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Gastrointestinal II Exam #2 > Pathology of the Liver > Flashcards

Pathology of the Liver Flashcards

1
Q

Which 3 cytosolic hepatocellular enzymes indicate hepatocyte injury?

A

AST

ALT

LDH

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2
Q

What labs can help determine biliary excretory function? (5)

A

Substances normally secreted in bile

  • serum BR (total and direct only)
  • urine BR
  • serum bile acids

Plasma membrane enzymes

  • ALP
  • GGT
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3
Q

What labs/tests can help determine hepatocyte synthetic function? (4)

A

Proteins secreted into the bloodstream

  • serum albumin
  • coagulation factors

Hepatocyte metabolism

  • serum ammonia
  • aminopyrine breath test (hepatic demethylation)
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4
Q

What is the definition of acute liver failure?

A

Acute liver illness with encephalpathy and coagulopathy that occurs within 26 weeks of initial liver injury in the absence of pre-existing liver disease

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5
Q

What are the major causes of acute liver failure?

A

Massive hepatic necrosis from drugs or toxins
-acetaminophen ingestion (50%)

Autoimmune hepatitis and Hep. A and B account for the other 50%

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6
Q

What is the clinical course of acute liver failure?

A

Manifests first with N/V and jaundice, followed by life-threatening encephalopathy and coagulation defects.

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7
Q

What is the pathological/morphological course of acute liver failure?

A
  • The liver typically enlarges at first due to inflammation and edema. ALT/AST are elevated.
  • As the process continues and the parenchyma is destroyed, the liver shrinks.
  • Jaundice, coagulopathy and encephalopathy can confirm the suspicion of extensive hepatic damage.
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8
Q

What is a sign of significant damage in ALF?

A

If ALT/AST declines as the parenchyma is destroyed and the liver shrinks

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9
Q

List other possible manifestations of ALF (5)

A

Changes in bile formation

Hepatic encephalopathy: mental status changes and asterixis; elevated ammonia

Coagulopathies

Portal HTN

Hepatorenal syndrome

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10
Q

What are the 3 most common causes of chronic liver failure worldwide?

A

Chronic Hep. B

Chronic Hep. C

NAFLD

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11
Q

Which liver enzyme tends to be more elevated in CLF?

A

ALT>AST

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12
Q

What are the clinical features of CLF?

A

Approx. 40% of patients with cirrhosis are asymptomatic until the most advanced stages of disease. When symptomatic, they present with non-specific manifestations; anorexia, weight loss, weakness, jaundice, ascites, etc.

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13
Q

What can cause pruritis in a patient with CLF?

A

Chronic jaundice

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14
Q

What hormone might be elevated in males with CLF? What does it cause?

A

Hyperestrogenemia - leads to palmer erythema, spider angiomas of the skin, hypogonadism and gynecomastia

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15
Q

What are examples of pre-,intra- and post-hepatic portal HTN?

A

Pre-: obstruction of the portal v.

Intra-: liver parenchymal disease

Post-: RSHF, constrictive pericarditis, outflow obstruction

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16
Q

Hep. A

Type of virus

Viral family

Route of transmission

Mean incubation period

Frequency of CLD

Diagnosis

A

Type of virus - ssRNA

Viral family - hepatovirus

Route of transmission - fecal-oral

Mean incubation period - 2-6 wks.

Frequency of CLD - never

Diagnosis - IgM Abs

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17
Q

Hep. B

Type of virus

Viral family

Route of transmission

Mean incubation period

Frequency of CLD

Diagnosis

A

Type of virus: partial dsDNA

Viral family - hepadnavirus

Route of transmission - parenteral, sexual contact, perinatal

Mean incubation period - 2-26 wks.

Frequency of CLD - 5-10%

Diagnosis - HBsAg or Ab to HBsAg

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18
Q

Hep. C

Type of virus

Viral family

Route of transmission

Mean incubation period

Frequency of CLD

Diagnosis

A

Type of virus - ssRNA

Viral family - flaviridae

Route of transmission - parenteral, intra-nasal cocaine

Mean incubation period - 4-26 wks.

Frequency of CLD - >80%

Diagnosis - 3rd gen. ELISA for Ab

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19
Q

What is autoimmune hepatitis?

A

Chronic, progressive hepatitis with autoimmune features

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20
Q

Which patients are at the greatest risk for autoimmune hepatitis?

