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BMS150 Post-MT2 > Liver Pathology Part II > Flashcards

Liver Pathology Part II Flashcards

1
Q

Hepatitis Genomes?

A

A, C, D, E - ssRNA
B - dsDNA

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2
Q

Hepatitis routes of transmission

A

A, E - fecal-oral
B - parenteral, sexual transmission
C, D, - parenteral

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3
Q

Hepatitis and chronic liver disease?

A

A - never
B - 5-10%
C - > 80%
D - same as HBV
E - Only immunocomprimised

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4
Q

Diagnosis of hepatitis?

A

A - Serum IgM against HAV
B - Hep B antigens
C - HCV RNA
D - HDV RNA or antibodies against
E - HEV RNA or antibodies against

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5
Q

Syndromes of hepatitis infection? (5)

A
  • Asymptomatic with recovery
  • Acute symptomatic with recovery
  • Chronic hepatitis
  • Fulminant hepatic failure (rare)
  • Long-term untreated HBV or HCV can progress to cirrhosis or carcinoma
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6
Q

Where is hepatitis A common?

A

Places with poorer hygiene

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7
Q

Clinical features of hepatitis A?

A
  • Usually fatigue, nausea, jaundice
  • Often asymptomatic
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8
Q

Hepatitis A is almost always ______ and never enters a chronic carrier state, but can rarely cause _______

A

Self-limited; fulminant hepatic failure

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9
Q

Most prevalent form of hepatitis worldwide?

A

Hepatitis B

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10
Q

Most people worldwide living with hepatitis B acquired it where?

A

At childbirth

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11
Q

Clinical course of hep B? (5)

A
  • Acute hepatitis w/ recovery/clearance
  • Non-progressive chronic hep
  • Progressive chronic disease = cirrhosis
  • Fulminant hepatitis w/ massive liver necrosis
  • Asymptomatic carrier state
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12
Q

What is the best predictor of hepatitis B chronicity?

A

Age

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13
Q

Clinical features of acute HBV? (5)

A
  • Nonspecific constitutional Sx: fever, anorexia
  • Jaundice
  • URQ pain
  • No sx
  • Hepatic failure (rare)
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14
Q

Risk factors for HCV?

A
  • IV drug use
  • Blood transfusions
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15
Q

What are hallmarks of HCV?

A

Persistent infections and chronic hepatitis

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16
Q

What occurs in majority of HCV-infected individuals?

A

Progression to chronic disease

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17
Q

How can chronic HCV be cured?

A

Antiviral regimes are matched to genotype of HCV - commonly 1a or 1b in NA

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18
Q

Most common indication for liver transplantation?

A

HCV

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19
Q

What form needs co-infection with hepatitis B for its life cycle?

A

HDV

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20
Q

Which form of viral hepatitis is from zoonosis resulting in self-limited hepatitis?

A

HEV

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21
Q

Hepatitis E is associated with a very high mortality rate in which population?

A

Pregnant women

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22
Q

3 forms of alcoholic liver injury?

A
  1. Hepatitis
  2. Hepatic steatosis
  3. Steatofibrosis including cirrhosis
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23
Q

Major pathologic pattern of hepatitis?

A
  • Liver cell necrosis
  • Inflammation
  • Mallory bodies
  • Fatty change
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24
Q

Major pathologic pattern of cirrhosis?

A
  • Fibrosis
  • Hyperplastic nodules
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25
Q

Major pathologic pattern of steatosis?

A
  • Fatty change
  • Perivenular fibrosis
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26
Q

Alcohol promotes movement of _________ from the gut into the _______ causing liver inflammation

A

Bacterial endotoxin; liver inflammation

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27
Q

Liver inflammation stimulates the release of ______ from sinusoidal endothelial cells, resulting in ________ and _______ of the activated stellate cells

A

Endothelins; Vasoconstriction and contraction

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28
Q

What are endothelins?

A

Potent vasoconstrictors released from capillary endothelial cells = decreased hepatic sinusoidal perfusion

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29
Q

What is alcohol metabolized into? What can this cause

A

Acetaldehyde = toxic and can cause lipid peroxidation if high concentrations

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30
Q

Alcohol metabolism reduced what? What is the result of this?

A

NAD+ => necessary for fatty acid oxidation therefore fat accumulates in liver

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31
Q

Metabolism of alcohol by CYP2E1 results in what?

A

Free radical production

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32
Q

Cellular findings of alcoholic steatohepatitis? (3)

A
  • Hepatocytes ballooned by accumulation of fat in vacuoles
  • Immune cells surrounded by dying hepatocytes
  • Ubiquitiniylated keratin = collapse of cytoskeleton
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33
Q

Clinical features of alcoholic liver disease?

A

Non-specific sx: malaise, anorexia, weight loss, upper ab discomfort, hepatomegaly

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34
Q

Forms of NAFLD?

A
  • Non-alcoholic steatohepatitis (NASH)
  • Simple hepatic steatosis and steatosis complicated by inflammation
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34
Q

When does alcoholic hepatitis hend to appear?

