• Nutrients/oxygenation 75% comes from the portal vein, 25% comes from the hepatic artery
  • SMV + splenic vein = portal vein –> R and L portal vein. Liver is drained by hepatic vein to the IVC.
    • Block off the hepatic vein = Budd-Chiari Syndrome
      • 2/2 hypercoagulable states (pregnancy,OCPs,lupus anticoagulant,PCV,HCCetc)
      • Can happen slow or fast. Slow = get collaterals.
      • Increased pressure = ascites, nutmeg liver
  • AST/ALT = liver enzymes that are important in ATP formation and formation of oxalaetic acid and pyruvic acid.
    • Depend on B6, ALT > AST. This is why there is an AST predominance in alcoholics b/c ALT activity is depressed.
    • ALT = Liver, Longer (47 hr half life), Localized (to cytoplasm)
    • AST = Skeletal muscle, heart, kidney, liver. Present in mitochondria mostly + cytoplasm. In Zone 3 of liver acinus –> most sensitive to ischemic or toxic damage b/c lowest O2.
  • Liver synthetic function measured by: PT/INR & albumin
  • Elevations in Liver Enzymes:
    • Hepatocellular pattern = AST/ALT > ALP/GGT
    • Cholestatic pattern = ALP/GGT > AST/ALT
  • Jaundice most common in acute Hep A (70%)> B > C (20%)
  • ALP = enzyme that delivers metabolites across cell membranes. Rests on biliary epithelium CM, and when you get obstruction the bile salts are irritative, and ALP is released. Also elevated in bone disease.
    • Normally elevated in 3rd trimester preggers (placenta) and growing kids (bones)
    • 1/2 life = 1 weeks, so it takes a while to return to normal
  • GGT can be elevated in COPD and renal dysfunction
  • Cholestatic drug rxn = elevated conjugated hyperbili + ALP, relatively normal AST/ALT

Liver disease processes

  • Autoimmune hepatitis = elevated AST/ALT + conj hyperbili + relatively normal AST/ALT
    • ANA, ASMA, Anti-liver kidney microsomal enzyme
  • Cnx btw UC and PSC
  • PBC = check AMA and IgM
  • NASH is the MCC of mildly elevated liver enzymes in the western world
  • Hepatitis B = check for surface antigen, then anti-HBV core, then anti-HBV surface
    • Just anti-Hbsurface IgG = immune b/c of vaccination
    • First Hb surface antigen pops up –> when that goes down before IgM surface antibodies are detectable (they are there, just bound up with the surface antigen), the IgM core antibodies are detectable, that is the window period



  • Hepatocerebral degeneration – not wilson’s disease, but 2/2 long standing portosystemic shunting and leads to deposition of manganese in the basal ganglia (Wilson’s is copper) in the basal ganglia. That leads to medication resistant choreo-athetotic movements of arms/hands/limbs, mood changes, dysarthria, gait ataxia, etc. Tremors of arm, twitches of hands may be first signs.
    • Etiology: unknown. Here’s what I do know: this disease is thought to be associated with manganese deposition in basal ganglia (globus pallidus and substantia nigra). This happens in hepatic encephalopathy as well because manganese is supposed to be cleared by the liver. When it’s not, the [] increases, and it can aberrantly deposit.