A

Caucasians, F>M

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21
Q

DRB1 allele is associated with:

A

Autoimmune hepatitis

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22
Q

Which patients are most likely to develop type 1 autoimmune hepatitis vs. type 2?

A

Type 1: middle-aged and older

Type 2: children and teens

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23
Q

Which labs are positive in type 1 autoimmune hepatitis (4) vs. type 2 (1)?

A

Type 1: + ANA, + SMA, + anti-SLA/LP, + AMA

Type 2: + anti-LKM-1

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24
Q

What morphological changes occur to the liver in acetaminophen injury?

A

CYP450 toxicity leads to death of hepatocytes in zone 3, while hepatocytes in zone 2 take over metabolic demands and can die, too. In severe, overdoses, the periportal hepatocytes may die and lead to ALF.

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25
Q

What neoplastic lesion can occur to the liver with anabolic steroids and oral contraceptives? What is its course?

A

Hepatocellular adenoma - benign, but can rupture and cause significant blood loss. 3 sub-types exist and each have their own risk of malignancy.

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26
Q

What can contribute to developing the following neoplasms?

Hepatocellular adenoma
Hepatocellular carcinoma
Cholangiocarcinoma
Angiosarcoma

A

Hepatocellular adenoma: OC, anabolic steroids

Hepatocellular carcinoma: alcohol, thorotrast

Cholangiocarcinoma: thorotrast

Angiosarcoma: thorotrast, vinyl chloride

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27
Q

What are the 3 stages of progression of alcholic liver disease?

A
  1. Hepatic steatosis (fatty liver)
  2. Alcoholic hepatitis
  3. Alcoholic steatofibrosis (alcoholic cirrhosis)
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28
Q

What lab findings are associated with hepatic steatosis?

What happens to the size of the liver?

A

Increased BR and ALP

Hepatomegaly - enlarges

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29
Q

Under what circumstances might hepatic steatosis be reversible?

A

If the patient abstains from drinking and there is no evidence of fibrosis/cirrhosis

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30
Q

What develops morphologically in alcoholic hepatitis? (3)

A

Hepatocytes swell (ballooning)

Mallory-Denk bodies (cytoskeleton breakdown) become apparent.

Neutrophils and inflammation appear.

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31
Q

What does the liver look like grossly in alcoholic steatofibrosis?

A

The liver is brown, shrunken and non-fatty

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32
Q

What liver enzyme tends to be more elevated in alcoholic steatofibrosis?

A

AST>ALT

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33
Q

Mallory-Denk bodies =

A

Alcoholic hepatitis

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34
Q

What causes NAFLD primarily?

A

Metabolic syndrome, obesity

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35
Q

What liver enzyme tends to be more elevated in NAFLD?

A

ALT>AST

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36
Q

AST>ALT

A

Alcoholic steatofibrosis (cirrhosis)

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37
Q

ALT>AST

A

Chronic liver failure

NAFLD

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38
Q

What morphologic change occurs in alcoholic steatofibrosis?

A

“Chicken-wire fibrosis”: sinusoidal and centrilobular fibrosis begins with sclerosis of the central v. and spreads outward

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39
Q

Which gender have a greater susceptibility for alcholic liver disease? Why?

Which ethnicity tends to be at greater risk?

A

Females are more susceptible, but men tend to get it more often because there are more male alcoholics. It is thought that this occurs due to the estrogen-dependent response to gut-derived endotoxin (LPS).

AA>W

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40
Q

In order to classify as Metabolic Syndrome, there must be 1 of the following:

And 2 of the following:

A

1 of the following:

  • DM
  • impaired glucose tolerance
  • impaired fasting glucose
  • insulin resistance

2 of the following:

  • BP > 140/90
  • dyslipidemia
  • central obesity
  • microalbuminemia
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41
Q

NAFLD is defined as…

A

A spectrum of disorders that have in common the presence of hepatic steatosis (fatty liver) and do not consume exorbitant amounts of alcohol.

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42
Q

What is the 2-hit pathogenesis for NAFLD?

A
  1. Insulin resistance gives rise to hepatic steatosis

2. Hepatocellular oxidative injury resulting in hepatocyte necrosis and inflammatory reactions to it

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43
Q

How does the morphology of NAFLD differ from alcoholic hepatitis?

