QUESTIONS

1. The blood supply to the liver is from the _______________ artery and the _______________ vein. Which one supplies 20% of the blood supply & which one supplies the other 80%?
    
2. What is the sphincter of Oddi?
    
3. What are the spaces of Disse?
    
4. The structural unit of the liver is the _______________ and it is centered on the _______________. The functional unit of the liver is the _______________ and it is centered on the _______________.
    
5. The three things making up a portal triad are:
    
6. What is an ITO cell?
    
7. The main hormone in charge of gall bladder contraction is
   _______________.
    
8. In what area of the GI tract are bile acids absorbed?
   
   OKay, that's enough anatomy. Now for some questions regarding what the liver does with itself all day.
    
9. Do you need insulin in order for the liver to take up glucose?
    
10. In the catabolic state, non-esterified fatty acids are released from
    peripheral stores & transported by albumin to the liver for repackaging into VLDL's for re-release or for burning as fuel. In repackaging the NEFA's they must be bound to glycerol to form triglycerides. What kind of feedback mechanism helps out when proteins to make up the VLDL's start running low?
     
11. In the catabolic state, beta oxidation is jamming and acetyl units are blasting into the Krebs cycle. When all the Coenzyme A is in use, the liver starts to free some up by making ketone bodies. What is the health food store name for CoA?  what are the three main ketone bodies?  What tissues burn ketone bodies?
     
12. True or False:
    
    Your liver contains > 1 years supply of Vitamin A.
     
13. The liver is very involved in Vitamin K and its dependent factors. In fact, in hepatic insufficiency, bleeding can result from problems in this arena. How might bleeding result?
     
14. What is a PIVKA test?
     
15. What is the difference between ferritin and transferrin?
     
16. What is haptoglobin?
     
17. Why is poop brown? (Second graders everywhere are waiting for your answer here.)
     
18. In liver disease, albumin is often low and globulins are often high. Why might globulins be high?
     
19. BSP is a dye metabolized in the liver similar to the way bilirubin is metabolized. Let's go back in time and pretend we are doing this test.  BSP can be cleared falsely fast (bsp is too low) or falsely slowly (bsp is too high). For each of the following conditions, say whether BSP would be high or low.
    
    a) obesity
     
    b) reduced albumin
    
    c) patient chronically on phenobarbital
    
    d) patient is really icteric
    
    e)patient not properly fasted before the test
     
20. Why is ALT not a good choice for monitoring chronic liver disease?
    
    
    
    
     

ANSWERS

1. The hepatic artery provides 20% of the blood supply to the liver and the portal vein supplies the other 80%.
   
   
   
   
    
2. The sphincter of Oddi sounds like something from Wayne's World but in reality it is the sphincter connecting the common bile duct to the duodenum. The area of the common bile duct between the gall bladder & its emergence from the liver is the cystic duct. It is not clear from my notes if the "common bile duct" is the part outside the liver or is the whole thing.
   
   
   
   
    
3. The sinusoids are lined by fenestrated endothelial cells which separate the blood from the actual hepatocytes.  The space between the hepatocytes & the endothelial cells is the Space of Disse. The hepatocytes have little microvilli reaching into the spaces.  It is through this space that the "stuff" in the blood is seen by the hepatocytes. Hepatocytes secrete bile but not into the spaces of Disse. Bile is secreted into canaliculi then to cholangioles & then bile ductules.
   
   
   
   
    
4. The structural unit of the liver is the lobule centered on the central hepatic vein. The functional unit of the liver is the acinus which is centered on the portal triad.
   
   
   
   
    
5. The three parts of the portal triad are the portal venule, the hepatic arteriole & the bile ductule. ( Yes, there are also nerves & lymphatics, too)
   
   
   
   
    
6. An Ito cell is a fat cell which lives in the liver & stores vitamin A. In CAH or similar fibrosing condition, it will transform into a fibroblast cell & begin to secrete collagen. (And you thought this was going to be an OJ Simpson joke, didn't you.)
   
