Liver, Gallbladder, and Pancrease

Question 1

What are the parts of the portal triad?

Answer 1

• Hepatic artery- brings in fresh blood
• hepatic portal vein- blood from GI tract
• bile duct- brings bile out of the liver
• lymphatics- bring lymph out of the liver towards portal triad

Question 2

How much of CO does liver get?

Answer 2

25%

80% enters liver from portal vein

20% from hepatic artery

Question 3

What is the function of the hepatocyte regarding glucose and protein?

Answer 3

• takes up glucose and stores it as glycogen, releases glucose between meals
• Takes up amino acids and synthesizes plasma proteins
  
  • makes lipoproteins
  • some protein is stored in the liver (reserve of one day’s worth of amino acids)

Question 4

What is the hepatocyte function regarding bile?

What is the function of bile?

Answer 4

• Liver makes bile
• bile salts are used to emulsify fats
  
  • negatively charged after the Na+ or H+ is removed
• bile is modified cholesterol
• Bile is released into bile canaliculi then to bile duct, then to gallbladder, then to duodenum
• In duodenum bile helps digest fat by emulsifying
• bile is reabsorbed in ileum and it is brought back to liver

Question 5

What is hepatocyte function regarding bilirubin?

Answer 5

• Bilirubin comes from broken down heme
  
  • Fe is recycled and porphyrin–>biliverdin–>bilirubin
  • when unconjugated it is lipophilic; must be conjugated in liver so it can be excreted in kidney
• Hepatocytes attach a glucuronic acid, making it water soluble
  
  • this is released into bile duct and into duodenum and out with feces

Question 6

What is fibrosis?

Answer 6

• inflammation: macrophages activate and stimulate fibroblasts to lay down collagen
• lots of collagen impairs blood flow through liver and liver function

Question 7

What laboratory test evaluates hepatocyte integrity?

Answer 7

• AST, ALT
  
  • these are enzymes that are found within hepatocytes.
  • they would only be found in the blood if the hepatocytes are dying (necrosis, not apoptosis)
  • the higher the values, the more hepatocyte death that is occuring.

Question 8

What lab values indicate biliary tract integrity?

Answer 8

• Serum alkaline phosphatase (AP, ALP, ALKP) and GGT
  
  • released if cells along the biliary tract are damaged
  • found in cells lining bile ducts
  • high numbers are indicative of bile duct damage

Question 9

What lab values indicate hepatocyte function?

Answer 9

• Serum bilirubin- liver’s ability to conjugate the bilirubin
  
  • tests for total and conjugated
  • total- conjugated = unconjugated
• Serum albumin- will not be made if liver is failing
  
  • decreased albumin and decreased total protein = liver damage
  • if all numbers are correct except albumin, might be a kidney problem
• INR (Prothrombin time)- measures clotting time
  
  • liver makes clotting factors, if liver is failing, pt will have increased clotting time
  • might be making clotting factors but not fibrinolytic factors (they would have more clotting)
  • coagulopathy- either too much or too little
• Serum ammonia- liver deaminates amino acids and sticks them together to form urea
  
  • if liver cannot do this, ammonia is released

Question 10

What is the MELD score?

Answer 10

• Model for End-stage Liver disease
  
  • 3.8 * ln(bilirubin) + 11.2 * ln (INR) + 9.6 * ln (creatinine) + 6.43
• higher score = higher risk of mortality

Question 11

What are the consequences of liver disease?

Answer 11

• jaundice and cholestasis
• hypoalbuminemia
• hyperammonemia
• hypoglycemia
• fetor hepaticus- smell of death/feces in lung
• hypogonadism-liver clears hormones (estrogen builds, decreased release of LH & FSH)
• gynecomastia- steroid hormones are lipophilic, must be conjugated in liver to be able to excrete
• palmar erythema- red palms, blamed on estrogen
• spider angiomas- red dilated capilaries, blamed on estrogen
• weight loss
• muscle wasting

Question 12

What does hepatic portal hypertension cause?