A

Looks almost identical to alcoholic hepatitis, except:

-mononuclear cells tend to be more prevalent than neutrophils or Mallory-Denk bodies

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44
Q

What is the progression of NAFLD?

A

NAFLD can cause isolated fatty liver disease (80%) or NASH.

NASH can go on to cause NASH cirrhosis (11% over 15 years) or HCC directly.

NASH cirrhosis can lead to decompensation (31% over 8 years) or HCC.

Figure 18-23

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45
Q

a-1 ATD pathogenesis

What is unique about the genetics?

What stain is positive?

A

AR disorder causing decreased a1-AT which allows elastase to accumulate. This causes panacinar emphysema and cirrhosis due to buildup of abnormal proteins.

It is codominant; mutations in the PiZ is most clinically significant.

PAS stain

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46
Q

What mutation and its heredity is associated with Wilson disease? What is its function?

A

AR mutation in ATP7B - impaired Cu excretion into bile and failure to incorporate Cu into ceruloplasmin.

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47
Q

Where does Cu accumulate in Wilson disease?

A

Liver, brain and eyes

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48
Q

How does Cu accumulation lead to damage in Wilson disease? (3)

A

ROS produced by the Fenton reaction

Cu binds sulfhydryl groups of cellular proteins

Cu displaces other metals from hepatic metalloenzymes

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49
Q

What morphological features are classic in extensive Wilson disease?

A

Mild to moderate fatty change in the liver.

Kayser-Fleischer rings (green to brown deposits of Cu in the cornea) are present if there is eye involvement.

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50
Q

What are the clinical features of Wilson disease? What age does it most often develop?

A

6-40 y/o

Neurologic involvement presents as movement disorders or rigid dystonia (may appear Parkinson-like) and possible psychiatric involvement.
Hemolytic anemia due to toxicity to RBC membranes.

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51
Q

What lab findings may indicate Wilson disease? (3)

A

Decreased serum ceruloplasmin
Increased hepatic Cu content
Increased urinary excretion of Cu

Presence of K-F bodies in the eye can also help with diagnosis

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52
Q

Which organs does iron get deposited in Hemochromatosis? What can each cause? (4)

A

Pancreas - DM
Joints - OA
Heart - CM
Skin - bronzing

53
Q

Iron causes buildup of ROS. What are 3 manners of cell injury mediated by iron excess?

A

Lipid peroxidation

Stimulation of collagen formation by activating hepatic stellate cells

ROS interaction with DNA causes cell injury

54
Q

What is the function of hepcidin?

A

Hepcidin lowers plasma iron levels, so a deficiency of hepcidin leads to iron overload.

55
Q

What mutation is most associated with the development of Hemochromatosis?

A

HFE

56
Q

Which mutations can lead to severe juvenile hemochromatosis?

A

HAMP and HJV

57
Q

What is the most common cause of death in hemochromatosis if left untreated?

A

HCC

58
Q

What stain is useful in diagnosing hemochromatosis?

A

Prussain blue stain

59
Q

What is an acquired (non-genetic) cause of hemochromatosis?

A

Recurrent blood transfusions (sickle cell disease, etc.)

60
Q

What are 2 causes of predominantly conjugated hyperbilirubinemia?

A

Deficiency of canalicular membrane transporters (Dubin-Johnson syndrome, Rotor syndrome)

Impaired bile flow (duct obstruction or autoimmune cholangiopathies)

61
Q

What are 3 “big picture” causes of predominantly unconjugated hyperbilirubinemia?

A

Excess BR production

Reduced hepatic uptake of BR

Impaired BR conjugation

(Crigler-Najjar syndrome type I and type II, Gilbert syndrome)

62
Q

Crigler-Najjar syndrome type I

Inheritance

Defects in BR metabolism

Liver pathology?

Clinical course

A

Inheritance: AR

Defects in BR metabolism: absent UGT1A1 activity

Liver pathology? None

Clinical course: fatal in neonatal period

63
Q

Crigler-Najjar syndrome type II

Inheritance

Defects in BR metabolism

Liver pathology?

Clinical course

A

Inheritance: AD with variable penetrance

Defects in BR metabolism: decreased UGT1A1 activity

Liver pathology? None

Clinical course: generally mild, occasional icterus

64
Q

Dubin-Johnson syndrome

Inheritance

Defects in BR metabolism

Liver pathology?

