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BHSC 2203 - Patho > Unit 10 - Hepatobiliary Disorders > Flashcards

Unit 10 - Hepatobiliary Disorders Flashcards

1
Q

How can you examine the liver?

A

Ask the patient to take a very deep breath

- diaphragm pushes liver downwards

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2
Q

What % of cardiac output goes to the liver?

A

25%

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3
Q

Of that 25%, how much of it is venous blood?

A

75 - 80% venous blood

  • high in nutrients from the GI tract
  • low in oxygen
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4
Q

Of that 25%, how much of it is arterial blood?

A

20 - 25% arterial blood

- high in OXYGEN

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5
Q

What is the vein that blood is able to flow to the liver?

A

Through the hepatic-portal vein

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6
Q

What are 5 examples of liver functions?

A
  1. Nutrient metabolism
  2. Production of serum proteins and enyzmes
  3. Drug and hormone metabolism
  4. Urea synthesis
  5. Bile synthesis
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7
Q

What is the main blood protein that is formed in the liver

A

Albumin

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8
Q

Why is biotransformation an important function of the liver?

A

Tylenol is not effective until it is BIOTRANSFORMED by the liver
- then it becomes active

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9
Q

What does the liver do to NH2?

A

Adds an H+ to yield NH3 (TOXIC)

- then coverts NH3 to urea to be safely excreted

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10
Q

What are the two possible fates of unconjugated bilirubin in the blood?

A
  1. Liver processes - converts to conjugated and excreted in bile
  2. Causes bilirubinemia, and results in jaundice
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11
Q

Why is it common for babies to experience jaundice?

A

Lots of cells are dying and the liver function hasn’t yet caught up to meet capacity

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12
Q

At what level does jaundice occur (mg/dl)?

A

Bilirubin level > 3 mg/dl

- normal is 0.2 - 1.2

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13
Q

What are the three causes of jaundice?

A
  1. Increased RBC breakdown
    - nothing to do with the liver!
  2. Impaired liver uptake of bilirubin
  3. Impaired excretion of bilirubin
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14
Q

What are the three types of jaundice?

A
  1. Prehepatic
  2. Hepatic
  3. Posthepatic
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15
Q

What is prehepatic jaundice caused by?

A

Increased levels of unconjugated bilirubin in blood

- jaundice happens before it reaches the liver

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16
Q

What is hepatic jaundice caused by?

A

Interference with the liver’s ability to conjugate bilirubin or to secrete it after conjugation
- can be unconjugated or conjugated

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17
Q

What is posthepatic jaundice caused by?

A

Obstruction of bile flow inside or outside of the liver

  • gallstones!
  • conjugated hyperbilirubinemia (backs up into the blood because the ducts are blocked = NOTHING wrong with the liver!)
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18
Q

What are the characteristics of indirect bilirubin?

A
  • unconjugated
  • elevated with increased RBC breakdown or impaired liver uptake
  • bound by albumin
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19
Q

With indirect bilirubin, will it be found in the urine?

A

No - because it is bound by albumin

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20
Q

What are the characteristics of direct bilirubin?

A
  • conjugated

- elevated with impaired excretion of bilirubin from liver

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21
Q

With direct bilirubin, will it be found in the urine?

A

Yes - because it is water-soluble

not bound to albumin

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22
Q

What is acute hepatitis?

A

Acute liver inflammation and cellular injury

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23
Q

What is acute hepatitis commonly caused by?

A 
Hepatitis viruses (A, B, C, D, E)
Hepatotoxins
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24
Q

What is the route of transmission for type B (and D) and C hepatitis?

A

Blood and bodily fluids

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25
Q

Is the prognosis more severe in B or C hepatitis?

A

B

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26
Q

How does acute hepatitis present?

A
  • JAUNDICE
  • anorexia
  • fatigue
  • diffuse abdominal discomfort
  • dark urine
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27
Q

What is acute toxic hepatitis caused by?

A

Exposure to hepatotoxin

- or its metabolite

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28
Q

If alcohol is the toxin causing acute toxic hepatitis - what is the ratio of AST to ALT? What should it be normally?

A

2: 1

- usually the ratio is 1:1

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29
Q

What are the outcomes for viral hepatitis?