Answer 12

• ascites
• esophageal varices
• hemorrhoids
• caput medusae
• splenomegaly

Question 13

What are the causes of jaundice?

Answer 13

• resulting in elevated unconjugated bili
  
  • excess bilirubin production
  • reduced hepatic uptake
  • impaired conjugation
• resulting in elevated conjugated bili
  
  • decreased hepatocellular excretion
  • impaired bile flow

Question 14

Whats the problem with increased unconjugated bilirubin?

Answer 14

• it is insoluble in water and tightly bound to albumin, so it cannot be excreted by the kidney
• the fraction that is not bound to albumin will:
  
  • diffuse into tissues (especially brain, causing brain damage)
  • produce toxic injury
  • may lead to severe neurological damage

Question 15

What is cholestasis?

What is biliary atresia?

Answer 15

• Cholestasis: The inability to move bile
  
  • passage gets clogged, bile can’t go through and this buildup will damage the hepatocytes
• Biliary atresia: bile duct doesnt form all the way, results in liver failure, seen in young children.

Question 16

What are the causes of hyperbilirubinemia without liver damage?

Answer 16

• Gilbert’s syndrome
• Crigler-Najjar syndrome
• Dubin-Johnson Syndrome
• Benign Postoperative Intrahepatic cholestasis
• Progressive Familial Intrahepatic Cholestasis

Question 17

What is Gilbert’s syndrome?

Answer 17

• Mild defect in glucoronosyltransferase enzyme (UGT1A1)
  
  • increase in unconjugated bilirubin (the only thing that is elevated)
  • Common 5%-10%, but benign

Question 18

What is Crigler-Najjar syndrome?

Answer 18

• Severe defect in glucuronosyltransferase enzyme (UGT1A1)
  
  • increase in unconjugated bilirubin
  • rare, but a severe problem
  • bilirubin can cause brain damage

Question 19

What is Dubin-Johnson Syndrome?

Answer 19

• Defect in protein needed to pump conjugated bilirubin into bile canaliculus
  
  • increase in conjugated bilirubin
  • rare and benign–liver is black!
• ** Joey didnt mention the sports thing, I was just looking at pictures of black livers and thought this was funny**

Question 20

What is benign postoperative intrahepatic cholestasis?

Answer 20

• increase in bilirubin production due to hemolysis or hematoma resorption
• increase in conugated bilirubin- excess bilirubin overwhelms biliary system
• benign, usuually resolves without problems

Question 21

What is progressive familial intrahepatic cholestasis?

Answer 21

• small group of genetic defects in transport proteins
• cause subsequent liver damage, requiring liver transplant
• rare, but severe

Question 22

What is the problem with cirrhosis? What does it cause?

Answer 22

• it impairs blood flow through the liver and causes hepatic portal hypertension, which causes:
  
  • ascites
  • portosystemic shunts
    
    • esophageal varices
    • hemorrhoids
    • caput medusae
  • splenomegaly

Question 23

How much liver function must be lost to have hepatic failure?

Answer 23

80-90%

Question 24

What are the clinical manifestations of cirrhosis?

(chart)

Answer 24

Question 25

Which hepatitises can be in carrier state/ asymptomatic infection?

Answer 25

* B, C, D

Question 26

Which hepatitises are chronic? \*all can be acute

Answer 26

B, C, D, G

Question 27

Hepatitis A & E how are they transmitted? is there a vaccine?

Answer 27

* transmitted through oral-fecal routes * occurs in places with poor infrastructure (bad sewage systems) * Not really present in US unless somebody travelled to another country * Vaccine for A, not for E

Question 28

Hepatitis B, C, & D transmission effects

Answer 28

* transmitted through intercourse and needles * Hep B- usually transmitted mother to baby in China * causes cancer * vaccine * Hep C- no vaccine * causes cancer * Hep D- can only be acquired **with** Hep B * Hep B vaccine effective

Question 29

What is hepatic steatosis?