Clinical course

A

Inheritance: AR

Defects in BR metabolism: impaired biliary excretion of BR glucuronides due to mutations in MRP2

Liver pathology? Pigmented cytoplasmic globules

Clinical course: innocuous

65
Q

Rotor syndrome

Inheritance

Defects in BR metabolism

Liver pathology?

Clinical course

A

Inheritance: AR

Defects in BR metabolism: possible decreased hepatic uptake/storage; decreased biliary excretion

Liver pathology? None

Clinical course: innocuous

66
Q

Gilbert syndrome

Inheritance

Defects in BR metabolism

Liver pathology?

Clinical course

A

Inheritance: AR

Defects in BR metabolism: decreased UGT1A1 activity

Liver pathology? None

Clinical course: innocuous

67
Q

What is the cause of cholestasis?

A

Impaired bile formation and bile flow that gives rise to accumulation of bile pigment in the hepatic parenchyma.

It can be caused by extra-hepatic or intra-hepatic obstruction of bile channels, or defects in hepatocytes bile secretion.

68
Q

What are some clinical signs of cholestasis? (5)

A

Jaundice

Pruritis

Xanthomas

Malabsorption

Vitamin ADEK deficiencies

69
Q

What are the lab findings in a patent with cholestasis?

A

Increased ALP and GGT (enzymes present on apical membranes of hepatocytes and bile duct epithelial cells)

70
Q

Primary biliary cirrhosis

Age of onset

Gender

Clinical course

Associated conditions

Serology

Radiology

Duct lesion

A

Age of onset: 30-70 y/o (median is 50 y/o)

Gender: 90% female

Clinical course: progressive

Associated conditions: Sjogren’s (70%), Scleroderma (5%), Thyroid disease (20%)

Serology: 95% + AMA, 50% + ANA, 40% + ANCA

Radiology: normal

Duct lesion: florid duct lesions and loss of small ducts only

71
Q

Primary sclerosing cholangitis

Age of onset

Gender

Clinical course

Associated conditions

Serology

Radiology

Duct lesion

A

Age of onset: 30 y/o (median age)

Gender: 70% male

Clinical course: unpredictable, but progressive

Associated conditions: IBD (70%), Pancreatitis (<25%), Retroperitoneal fibrosis

Serology: 65% + ANCA, 6% + ANA

Radiology: strictures and beading of large bile ducts

Duct lesion: inflammatory destruction of extra-hepatic and large intra-hepatic ducts

72
Q

What are the 2 autoimmune cholangiopathies?

A

Primary biliary cirrhosis and Primary sclerosing cholngitis

73
Q

What 2 pathologies can result in impaired blood flow into the liver?

A

Hepatic a. compromise

Portal v. obstruction and thrombosis

74
Q

What causes hepatic a. compromise?

A

Thrombosis or compression of an intra-hepatic branch of the hepatic a. by embolism, neoplasia, etc. can cause necrotic damage to the liver. These liver infarcts are rare, because of the dual blood supply (portal v. and hepatic a.).

75
Q

Portal v. obstruction and thrombosis can occur extra-, and intra-hepatically. What are the causes of each?

A

Extra-hepatic: idiopathic (30%), or some degree of obstruction of the portal v. prior to reaching the liver (intra-abdominal sepsis, hypercoagulability, trauma, HCC, cirrhosis, etc.)

Intra-hepatic: portal v. radicles obstructed by acute thrombosis -> lines of Zahn

76
Q

What is the most common cause of small portal v. branch obstruction (causing impaired blood flow into the liver)?

A

Schistosomiasis

77
Q

What are the 3 major manifestations of impaired blood flow into the liver (Hepatic a. compromise, Portal v. obstruction and thrombosis)?

A

Esophageal varices

Splenomegaly

Intestinal congestion

78
Q

What is the most common cause of impaired intra-hepatic blood flow?

What are 6 other, less likely, causes?

A

Cirrhosis

Sickle cell disease
DIC
Eclampsia
Malignancy
Peliosis hepatitis - sinusoidal dilation from impeded efflux of hepatic blood
Bartonella infection
79
Q

What are 4 major manifestations of impaired intra-hepatic blood flow?

