Term
| What are the principle complications of Cirrhosis? |
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Definition
Cirrhosis= formation of micro or macro nodules that disrupt hepatic architecture and produce portal HTN and compromised function (may progress to HCC).
**Varices are most common and patients die mostly of HCC (10% will die overall)
1) Bleeding (esophageal varices from portal HTN)
2) Ascites and hepatic encephalopathy
3) Coagulopathy (abnormal protein production)
4) Renal Failure
- also present with jaundice (bilirubin buildup), muscle wasting, gynecomastia (gonadal atrophy), pruritis (itching) and osteopenia (vitamin D and calcium) |
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Term
| What is the basic anatomy of the portal vein and its tributaries? |
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Definition
Portal Vein (70% of hepatic blood supply) forms as confluence of SMV and Splenic vein (which drains IMV from left colon) and is sandwiched between Sinusoidal and Splanchnic capillary beds.
- Main portal vein (drain right and left gastric veins) divides into left (drains umbilical vein) and right branches to supply corresponding hepatic lobes.
**Portal HTN develops when portal pressure gradient ("effective" sinusoidal pressure) > 12 mm Hg (normally <5) |
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Term
| What is the "portal pressure gradient" and how is it interpreted clinically? |
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Definition
Difference between hepatic vein pressure and portal vein pressure (normally <5 mm Hg)- "effective sinusoidal pressure"
Gradient becomes elevated either when inflow increases (splenic AFV), or when resistance increases (most common)
Generally measured by hepatic vein cath through trans-jugular or trans-femoral approach. Compare free hepatic vein pressure to "wedged venous pressure" as measured by balloon cath.
deltaP= Q/R and R= 8nl/pir^4 |
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Term
| What are the primary causes of portal hypertension and how are they categorized clinically? |
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Definition
Generally due to increased vascular resistance
Can be Intra-hepatic or Extra-hepatic
1) Extra-hepatic
- Portal or Splenic vein thrombosis (pre-hepatic), or Hepatic vein thrombosis (post-hepatic)
2) Intra-hepatic
- Pre-sinusoidal (Schistosomiasis, early primary biliary cirrhosis)
- Sinusoidal (Alcoholic cirrhosis)
- Post-sinusoidal (Alcoholic hepatitis, veno-occlusive disease) |
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Term
| How does portal hypertension cause varices? |
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Definition
Bleeding varices is a principle complication of cirrhosis that is due to portal HTN.
1) Portal HTN leads to dilation of esophago-gastric collaterals that communicate between the coronary vein and the esophageal veins with drainage into the azygous.
2) Varices develop that tend to hemorrhage
**other sites include umbilicus, splenic bed via short gastric veins, retroperitoneum, rectum, intestine. |
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Term
| How does portal hypertension produce ascites? |
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Definition
Ascites is a principle complication of cirrhosis associated with portal hypertension due to macro and micro-nodular formation and disrupted venous architecture and increased resistance.
1) Portal HTN
- As intra-sinusoidal pressure increases causing fluid to leak out (capillaries are already fenestrated w/o a BM) into the liver and then exudes into the peritoneal cavity.
- Intra-sinusoidal hydrostatic pressure is great and causes serum efflux (secondary volume depletion)
2) Functional renal abnormalities
- sodium/water retention
- renal vasoconstriction
3) Hyperndynamic circulation
- Peripheral arterial vasodilation (NO)
- Decreased SVR |
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Term
| How can cirrhosis produce hepatic encephalopathy? |
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Definition
Presents with "flapping tremor" (asterixis) and variable personality changes that may be as severe as coma.
caused by AMMONIA produced by gut flora by the breakdown of nitrogenous substances.
1) Hepatic metabolism of ammonia is impaired and substantial volumes of portal blood bypass liver through porto-systemic collaterals, raising NH4+ that crosses BBB
2) Brain has no TCA cycle to deal with NH4+, and it can only be handled by converting glutamate to glutamine, leading to suppressed neuronal excitability.
**other monamines may also be involved** |
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Term
| What physical signs are most associated with advanced liver disease? |
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Definition
1) Jaundice
2) Muscle wasting
3) Portal HTN
4) Variceal bleeding
5) Ascites
6) Hepatic encephalopathy
7) Coagulopathy (legs)
8) Hepatorenal syndrome (renal failure) |
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Term
| What are the 3 major theories of ascites generation in cirrhosis? |
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Definition
All agree that portal htn causes splanchnic vasodilation and increased splanchnic pressure.
1) Classic underfilling theory
- Increased hydrostatic pressure
2) Overflow theory
- Sodium-retaining signal
3) Forward theory
- Peripheral arterial vasodilation |
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Term
| Who should receive HCC screening? |
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Definition
AFP and ultrasound every 6 months for
1) cirrhosis of any cause
2) certain inherited metabolic disorders (hemochromatosis, tyrosinemia, porphyrias)
Healthy HBV carriers need screening every 12 months with AFP.
CT/MRI NOT for screening! |
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Term
Which of the following is an appropriate HCC screening method for a patient with cirrhosis from alcoholism?
1) AFP with LFTs every 6 months
2) CT scan every 12 months
3) AFT without LFTs every 12 months
4) AFT with US every 6 months |
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Definition
4!
healthy Hep B gets AFT +/- every 12 months |
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Term
| Which patients with HCC qualify for liver transplant? |
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Definition
80% have cirrhosis and 5yr survival is 70% with 15% recurrence rate.
1) Single tumor not > 5cm
2) Multiple (up to 3) tumors- none > 3cm |
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