Answer 29

* Fatty liver disease- fat builds up inside hepatocytes, enlarges liver * Usually caused by high alcohol intake, the hepatocytes will take up the alcohol (as fats?) faster than they can make the fats into lipoproteins * Will see elevated AST, ALT and unconjugated bili, but all will return to normal after the binge drinking stops

Question 30

What are the different stages of alcoholic liver disease?

Answer 30

* hepatic steatosis (90-100%) * alcoholic hepatitis (10-35%) * Cirrhosis (8-20%)

Question 31

What is hemochromatosis? who gets it? genetics? How is it "cured"?

Answer 31

* hereditary uncontrolled uptake of iron, about 1 g/year * mostly males; 5-7:1 * because women lose the iron through menstruation * autosomal recessive * heterozygous carriers (about 10%) * problems appear around 50+ years old * "cured" by having person regularly donate blood

Question 32

What problems does a person with fully developed hemochromatosis disease likely have?

Answer 32

* cirrhosis (100%) * DM (75-80%) * grey skin pigmentation (75-80%)

Question 33

What is another primary iron overload disease?

Answer 33

* Bantu siderosis * liss common, genetic mutation in Africa * also recessive * also takes up iron at too fast of a rate

Question 34

What is **primary** obstructive biliary tract disease?

Answer 34

* the destruction of hepatic biliary ducts * will see elevated alkaline phos and cholesterol * hyperbili later in disease * antimitochondrial antibodies (autoimmune) in \>90% * often fatal

Question 35

What is **secondary** obstructive biliary tract disease?

Answer 35

* **obstruction** of extrahepatic biliary tract * usually caused by: gallstones * biliary atresia * malignancies (tumor) of biliary tree or pancrease * strictures resulting from surgery

Question 36

What are the four circulatory problems of the liver?

Answer 36

* Hepatic vein outflow obstruction * impaired intrahepatic blood flow * impaired blood flow into liver * impaired hepatic artery flow

Question 37

What are some causes of primary liver cancer?

Answer 37

* Hep B- the earlier you get hep B, the earlier you are likely to get cancer * chronic liver disease- Hep C and cirrhosis * Aflatoxin- used to be common in peanut butter, toxin made by fungus * cirrhosis (85-90%)- definite correlation, but not necessarily cause

Question 38

What is the survival rate of primary carcinoma of the liver?

Answer 38

about 7 months. prognosis is also poor for metastatic

Question 39

What is cholelithiasis? How many people are affected by it?

Answer 39

* Gallstones * \>20 million american (about 10% of adults) * about 1 million new cases/yr * 2/3 requiring surgery * about 1000 deaths per year * usually asymptomatic (70-80%) * until stones start moving or gallbladder becomes inflamed

Question 40

What are the different types of stones?

Answer 40

cholesterol (front) pigment (below)

Question 41

What are the risk factors for cholesterol stones?

Answer 41

* fair- also Pima, Hope, navajo * forty- increase with age * female * fertile- pregnancy, also oral contraceptive use * fat * gallbladder stasis * hyperlipidemia

Question 42

What are the risk factors for pigment stones?

Answer 42

* Made of bilirubin * chronic hemolytic syndromes * biliary infection * GI disorders- crohns * Asian \> westerners

Question 43

What is choledocholithiasis? What problems does it cause?

Answer 43

* the presence of stones in the biliary tree * **biliary obstruction**- become very painful when stuck in ducts. Bilirubin levels elevate * **pancreatitis**- enzymes can't get out and instead become active in pancrease * **cholangitis**- inflammation of gallbladder * **hepatic abscess** * **chronic liver disease with biliary cirrhosis** * **acute calculous cholecystitis**- inflammation

Question 44

What is acute pancreatitis? What causes it?

Answer 44

* digestive enzymes auto digesting the pancreas * "I GETS" * **I**diopathic * **g**allstone- blocking ampulla of vater * **e**thanol (alcohol)- alcoholics will usually get cirrhosis or pancreatitis, usually not both * **t**rauma * **s**teroids