A

Ascites (cirrhosis)

Esophageal varices (cirrhosis)

Hepatomegaly

Elevated liver enzymes

80
Q

What are the 2 major causes of hepatic venous outflow obstruction?

A

Hepatic v. thrombosis (Budd-Chiari syndrome) and Sinusoidal obstruction syndrome

81
Q

What is the pathogenesis of Budd-Chiari syndrome?

A

Obstruction of >/2 major hepatic vv. produces liver enlargement, pain and ascites = Budd-Chiari syndrome

82
Q

What causes sinusoidal obstruction syndrome?

A

Toxic injury to the sinusoidal endothelium

83
Q

What are 5 major manifestations of hepatic v. outflow obstruction?

A

Ascites

Hepatomegaly

Abdominal pain

Elevated liver enzymes

Jaundice

84
Q

What is the common cause of nodular regenerative or focal nodular hyperplasia?

A

Focal or diffuse alterations in hepatic blood supply, arising from obliteration of portal v. radicles and compensatory augmentation of arterial blood supply.

85
Q

What is the major risk factor for developing hepatic adenomas?

A

Oral contraceptives

86
Q

What is a clinical complication of hepatic adenomas?

A

They can rupture and cause excessive abdominal bleeding

87
Q

Hepatoblastoma is the most common liver tumor of:

What is a genetic mutation associated with it?

What is the outcome?

A

Young children (<3 y/o)

WNT pathway, including mutations in APC gene

If untreated, the tumor is usually fatal within a few years, but therapy has raised the 5-year survival to 80%

88
Q

What are the most important factors in hepatocarcinogenesis?

At what age does it present? What sex is at greater risk?

A

Viral infections (HBV, HCV) and toxic injuries (aflatoxin, EtOH)

<60 y/o, M>F

89
Q

What are the 2 most common early mutational events in development of HCC?

A

B-catenin activation and p53 inactivation

90
Q

HCC may appear grossly in which forms? (3)

A

Unifocal mass

Multifocal, widely distributed nodules of variable size

Diffusely infiltrative cancer

91
Q

Cholangiocarcinoma (CCA) begins where?

What is its prognosis generally?

A

In the biliary tree, arising from bile ducts within and outside of the liver.

Poor prognosis generally.

92
Q

What is a Klatskin tumor?

A

An extra-hepatic form of perihilar tumors from CCA

93
Q

What are the precursor lesions of CCA?

A

Biliary intra-epithelial neoplasias (low to high grade, BiIIN-1, -2, or -3 (-3 is highest risk for malignant transformation))

94
Q

What are some risk factors for CCA? (2)

A

Liver fluke infections (Opisthorchis, Clonorchis)

Chronic inflammatory disease of bile ducts

95
Q

Angiosarcoma is mainly associated with which toxins?

A

Vinyl chloride and Thorotrast

96
Q

In what population is a hepatic lymphoma most prominent?

What are the 3 important sub-types?

A

M>F

Diffuse large B-cell lymphomas - most common
MALT lymphomas
Hepatosplenic delta-gamma T cell lymphoma - most common in young males

97
Q

What 4 primary tumors sites often metastasize to the liver?

A

Colon
Breast
Lung
Pancreas

98
Q

Ground glass hepatocyte is present on biopsy. Likely diagnosis?

A

Hep. B

99
Q

How do hepatic stellate cells contribute to scar formation in the liver?

A

Hepatic stellate cells (in the quiescent form) store vitamin A, but in several forms of acute and chronic injury, they can be cativated and converted into highly fibrogenic myofibroblasts.

100
Q

What are the 2 major mechanisms of liver regeneration?

A
  1. Proliferation of remaining hepatocytes

2. Repopulation from progenitor cells

101
Q

What are 4 unique signs of CLF in males?

A

Palmer erythema
Spider angiomata
Hypogonadism
Gynecomastia

102
Q

What is the best predictor of chronicity in HBV?

A

Age at time of infection (younger patients have higher risk of chronicity)

103
Q

Hallmark of chronic hepatitis

A

Portal chronic inflammation

104
Q

Hallmark of progressive chronic liver damage

A

Scarring

105
Q

What is interface hepatitis?

A

It is a feature of viral hepatitis, as well as AIH and steatohepatitis.

It is associated with a lymphocytic infiltrate into the adjacent parenchyma along with destruction of individual hepatocytes along the edges of the portal tract.

