Liver, Gallbladder, and Pancrease Flashcards
What are the parts of the portal triad?
- 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
How much of CO does liver get?
25%
80% enters liver from portal vein
20% from hepatic artery
What is the function of the hepatocyte regarding glucose and protein?
- 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)
What is the hepatocyte function regarding bile?
What is the function of bile?
- 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
What is hepatocyte function regarding bilirubin?
- 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
What is fibrosis?
- inflammation: macrophages activate and stimulate fibroblasts to lay down collagen
- lots of collagen impairs blood flow through liver and liver function
What laboratory test evaluates hepatocyte integrity?
- 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.
What lab values indicate biliary tract integrity?
- 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
What lab values indicate hepatocyte function?
- 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
What is the MELD score?
- 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
What are the consequences of liver disease?
- 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
What does hepatic portal hypertension cause?
- ascites
- esophageal varices
- hemorrhoids
- caput medusae
- splenomegaly
What are the causes of jaundice?
- resulting in elevated unconjugated bili
- excess bilirubin production
- reduced hepatic uptake
- impaired conjugation
- resulting in elevated conjugated bili
- decreased hepatocellular excretion
- impaired bile flow
Whats the problem with increased unconjugated bilirubin?
- 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
What is cholestasis?
What is biliary atresia?
- 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.
What are the causes of hyperbilirubinemia without liver damage?
- Gilbert’s syndrome
- Crigler-Najjar syndrome
- Dubin-Johnson Syndrome
- Benign Postoperative Intrahepatic cholestasis
- Progressive Familial Intrahepatic Cholestasis
What is Gilbert’s syndrome?
- Mild defect in glucoronosyltransferase enzyme (UGT1A1)
- increase in unconjugated bilirubin (the only thing that is elevated)
- Common 5%-10%, but benign
What is Crigler-Najjar syndrome?
- Severe defect in glucuronosyltransferase enzyme (UGT1A1)
- increase in unconjugated bilirubin
- rare, but a severe problem
- bilirubin can cause brain damage
What is Dubin-Johnson Syndrome?
- 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**
What is benign postoperative intrahepatic cholestasis?
- increase in bilirubin production due to hemolysis or hematoma resorption
- increase in conugated bilirubin- excess bilirubin overwhelms biliary system
- benign, usuually resolves without problems
What is progressive familial intrahepatic cholestasis?
- small group of genetic defects in transport proteins
- cause subsequent liver damage, requiring liver transplant
- rare, but severe
What is the problem with cirrhosis? What does it cause?
- it impairs blood flow through the liver and causes hepatic portal hypertension, which causes:
- ascites
- portosystemic shunts
- esophageal varices
- hemorrhoids
- caput medusae
- splenomegaly
How much liver function must be lost to have hepatic failure?
80-90%
What are the clinical manifestations of cirrhosis?
(chart)
Which hepatitises can be in carrier state/ asymptomatic infection?
- B, C, D
Which hepatitises are chronic?
*all can be acute
B, C, D, G
Hepatitis A & E
how are they transmitted?
is there a vaccine?
- 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
Hepatitis B, C, & D
transmission
effects
- 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
What is hepatic steatosis?
- 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
What are the different stages of alcoholic liver disease?
- hepatic steatosis (90-100%)
- alcoholic hepatitis (10-35%)
- Cirrhosis (8-20%)
What is hemochromatosis?
who gets it?
genetics?
How is it “cured”?
- 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
What problems does a person with fully developed hemochromatosis disease likely have?
- cirrhosis (100%)
- DM (75-80%)
- grey skin pigmentation (75-80%)
What is another primary iron overload disease?
- Bantu siderosis
- liss common, genetic mutation in Africa
- also recessive
- also takes up iron at too fast of a rate
What is primary obstructive biliary tract disease?
- the destruction of hepatic biliary ducts
- will see elevated alkaline phos and cholesterol
- hyperbili later in disease
- antimitochondrial antibodies (autoimmune) in >90%
- often fatal
What is secondary obstructive biliary tract disease?
-
obstruction of extrahepatic biliary tract
- usually caused by: gallstones
- biliary atresia
- malignancies (tumor) of biliary tree or pancrease
- strictures resulting from surgery
What are the four circulatory problems of the liver?
- Hepatic vein outflow obstruction
- impaired intrahepatic blood flow
- impaired blood flow into liver
- impaired hepatic artery flow
What are some causes of primary liver cancer?
- 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
What is the survival rate of primary carcinoma of the liver?
about 7 months.
prognosis is also poor for metastatic
What is cholelithiasis?
How many people are affected by it?
- 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
What are the different types of stones?
cholesterol (front)
pigment (below)
What are the risk factors for cholesterol stones?
- fair- also Pima, Hope, navajo
- forty- increase with age
- female
- fertile- pregnancy, also oral contraceptive use
- fat
- gallbladder stasis
- hyperlipidemia
What are the risk factors for pigment stones?
- Made of bilirubin
- chronic hemolytic syndromes
- biliary infection
- GI disorders- crohns
- Asian > westerners
What is choledocholithiasis?
What problems does it cause?
- 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
What is acute pancreatitis?
What causes it?
- digestive enzymes auto digesting the pancreas
- “I GETS”
- Idiopathic
- gallstone- blocking ampulla of vater
- ethanol (alcohol)- alcoholics will usually get cirrhosis or pancreatitis, usually not both
- trauma
- steroids