   
   
   
    
7. The main hormone for gall bladder contraction is cholecystokinin.
   
   
   
   
    
8. Bile acids are absorbed in the ileum
   
   
   
   
    
9. No, insulin is not needed for the liver to take up glucose.  (It is needed for any other organ/tissue) Instead of regulating glucose metab. at the cell membrane, insulin is needed to regulate intracellular enzymes. Hypoglycemia can be a problem in hepatic insufficiency as there is reduced capacity for gluconeogenesis as well as reduced glycogen storage but all you need is 30% functional liver tissue to keep blood sugar level maintained.
   
   
   
   
    
10. There is no feedback mechanism when lipoprotein apoproteins start running low. Lipid just starts accumulating and voila! Fatty liver.
    
    
    
    
     
11. Coenzyme A is panthothenic acid. The three amigos of the ketone body world are Acetone, acetoacetic acid, and beta-hydroxybutyric acid.
    
    
    
    
     
12. Wouldn't I be a stinker if I made that up about the liver? It's true,
    you have > 1 year's supply of vitamin A in your liver.
    
    
    
    
     
13. In liver failure
    
    1) the liver cannot reactivate used vitamin K1
    
    2) The K factors (2,7,9,10)  cannot be synthesized in the liver
    
    3) If you have cholestasis, there are no bile acids available to enable the absorption of dietary K1
    
    4) If your patient is on antibiotics, you will probably have screwed up the GI flora able to make K2 (K2 has 60% the activity
    of K1 and doesn't require bile acids for absorption.)
    
    
    
    
     
14. PIVKA stands for proteins induced by Vitamin K absence & they consist of inactive K factors. The test is called a thrombotest & is written up nicely in CVT10. Sharon Center likes this test much better than PT pre--biopsy.
    
    
    
    
     
15. Welcome to iron metabolism.  Old red blood cells are broken down & their hemoglobin is taken up by the RE system of the spleen & liver.  The iron is removed & released to the plasma where it is picked up by transferrin & carried around. It hopefully
    is carried to the bone marrow for recycling but it can get returned to the RE system storage depots  (or it may have never left the RE cell). Within the RE cell it binds to ferritin for storage. If ferritin stores fill, it is stored as hemosiderin.  No body really knows how iron gets away from ferritin or hemosiderin but it can get away, get back to the plasma, & back to the bone marrow.
    
    
    
    
     
16. As old red cells are processed and iron is removed from the heme unit, the rest of the heme is processed first to biliverdin (by heme oxygenase) & then to bilirubin (by biliverdin reductase).  Bilirubin is then released into the circulation. It is now unconjugated & not water soluble so it travels around bound to albumin. It gets to the liver & gets conjugated.  From here it goes into the bile system & into the GI tract.  It gets unconjugated in the GI tract & converted by bacteria to urobilingen (which gets reabsorbed & excreted back in to bile - 80% or gets excreted renally 20%).
    
    Okay, so where does haptoglobin fit in?  Haptoglobin is the protein that picks up old hemoglobin from the old broken red cells & transports it to the RE system.
    
    
    
    
     
17. Poop is brown because urobilinogen is broken down by GI flora to stercobilin which is brown. The idea is that if there is cholestasis, there won't be any bilirubin to convert to urobilinogen to convert to stercobilin & the stool will be "clay colored".  In reality, poop color is also determined by diet, dyes & lots of factors so they clay rule isn't iron clad.
    
    
    
    
     
18. There are several reasons for globulins to be high in liver disease.
    First, it helps that globulin production is considered to be of higher priority than albumin production; globulins are produced at the expense of albumin. Next, gamma globulins are basically antibodies so they are produced by lymphoid tissues (not the liver) & there is plenty of reason for immune stimulation. For one thing, the damaged liver is releasing antigens & for another thing the liver isn't very efficient at removing intestinal bugs or other antigenic type stuff coming in from the portal circulation.
    
    
    
    
     
19. BSP is cleared fast when albumin is low, when phenobarb has induced the enzymes used to process it, or if the fed patient's gall bladder is contracting along moving the BSP through quicker than usual.  BSP is cleared more slowly if you over-dosed your patient because you used your obese patient's actual weight & not lean body mass to dose the stuff, or if there is so much bilirubin circulating that there is competition to get into the liver.
    
    
    
    
     
20. Leakage enzymes such as ALT are not so good for chronic liver monitoring because they deplete :(