A

Acutely following bouts of heavy drinking

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35
Q

Is alcoholic steatosis reversible?

A

Usually reversible upon cessation of alcohol use

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35
Q

Most common cause of liver disease in the USA?

A

Non-alcoholic fatty liver disease (NAFLD)

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36
Q

NASH progression?

A
  • 10-20% of cases = liver cirrhosis
  • If cirrhosis, possibly liver cancer
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37
Q

Pathologic findings of NASH?

A
  • Hepatocyte ballooning, lobular inflammation. steatosis
  • Fibrosis => cirrhosis
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38
Q

What is NASH strongly associated with?

A

Obesity and metabolic syndrome

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39
Q

Pathophysiology of NASH is a two hit model involving?

A
  1. Hepatic fat accumulation
  2. Increased oxidative stress
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40
Q

What do free radicals cause?

A

Lipid peroxidation of the accumulated intracellular fat

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41
Q

Obesity seems to be associated with reduced intestinal barrier function, resulting in what?

A

Increased inflammation in the liver

42
Q

Clinical features of NASH?

A
  • Usually asymptomatic until hepatic failure
  • Fatigue and right-sided abdominal pain
  • Increased risk of hepatocellular carcinoma
43
Q

What is a frequent cause of heath in those with NASH?

A

CVD

44
Q

NASH definitive diagnosis?

A

Detection of fibrosis via imaging or biopsy

45
Q

Most common cause of fulminant hepatitis?

A

Drug and toxin-induced liver disease

46
Q

Pathological patterns and clinical presentations of drug and toxin-induced liver disease?

A
  • Insidious onset or rapid
  • Hepatocyte necrosis, cholestasis, or insidious onset liver dysfunction
  • Histologically similar to viral hep
47
Q

Toxins can: (3)

A
  • Be directly toxic
  • Be converted by the lier into an active toxin
  • Elicit an immune response by acting as a hapten
48
Q

Most drugs or toxins affecting the liver can be classified as what?

A
  1. Predictable hepatotoxins
  2. Unpredictable or idiosyncratic hepatotoxins
49
Q

What are predictable hepatotoxins?

A

Dose-dependent, occur in most individuals

50
Q

What are unpredictable or idiosyncratic hepatotoxins?

A

Independent of dose, rare

51
Q

What is the most common hepatotoxin causing acute liver failure?

A

Acetaminophen

52
Q

What is the most common hepatotoxin causing chronic liver failure?

A

Alcohol

53
Q

Acetaminophen in low-doses?

A

95% of the time = Detoxification by phase II enzymes, conjugated and excreted in the urine

54
Q

Acetaminophen in high doses?

A

5% of the time = increased production of NAPQI, if GSH reserves are insufficient, then this molecule will damage hepatocytes

55
Q

Etiology of autoimmune hepatitis?

A
  • Involves attack by cytotoxic T lymphocytes
  • Likely genetic, can be triggered by certain medications (statins) or viral infection
56
Q

Type of autoimmune hepatitis with presence of ANA and anti-smooth muscle antibodies, HLA DR3?

A

Type I (most common)

57
Q

Population that type I autoimmune hepatitis is most common in?

A

Middle-ages to older individuals

58
Q

Type of autoimmune hepatitis with presence of anti-CYP450 antibodies?

A

Type II

59
Q

Population that type II autoimmune hepatitis is most common in?

A

Children and teenagers

60
Q

Prognosis of autoimmune hepatitis?

A
  • Most patients have mild disease = watch and wait with good prognosis
  • Severe untreated has mortality of 40%
61
Q

What is caused by a combination of increased resistance to blood flow
through the portal circulation, and a “hyperdynamic circulation”?

A

Portal hypertension

62
Q

Pre-hepatic causes of portal hypertension?

A

Thrombosis and obstruction of portal vein

63
Q

Intra-hepatic causes of portal hypertension?

A

Cirrhosis from any cause

64
Q

Post-hepatic causes of portal hypertension?

A

Severe R-sided CHF

65
Q

Typical complications of portal hypertension? (4)

A
  • Ascites
  • Formation of portosystemic venous shunts
  • Congestive splenomegaly
  • Hepatic encephalopathy
66
Q

Features of portal hypertension? (7)

A
  • Hepatic encephlaopathy
  • Esophageal varices
  • Splenomegaly
  • Malnutrition
  • Spider angiomas
  • Caput medusae
  • Ascites
67
Q

Why might hyperdynamic circulation occur to intestines and stomach?

A

Possibly impaired lier clearance of vasodilatory substances

68
Q

What are esophageal varices?

A

Collateral veins that allow some drainage to occur, but result in enlarged, fragile, congested subepithelial and
submucosal venous plexus within the distal esophagus

69
Q

Why does cirrhosis result in portal hypertension and the development of varices?

A

Cirrhosis causes necrosis and fibrotic bridging that interrupts the normal flow from triad to hepatic vein = blood being diverted from liver to systemic veins nearby

70
Q

How bad are esophageal varices?

