Liver Document - Sequelae of liver disease

What is normal portal vein pressure in dogs and cats?

5–7 mmHg — similar to right atrial pressure.

Define portal hypertension.

Increased pressure within the portal venous system due to prehepatic, intrahepatic, or posthepatic obstruction.

Which forms of portal hypertension lead to acquired portosystemic shunts?

Pre-hepatic and intra-hepatic causes (not post-hepatic).

Why don’t post-hepatic causes create collateral vessels?

Because both portal and systemic venous pressures are elevated and equilibrated — no pressure gradient.

What are the major clinical signs of portal hypertension?

Ascites, hepatic encephalopathy, gastric ulceration, acquired shunts, and sometimes GI bleeding.

What secondary change can portal hypertension cause in the intestine?

Ischemic necrosis, ulceration, and hemorrhage — worsening hepatic encephalopathy.

What is the difference between transudate and modified transudate in hepatic effusions?

Transudate = low protein (<2.5 g/dL);

Modified = mild increase due to sinusoidal leakage (fenestrated endothelium).

What type of effusion is typical of post-hepatic portal hypertension?

Low-protein effusion if acute; vessels have tight endothelium, limiting leakage.

What can exacerbate ascites in liver disease?

Concurrent hypoalbuminemia — reduces oncotic pressure.

What are pre-hepatic causes of portal hypertension?

Portal vein thrombosis, congenital atresia/stenosis, invasive neoplasia, fibrosis/stricture, A-V fistula, cyst, abscess, post-shunt ligation.

What are intra-hepatic pre-sinusoidal causes?

Portal vein hypoplasia, congenital hepatic fibrosis, Carolis’ disease, hepatic flukes.

What are intra-hepatic sinusoidal causes?

Chronic hepatitis and cirrhosis.

What are post-sinusoidal causes?

Veno-occlusive disease (hepatic venule fibrosis or thrombosis).

What are post-hepatic causes of portal hypertension?

 Right-sided heart failure, pericardial disease, pulmonary hypertension, Budd-Chiari syndrome.

How is portal hypertension measured directly?

Catheterization of the portal vein (rare in clinical practice).

How is portal hypertension suspected clinically?

Signs of liver disease + ascites ± encephalopathy ± gastric ulceration ± collateral vessels on imaging.

What ultrasound findings suggest PH?

Low-velocity or reversed portal blood flow and a portal vein-to-aorta ratio > 0.65 with no congenital shunt.

What is the prognostic implication of ascites in chronic liver disease?

Negative prognostic factor in cirrhosis and chronic hepatitis, but not necessarily in non-cirrhotic PH or PHPV.

Why can portal hypertension cause gastric ulceration?

Due to intestinal mucosal ischemia and necrosis from elevated venous pressure.

In chronic hepatitsi , inflammation → __ → __ → __ → __

fibrosis → increased vascular resistance → PH → ascites + shunts

Define hepatic encephalopathy

Neurologic dysfunction due to accumulation of toxins (mainly ammonia) that the liver fails to detoxify.

What is the most important toxin implicated in HE?

Ammonia, but others include aromatic amino acids, GABA, benzodiazepine-like substances, tryptophan, and manganese.

How does HE affect the brain?

Alters neurotransmission (glutamate, GABA, serotonin) and can cause cerebral edema.

What are the clinical signs of hepatic encephalopathy?

Lethargy, disorientation, aggression, vocalization, head pressing, seizures, coma, and death.

What condition allows toxins to bypass hepatic detoxification?

Portosystemic shunting (congenital or acquired).

What is Type I HE?

Congenital portosystemic shunt without intrinsic liver disease.

What is Type II HE?

Chronic hepatic disease with portal hypertension and acquired shunts.

What is Type III HE?

Fulminant acute hepatic failure (massive hepatocellular loss).

Why can cats develop HE even without a shunt?

Fasting causes arginine deficiency, impairing the urea cycle and ammonia detoxification.

What are key exacerbating factors of HE?

GI bleeding, infection, hypoglycemia, dehydration, protein catabolism, alkalosis, and hypokalemia.

Why does GI bleeding worsen HE?

Blood is highly ammoniagenic — digestion increases ammonia absorption.

How does metabolic alkalosis affect HE?

Increases CNS uptake of ammonia (NH₃ form is more diffusible at higher pH).

Why does hypokalemia worsen HE?

Increases renal ammoniagenesis and impairs ammonia trapping inside cells.

What common medications can cause hypokalemia and exacerbate HE?

Loop and thiazide diuretics.

Why is spironolactone preferred for ascites with HE?

It is potassium-sparing and reduces RAAS activation.

How can removing too much ascitic fluid worsen HE?

Causes hypovolemia → RAAS activation → more ammonia and sodium retention.

What is the main dietary goal in HE management?

Moderate protein restriction using non-ammoniagenic proteins (eggs, dairy, soy).

Why should severe protein restriction be avoided?

Leads to muscle catabolism → endogenous ammonia production → worsened HE.

What is the role of lactulose in HE?

Traps ammonia as ammonium in the acidic colon and increases its excretion in feces.

What is the starting dose of lactulose?

0.25 mL/kg PO 2–3×/day, adjusted to produce soft stool.

How does lactulose reduce ammonia absorption?

Bacterial fermentation produces acids → lowers pH → converts NH₃ → NH₄⁺ (non-absorbable).

Why is hydration important in HE?

Dehydration increases ammonia concentration and worsens neurologic signs.

What antibiotics are commonly used for HE and why?

Metronidazole — targets anaerobes that produce ammonia via urease activity.

What recent evidence exists about antibiotic necessity in HE?

Some studies show diet and lactulose alone can control HE, reducing the need for chronic antibiotics.

What type of diuretics are preferred for ascites in PH and HE?

Aldosterone receptor antagonists (spironolactone).

Why can aggressive diuresis worsen HE?

Causes hypokalemia and dehydration, both of which promote ammonia toxicity.

What are the effects of RAAS activation in liver disease?

Sodium/water retention, potassium loss, and worsening ascites and encephalopathy.

Why are PPIs used in dogs and cats with PH?

Believed to be predisposed to ulceration through gut ischemia so to prevent ulceration, decrease acid secretion.

Why must PPIs (like omeprazole) be used cautiously in PH?

Long-term use alters GI flora, potentially worsening HE.

What happens if PPIs are stopped abruptly?

Rebound hypergastrinemia, hyperacidity, vomiting 

Portal hypertention → __, __, __

ascities, shunts, ulceration

Shunting/failure → __ → __

toxins bypass liver, HE