Liver, Gallbladder, and Pancrease Flashcards

1
Q

What are the parts of the portal triad?

A
  • 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
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2
Q

How much of CO does liver get?

A

25%

80% enters liver from portal vein

20% from hepatic artery

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3
Q

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

A
  • 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)
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4
Q

What is the hepatocyte function regarding bile?

What is the function of bile?

A
  • 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
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5
Q

What is hepatocyte function regarding bilirubin?

A
  • 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
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6
Q

What is fibrosis?

A
  • inflammation: macrophages activate and stimulate fibroblasts to lay down collagen
  • lots of collagen impairs blood flow through liver and liver function
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7
Q

What laboratory test evaluates hepatocyte integrity?

A
  • 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.
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8
Q

What lab values indicate biliary tract integrity?

A
  • 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
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9
Q

What lab values indicate hepatocyte function?

A
  • 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
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10
Q

What is the MELD score?

A
  • 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
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11
Q

What are the consequences of liver disease?

A
  • 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
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12
Q

What does hepatic portal hypertension cause?

A
  • ascites
  • esophageal varices
  • hemorrhoids
  • caput medusae
  • splenomegaly
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13
Q

What are the causes of jaundice?

A
  • resulting in elevated unconjugated bili
    • excess bilirubin production
    • reduced hepatic uptake
    • impaired conjugation
  • resulting in elevated conjugated bili
    • decreased hepatocellular excretion
    • impaired bile flow
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14
Q

Whats the problem with increased unconjugated bilirubin?

A
  • 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
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15
Q

What is cholestasis?

What is biliary atresia?

A
  • 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.
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16
Q

What are the causes of hyperbilirubinemia without liver damage?

A
  • Gilbert’s syndrome
  • Crigler-Najjar syndrome
  • Dubin-Johnson Syndrome
  • Benign Postoperative Intrahepatic cholestasis
  • Progressive Familial Intrahepatic Cholestasis
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17
Q

What is Gilbert’s syndrome?

A
  • Mild defect in glucoronosyltransferase enzyme (UGT1A1)
    • increase in unconjugated bilirubin (the only thing that is elevated)
    • Common 5%-10%, but benign
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18
Q

What is Crigler-Najjar syndrome?

A
  • Severe defect in glucuronosyltransferase enzyme (UGT1A1)
    • increase in unconjugated bilirubin
    • rare, but a severe problem
    • bilirubin can cause brain damage
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19
Q

What is Dubin-Johnson Syndrome?

A
  • 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**
20
Q

What is benign postoperative intrahepatic cholestasis?

A
  • increase in bilirubin production due to hemolysis or hematoma resorption
  • increase in conugated bilirubin- excess bilirubin overwhelms biliary system
  • benign, usuually resolves without problems
21
Q

What is progressive familial intrahepatic cholestasis?

A
  • small group of genetic defects in transport proteins
  • cause subsequent liver damage, requiring liver transplant
  • rare, but severe
22
Q

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

A
  • it impairs blood flow through the liver and causes hepatic portal hypertension, which causes:
    • ascites
    • portosystemic shunts
      • esophageal varices
      • hemorrhoids
      • caput medusae
    • splenomegaly
23
Q

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

A

80-90%

24
Q

What are the clinical manifestations of cirrhosis?

(chart)

A
25
Q

Which hepatitises can be in carrier state/ asymptomatic infection?

A
  • B, C, D
26
Q

Which hepatitises are chronic?

*all can be acute

A

B, C, D, G

27
Q

Hepatitis A & E

how are they transmitted?

is there a vaccine?

A
  • 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
28
Q

Hepatitis B, C, & D

transmission

effects

A
  • 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
29
Q

What is hepatic steatosis?

A
  • 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
30
Q

What are the different stages of alcoholic liver disease?

A
  • hepatic steatosis (90-100%)
  • alcoholic hepatitis (10-35%)
  • Cirrhosis (8-20%)
31
Q

What is hemochromatosis?

who gets it?

genetics?

How is it “cured”?

A
  • 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
32
Q

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

A
  • cirrhosis (100%)
  • DM (75-80%)
  • grey skin pigmentation (75-80%)
33
Q

What is another primary iron overload disease?

A
  • Bantu siderosis
    • liss common, genetic mutation in Africa
    • also recessive
    • also takes up iron at too fast of a rate
34
Q

What is primary obstructive biliary tract disease?

A
  • the destruction of hepatic biliary ducts
    • will see elevated alkaline phos and cholesterol
    • hyperbili later in disease
  • antimitochondrial antibodies (autoimmune) in >90%
  • often fatal
35
Q

What is secondary obstructive biliary tract disease?

A
  • obstruction of extrahepatic biliary tract
    • usually caused by: gallstones
    • biliary atresia
    • malignancies (tumor) of biliary tree or pancrease
    • strictures resulting from surgery
36
Q

What are the four circulatory problems of the liver?

A
  • Hepatic vein outflow obstruction
  • impaired intrahepatic blood flow
  • impaired blood flow into liver
  • impaired hepatic artery flow
37
Q

What are some causes of primary liver cancer?

A
  • 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
38
Q

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

A

about 7 months.

prognosis is also poor for metastatic

39
Q

What is cholelithiasis?

How many people are affected by it?

A
  • 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
40
Q

What are the different types of stones?

A

cholesterol (front)

pigment (below)

41
Q

What are the risk factors for cholesterol stones?

A
  • fair- also Pima, Hope, navajo
  • forty- increase with age
  • female
  • fertile- pregnancy, also oral contraceptive use
  • fat
  • gallbladder stasis
  • hyperlipidemia
42
Q

What are the risk factors for pigment stones?

A
  • Made of bilirubin
    • chronic hemolytic syndromes
    • biliary infection
    • GI disorders- crohns
    • Asian > westerners
43
Q

What is choledocholithiasis?

What problems does it cause?

A
  • 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
44
Q

What is acute pancreatitis?

What causes it?

A
  • 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
45
Q
A