A
  1. Subclinical disease
  2. Acute icteric disease (could recover or lead to chronic hepatitis and then cirrhosis)
  3. Acute liver failure
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30
Q

Why is the incidence of Hepatitis B low in developed countries?

A

There is a vaccine

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31
Q

True or False:

Hepatitis B has worse outcomes than hepatitis C

A

False

  • Type C is worse
  • There is no vaccine for C
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32
Q

What is the etiology of chronic alcoholic liver disease?

A

Chronic, heavy alcohol exposure

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33
Q

What happens if you have high levels of alcohol dehydrogenase activity?

A

You can have a lot of drinks and not be affected for the toxic effects of alcohol

34
Q

How does the liver present in cases of alcoholic liver disease?

A

Fatter liver (steatosis)

  • liver cells contain fat deposits
  • liver is enlarged
35
Q

True or False:

A fatty liver is reversible

A

True

36
Q

True or False:

Cirrhosis is reversible

A

False

37
Q

Name one common acute and one common chronic change induced in the liver due to alcohol abuse

A 
Acute = steatosis (fatty liver)
Chronic = cirrhosis
38
Q

Describe the characteristics of a cirrhotic liver

A 
Smaller
Nodular
Yellow
Very firm
Poor blood flow
Bile ducts are squeezed (reducing flow)
39
Q

Why does portal hypertension occur in cirrhosis?

A

There is an obstruciton (or reduction) of portal blood flow caused by the choking action of the dense fibrous bands of cirrhosis
- scar and shrink the liver

40
Q

What are the manifestations of cirrhosis?

A
  • jaundice
  • bleeding (clotting factors not being produced at normal rates)
  • low albumin (and then edema)
  • immune deficient
  • estrogen excess
  • encephalopathy
41
Q

Why is there an estrogen excess in cirrhosis?

A

Liver breaks down estrogen and other hormones

42
Q

Why does cirrhosis cause encephalopathy?

A

Conversion of ammonia to urea is compromised

43
Q

What are the complications of portal hypertension (3)?

A
  1. Ascites
  2. Splenomegaly
  3. Anastomoses (between portal and systemic circulation)
44
Q

What is anastomoses?

A

Small connections between two blood vessels

45
Q

What is ascites?

A

Abdominal distention with ascitic fluid

46
Q

What are the three causes of ascites?

A
  1. Reduction production of albumin (reduced oncotic pressure of the plasma)
  2. Portal hypertension (increased transudation of fluid into the abdomen)
  3. Hyperaldosteronism (sodium and water retention in the kidneys)
47
Q

Explain why ascites can happen if there is a low level of plasma albumin

A

Albumin is a blood protein

  • keeps water in the blood
  • if Albumin levels are low, water leaves the blood vessels and enters the abdominal cavity
  • happens if the liver is not functioning properly and producing albumin (fatty liver or cirrhosis)
48
Q

Explain why ascites can happen if hyperaldosteronism - what causes this?

A

Caused by cirrhosis

  • Cells of the liver are not breaking down aldosterone
  • Aldosterone rises in circulation - causing the retention of sodium and water
49
Q

What is the relationship between splenomegaly and cirrhosis

A

If the liver is firm - blood gets backed up into the spleen = spleen enlarges
- blood flow to liver is compromised

50
Q

Approximately how much blood volume dose the spleen hold?

A

20% of blood volume

51
Q

What are three consequences of portal-systemic anastomoses? (Which is a consequence of portal-hypertension)

A
  1. Hemorrhoids
  2. Esophageal varices - enlargement of esophageal veins
  3. Caput medusa - prominent periumbilical veins
52
Q

What are the laboratory findings that can be seen in cirrhosis?

A
  1. Serum transaminases (ALT and AST) are elevated
  2. Hypoalbuminemia (loss of liver function)
  3. Blood ammonia elevated (less urea synthesis)
53
Q

What are the distant and systemic complications of cirrhosis?

A
  • jaundice
  • bleeding tendency (low clotting factors)
  • hematemesis (vomiting blood)
  • exsanguination (loss of blood) from esophageal varices
  • hyperestrinism (spider nevi, palmar erythema, gynecomastia, testicular atrophy)
  • hepatic encephalopathy
  • hepatorenal syndrome
54
Q

What is hepatorenal syndrome?

A

When there is something wrong with the liver, there is something wrong with the kidneys

  • we don’t understand the exact mechanism
  • decreased blood flow to kidneys
55
Q

What organ produces bile?