106
Q

Characteristic feature of chronic viral hepatitis due to HCV

A

Portal tract expansion by a lymphoid follicle

107
Q

Major extrahepatic cause of cholestasis in adults is…

A

LDO - large duct obstruction

108
Q

“Giant cell transformation” =

A

Neonatal hepatitis

109
Q

What is the single most frequenct cause of death from liver disease in early childhood?

What is the definition of it?

What are the 2 forms?

A

Biliary atresia - complete or partial obstruction of the lumen of the extrahepatic biliary tree within the first 3 months of life.

Fetal: 20%
Perinatal: 80%

110
Q

+ AMA should make you think…

A

PBC

111
Q

+ ANCA should make you think…

A

PSC

112
Q

“Onion-skinning”

A

PSC

113
Q

What are choledochal cysts?

A

Congenital dilations of the common bile duct

114
Q

What is fibropolycytic disease of the liver?

Von Meyenburg complexes
Caroli disease
Caroli syndrome

A

They are a group of lesions in which the primary abnormalities are congenital malformations of the biliary tree

Von Meyenburg complexes = hamartomas
Caroli disease = simple multiple biliary cysts
Caroli syndrome = Caroli disease + congenital hepatic fibrosis

115
Q

Most common cause of jaundice in pregnancy is:

A

Viral hepatitis

116
Q

Pre-eclampsia and eclampsia

A

Maternal HTN, proteinuria, edema and coagulation abnormalities (pre-eclampsia)

When hyperreflexia and convulsions occur it is termed eclampsia and can be life threatening

117
Q

Cholestasis of pregnancy

A

Onset of pruritis in the 3rd trimester, followed, in some cases, by dark urine and light stools and jaundice

118
Q

Acute fatty liver of pregnancy can present as..

A

A spectrum of disorders ranging from subclinical or modest hepatic dysfunction to hepatic failure, coma and death.

119
Q

Focal nodular hyperplasia definition:

What age?

A

A single well-demarcated lesion with a central scar that arises spontaneously in an otherwise normal liver.

Young to middle-aged adults

120
Q

Nodular regenerative hyperplasia definition:

What can develop as a result?

What are 2 associations?

A

Multiple nodules (looks like cirrhosis) but no fibrous septa.

Portal HTN

HIV, rheumatologic dz

121
Q

Most common benign neoplasm of the liver:

Which gender is at a bigger risk?

How is it discovered?

A

Cavenrous hemangioma

F>M

Incidental discovery or a cause of hemorrhage due to subcapsular location

122
Q

What are the 3 sub-types of hepatic adenomas?

What are the risk for malignancies of each? What morphologic changes occur?

A

HNF1-ainactivated adeoma - no risk; fatty with no atypia

B-catenin activated adenoma - very high risk; B-catenin and dysplasia

Inflammatory adenoma - small but definite risk; CRP and amyloid A

123
Q

What are the 2 anatomic variants of Hepatoblastomas?

A

Epithelial type - composed of fetal or embryonal cells

Mixed epithelial and mesenchymal type - primitive mesenchyme, osteoid, cartilage or striated muscle

124
Q

What is the fibrolamellar variant of HCC?

A

Only 5% of cases, but 85% of them occur under age 35. It presents as a single large, hard “scirrhous” tumor with fibrous bands coursing through it.

125
Q

If + SMA, you should think…

A

AIH type I

126
Q

In HCC, what is the clinical importance of large cell and small cell pre-malignant lesions? What disease are they associated with?

A

Large cell: increased risk for HCC
Small cell: pre-malignant changes

They’re associated with CLD

127
Q

What is the clinical importance of low grade dysplasia and high grade dysplasia in the development of HCC?

A

Low grade: suggest an increased risk for HCC

High grade: “most important primary pathway for emergence of HCC in viral hepatitis and alcoholic liver disease”

128
Q

What morphological change occurs in pre-eclampsia?

A

Periportal sinusoids contain fibrin deposits associated with hemorrhage into the space of Disse.

129
Q

What is the primary hepatolithiasis? What does it lead to?

A

Disorder of intrahepatic gallstone formation that leads to:

  • repeated bouts of ascending cholangitis
  • progressive destruction of hepatic parenchyma
  • increased risk for hepatic neoplasia

Gastrointestinal II Exam #2 (3 decks)

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