contributing to
increased hydrostatic pressure and ascites.
What role do hepatocytes play in coagulation?
○ Synthesize nearly all pro- and anticoagulants, compounds that
promote/inhibit fibrinolysis, and are responsible for vitamin K-
dependent activation of coagulation factors II, VII, IX, and X.
How is vitamin K related to coagulation?
○ Necessary for the activation of coagulation factors II, VII, IX, and X; its
uptake depends on bile production.
Which coagulation factors and proteins are synthesized by the liver?
Procoagulants include Fibrinogen, Prothrombin, Factors V, VII, VIII, IX,
X, XI, XII, XIII, and Thrombopoietin.
○ Anticoagulants include Protein C, Protein S, Tissue Factor pathway
inhibitor, and Antithrombin.
What is the risk of coagulopathy in cirrhosis?
People with cirrhosis have a higher risk of thrombosis than
hemorrhage, which may be true for hepatic fibrotic disease in dogs and
cats. Splanchnic thrombosis is increasingly recognized with advanced
imaging (CT) . 42% of the dogs with PV thrombosis have hepathopathy
What are the risks associated with hepatic biopsy in dogs?
○ A study found 42% of dogs had a significant decrease in PCV post-
biopsy, but only 2 required intervention.
How does coagulopathy present in acute versus chronic hepatopathies?
Acute: might show mild/moderate decreased PLT, increased PT/PTT,
decreased fibrinogen, AT, and Protein C, with TEG indicating normal to
hypo/hyperfibrinolytic states.
○ Chronic: similar platelet trends, with potential thrombosis risk,
especially noted in dogs with chronic liver disease (CLD).
What criteria indicate a high risk for bleeding in dogs with chronic
hepatitis?
Platelets <50K, PT or aPTT >1.5 times upper limit, Fibrinogen <
100mg/dL, vWF activity <50%, BMBT > 5min, PCV < 30.
How is active bleeding treated in liver disease?
Administering a wide variety of factors recommended, including FFP
and Cryoprecipitate, due to nonspecific coagulation abnormalities.
What is the approach to treating hypercoagulable states in liver disease?
○ No evidence that prior treatment mitigates or prevents thrombosis; drug
pharmacokinetics in hepatic failure are unpredictable. prophylaxis is
not recommended
At what bilirubin levels does jaundice become detectable in separated
plasma, sclera, and mucosa?
○ Plasma at >1 mg/dL, sclera at >1.5 mg/dL, and mucosa at >2.0-2.5
mg/dL.
What is bilirubin encephalopathy, and how does it occur?
○ High levels of unconjugated bilirubin can cross the blood-brain barrier,
accumulate in the basal ganglia, causing neurological signs similar to
HE.
What is the functional role of bilirubin?
Bilirubin is not just a waste product; it acts as a functional compound
with hormonal activities.