A
  • May rupture and cause massive hematemesis = medical emergency
  • As many as half of patients die from the first bleeding episode
71
Q

Pathology that affects the ducts and ductules within the liver?

A

Intrahepatic biliary tract disease

72
Q

Secondary biliary cirrhosis?

A

Secondary to uncorrected bile duct obstruction of the extrahepatic biliary tree

73
Q

Primary biliary cirrhosis (PBC)?

A
  • Autoimmune, non-supparative inflammation that destroys the intrahepatic bile ducts
  • Portal inflammation leads to scarring and eventually cirrhosis
74
Q

Primary sclerosing cholangiitis (PSC)?

A
  • Intrahepatic and extrahepatic bile ducts become inflamed and the ducts become obliterated
  • The unaffected areas dilate, leading to the appearance of ‘beads on a string’
75
Q

Major initial presentation of primary biliary cirrhosis (PBC)?

A
  • Pruritus
  • Fatigue
  • Abdominal discomfort
76
Q

What are later presentations of PBD?

A
  • Skin pigmentation
  • Xanthelasmas
  • Steatorrhea
  • Vitamin D malabsorption
77
Q

Pathogenesis of PBC?

A

Anti-mitochondrial antibodies against pyruvate DH and T cells that recognize this antigen are present

78
Q

Major initial presentation of primary sclerosing cirrhosis (PSC)?

A
  • Fatigue
  • Pruritis
  • Jaundice
79
Q

Later presentation of PSC?

A
  • Chronic liver disease => cirrhosis usually occur
  • 7% develop cholangiocarcinoma
  • Increased risk of colon cancer
80
Q

Pathophysiology of PSC?

A
  • Likely autoimmune
  • Associated with HLA-B8 and p-ANCA
81
Q

PSC epidemiology?

A
  • Presents in early adulthood-middle age
  • M > F
  • Greatly increased in those with ulcerative colitis
82
Q

Specific pathologic findings for PBC?

A
  • Destruction of interlobular bile ducts
  • Patchy involvement (not all ducts)
  • Severe cholestatic findings at end-stages and hepatomegaly
83
Q

Specific pathologic findings for PSC?

A
  • Large duct inflammation similar to UC
  • Strictures can develop
  • Smaller ducts often have little inflammation and show “onion skin” fibrosis
  • Similar severe cholestatic findings at end-stage as PBC
84
Q

Acute inflammation of the gallbladder, precipitated 90% of the time by obstruction of the neck or cystic duct

A

Acute cholecystitis

85
Q

Most common reason for emergency cholecystectomy?

A

Acute cholecystitis

86
Q

What causes acute cholecystisis?

A

Results from chemical irritation and inflammation of the obstructed gallbladder

87
Q

In acute cholecystitis, mucosal phospholipases _____ luminal lecithins to what?

A

Hydrolyze; toxic lysolecithins

88
Q

In acute cholecystitis, what happens to the normally protective mucous layer, what does this cause?

A

Layer is disrupted => exposing mucosal epithelium to bile salt detergent action

89
Q

In acute cholecystitis, PGs released and GB distention cause what?

A

Inflammation = dysmotility

90
Q

Clinical features of acute cholecystitis?

A
  • Begins with progressive RUQ pain
  • Mild fever
  • Anorexia
  • Tachycardia
  • Sweating
  • Nausea and vomiting
91
Q

What are most patients with acute cholecystitis free of?

A

Jaundice

92
Q

In acute cholecystitis, what will rupture cause?

A

Severe peritonitis and bleeding

93
Q

Chronic cholecystitis is associated with that in >90% of cases?

A

Cholelithiasis

94
Q

Why is the cause of chronic cholecystitis obscure?

A

Not clear that gallstones play a direct role in initiation of inflammation or pain

95
Q

What does supersaturation of bile do?

A

Predisposes to chronic inflammation

96
Q

Clinical features of chronic cholecystitis?

A

Recurrent attacks of either steady or colicky epigastric or RUQ pain

97
Q

Complications of chronic cholecystitis?

A
  • Bacterial superinfection with cholangitis or sepsis
  • GB perforation/local abscess formation
  • Biliary enteric fistula
    Porcelain GB
98
Q

What is porcelain GB?

A

Dystrophic calcification within the wall of the gall bladder, greatly increases risk of cancer

99
Q

Bacterial infection of the bile ducts?

A

Cholangitis

100
Q

What can cholangitis be a result of?

A

Any lesion that creates obstruction to bile flow, most commonly choledocholithiasis and biliary strictures

101
Q

What bacteria can cause cholangitis?

A

Gram (-) aerobes: E. coli, Klebsiella, Enterococcus, Enterobacter

102
Q

Clinical presentation of cholangitis?

A
  • Acute onset fever, chills, abdominal pain, jaundice
  • Acute inflammation of bile duct walls = entry of neutrophils
103
Q

What is the main concern of cholangitis?

A

Sepsis

BMS150 Post-MT2 (17 decks)

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