Cirrhosis – fibrosis of liver ; irreversible

  • Ascites – fluid build up in the peritoneal cavity of pts with cirrhosis. Most common complication of cirrhosis. Within 10 yrs of diagnosis, 50% of ppl will devleop ascites. Must have portal HTN (PHT) in order to develop ascites.
    • Thought to be 2/2 arterial vasodilation, particularly splanchnic VD.
    • Requires sinusoidal HTN, portal pressure > 12 mmHg, if reduced to < 12 via portosystemic shunt, will likely subside.
    • Is not caused by pre-sinusoidal portal HTN, i.e. portal venous thrombosis will not result in ascites unless there is some other insult. ‘
    • Fluid builds up for multifactorial reasons: increased hydrostatic pressure, decreased oncotic pressure holding fluid in, increased sodium reabsorption b/c of aberrant RAAS activation (briefly, because of decreased SVR due to NO/prostacyclin), and markedly increased H2O reabsorption because of aberrantly increased ADH (also 2/2 to intravascular volume depletion/SNS activation/RAAS stimulation).  
  • Hepatic Venous Pressure Gradient = a way to tell if there is portal hypertension
    • Functionally measuring the difference between the IVC (systemic) venous pressure and the wedged hepatic vein pressure which represents to some approximation the portal vein pressure (it is slightly lower than the PVP normally)
    • What you do: measure the pressure in the hepatic vein with a balloon, then push it through until it is wedged get the wedge pressure. Take the difference (wedge – free), normal = 1-5 mmHg. >5mmHg = portal HTN, >10 = clinically significant portal HTN, >12 = risk of variceal bleeding
  • Varices
    • form when portal HTN exists and resistance to flow is greater through the portal system than it is through collateral circulation, so instead of flowing through the portal venous system, blood goes to the path of least resistance and buffs up the collateral circulation to drain directly into systemic circulation.
    • Problem is that these vessels can rupture and cause massive bleeding.




  • Hepatopulmonary syndrome
    • Etiology: pathophys unknown ; thought to be similar to HRS, where you have overproduction of NO and other vasodilators that lead to vasodilitation and angiogenesis. This leads to increased perfusion in comparison to ventilation, leading to a ventilation-perfusion mismatch. This is exacerbated by the fact that cirrhotic pts already have high CO that increases their perfusion.
    • Diagnosis: Need 1) liver disease/cirrhosis 2) Impaired oxygenation 3) Intrapulmonary vascular abnormalities
      • A-a gradient is elevated (>15 mmHg) demonstrating impaired oxygenation on room air (very important)
        • PAO2 – PaO2 (from ABG)
          • PAO2 = Partial pressure of oxygen in the alveoli = [FiO2 (21%) * (Patm – PH2O)] – (PaCO2/RQ)
      • Dx w/ agitated saline echocardiography — agitating NS makes microbubbles that are normally blocked by pulmonary vasculature, but in HPS, the vasculature is dilated, so within about 7 beats after injecting, you can see the bubbles pop up in the LA.
      • Roughly, you can also look at PaO2 and if it’s less than 80 mmHg, it demonstrates impaired O2.
      • Treatment: Liver tx, O2, rouvastatin (some evidence).


  • Portopulmonary HTN – when pt has pulmonary arterial HTN and portal HTN & no other cause for pHTN.
    • dx w/ RHC = mean pulmonary artery pressure > 25 mmHg at rest and PCWP < 15 mmHg
    • Etiology: unknown, few hypothesis including sheer stress 2/2 hyperdynamic flow from collateralization of vasculature 2/2 portal HTN. Also possibly due to various substances that should have been filtered out by the liver reaching the pulmonary vasculature and –> HTN (IL-1, endothelin, etc.)
    • Clinical presentation: DOE, chest pain, hemoptysis, fatigue, syncope. Tricuspid regurg, accentuated pulmonic valve closing sound (S2).


  • Hepatorenal Syndrome – dx of exclusion, kidney injury
    • Etiology: arterial vasodiolation + splanchnic vasodilation (primarily NO) leads to this. There is increase in CO, decrease in SVR –> localized decrease in renal perfusion –> noted by the JGA –> RAAS system activated –> decreased GFR + decreased urine sodium output
    • Diagnosis: 1) Chronic /acute hepatic disease with liver failure and portal HTN 2) AKI (>0.3 mg/dL or more in 48 hrs) 3) No other reason for AKI rising serum Cr, limited proteinuria  (<500 mg per day), normal urine sediment, low urine sodium (<10 mEq/day), oliguria
      • Type 1: worse; dramatic rise in serum Cr (increase by 50% in two days)
      • Type 2: Does not respond to diuretics


Please note, the information on this page is not to be taken as medical advice in any form. It is used by me as an easily accessible “study guide” and for anyone else as open-access med-ucation. The contents are accurate to the best of my knowledge. However if you see any mistakes, please comment below and I will either verify my material or correct the mistake ASAP. Further, if you have individual medical questions, you should contact your personal medical provider.