A

Liver

56
Q

What organ stores bile?

A

Gallbladder

57
Q

What are the components of bile (3)?

A
  1. Bile salts
  2. Bile pigments
  3. Cholesterol
58
Q

When do gallstones form?

A

When ratio of bile salts is low compared to other components
(Bile salts make bile soluable)

59
Q

What are 4 disorders of the gallbladder?

A
  1. Cholelithiasis (gallstones)
  2. Acute and chronic cholecystitis
  3. Choledocholithiasis
  4. Cholangitis
60
Q

What is choledocholithiasis?

A

Stones in the common bile duct

61
Q

What is cholangitis?

A

Inflammation of the common bile duct

62
Q

What is acute and chronic cholecystitis caused by?

A

Inflammation caused by irritation due to concentrated bile

63
Q

What are cholelithiasis?

A

Gallstones

64
Q

What are the types of gallstones?

A
  1. Cholesterol
  2. Black stones (polybilirubinate stone)
  3. Brown stones (mixture of calcium and bile pigments)
65
Q

What is the most common form of gallstone?

A

Cholesterol

  • 75 - 80% of stone
  • also called yellow stones
66
Q

What kind of gallstone is common in people with hemolytic anemia or sickle cell anemia?

A

Black stones

67
Q

What is the rarest form of gallstone?

A

Brown stones

68
Q

Where do brown stones form?

A

In the bile DUCTS, not in the gallbladder

- form in association with infection

69
Q

True or False:

Regardless of the type of gallstones, the clinical manifestations are the same

A

True

70
Q

What are some examples of complications that can arise as a result of gallstones?

A
  • Cholycystitis
  • Ulceration of gallbladder wall
  • Cholecystoenteric fistula
  • Obstruction of bile duct system
  • Obstructive jaundice
  • Biliary cirrhosis
  • Cholangitis and liver abscess
71
Q

What happens during a cholecystoenteric fistula?

A

Chronic inflammation of the gallbladder that results in burrowing or tunneling

  • might end up joining the duodenum
  • enzymes present in the duodenum could end up digesting the gallbladder
72
Q

How can pancreatitis be caused by a bile duct obstruction (6 steps)?

A
  1. Gallbladder contracts
  2. Bile is sent down the common bile duct
  3. Blockage forms in Ampulla of Vater (cannot enter duodenum)
  4. Bile goes up PANCREATIC duct
  5. Bile in pancreas disrupts tissues, digestive enzymes become activated
  6. Pancreas starts digesting ITSELF!
73
Q

What does acute pancreatitis manifest with clinically?

A
  • excruciating pain that radiates to the back and to the left
  • results in death in 3 days
  • can be triggered by overeating and overdrinking
74
Q

What are intrahepatic consequences of a biliary obstruction?

A
  • bile flow in the liver slows down
  • bile accumulates for forms plugs in the ducts
  • ducts rupture and damage liver cells
  • liver is unable to continue processing bilirubin
  • increased bile acids in blood and skin
75
Q

If there is an increase in ALP (alkaline phosphatase), what does that suggest?

A

An elevation in blood suggests that there is rupturing of the bile ducts in the liver

  • liver is not able to process bilirubin as normal = jaundice
  • could be post OR hepatic jaundice
76
Q

What is primary biliary cirrhosis?

A

Intrahepatic bile duct inflammation

- autoimmune disease

77
Q

What happens to the wall of the bile duct in primary biliary cirrhosis?

A

Walls become thicker

  • Lymphocytes surround the duct
  • makes the lumen more narrow
78
Q

What is primary sclerosing cholangitis?

A

A chronic inflammatory disease of intrahepatic and extrahepatic BILE DUCTS
- usually associated with ulcerative colitis

79
Q

True or False:

Primary biliary cirrhosis occurs primarily in males

A

False

  • occurs in females
  • b/c it is an autoimmune disease
80
Q

Who is most affected by primary sclerosing cholangitis?

A

YOUNG men

81
Q

What do the bile ducts look like in primary sclerosing cholangitis?

A

Appear beaded with alternating narrow and flared segments

82
Q

What is a common finding in primary sclerosing cholangitis?

A

Jaundice

BHSC 2203 - Patho (13 decks)

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