Unit 4 - Liver 2 Flashcards

1
Q

What does Fusobacterium necrophorum do to the liver?

A

it causes liver necrosis

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2
Q

What is the pathogenesis of liver necrosis caused by Fusobacterium necrophorum?

A
  1. Fusobacterium necrophorum is present in the rumen 2. Ruminal acidosis 3. Loss of ruminal mucosal integrity 4. Fusobacterium necrophorum enters portal circulation 5. Liver becomes infected 6. liver necrosis
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3
Q

What microscopic pattern is observed in a liver with an ascending bacterial infection via the biliary tree?

A

there is inflammation involving the bile ducts and adjacent liver with neutrophils as an infiltrate (+/- lymphocytes and plasma cells)

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4
Q

What two liver flukes are the cause of hepatic trematodosis in the United States?

A

Fasciola hepatica and Fascioloides magna

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5
Q

How can liver flukes cause liver damage?

A
  1. the larvae wonder through the liver for more than a month causing necrosis with eosinophils and fibrous tracts or 2. adults in the bile ducts or in cysts in the liver causing cholangiohepatitis
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6
Q

What liver lesion is associated with ascarid larval migration in the pig?

A

milk spot liver - randomly scattered irregular, slightly depressed, firm, white lesions

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7
Q

What typically causes hepatic necrosis?

A

hypoxia and hepatotoxins

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8
Q

What gross lesions are associated with hepatic necrosis?

A

diffuse injury to a specific region of the hepatic lobule leads to an accentuated lobular pattern

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9
Q

Microscopically, what does centrilobular necrosis indicate as the potential differential?

A

hypoxia or metabolized hepatotoxins

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10
Q

Microscopically, what does mid-zonal necrosis indicate as the potential differential?

A

hexachlorophene or alphatoxins

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11
Q

Microscopically, what does periportal necrosis indicate as the potential differential?

A

direct-acting hepatotoxins

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12
Q

Microscopically, what does massive neccrosis indicate as a potential differential?

A

specific toxins or specific infectious agents

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13
Q

What are some special attributes of the centrilobular region?

A

part of the lobule with the lowest oxygen tension and part of the lobule with the greatest concentration of cytochrome P-450 mixed function oxidases

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14
Q

What is the most common cause of centrilobular necrosis?

A

hypoxia

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15
Q

What can cause hypoxia?

A

anemia, pneumonia/pulmonary edema, passive congestion due to heart failure, or shock

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16
Q

Where is the highest concentration of mixed function oxidases found?

A

in centrilobular hepatocytes

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17
Q

What gross changes are seen with centrilobular necrosis?

A

you will see an accentuated lobular pattern +/- hepatomegaly

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18
Q

What microscopic changes do you see with centrilobular necrosis?

A

dgeneration and loss of centrilobular hepatocytes

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19
Q

What are the two major types of hepatotoxins?

A

toxins that cause direct hepatocellular injury or toxins that are transformed by liver to toxic metabolies

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20
Q

Where is the expected pattern of injury to occur with toxins that cause direct hepatocellular injury?

A

periportal

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21
Q

Where is the expected pattern of injury to occur with toxins transformed by the liver into toxic metabolites?

A

centrilobular

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22
Q

What does carbon tetrachloride metabolize into and what does it do to the liver?

A

trihalomethane leads to oxygen free radical formation and centrilobular hepatocyte necrosis

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23
Q

Where does periportal necrosis occur?

A

around vessels in portal triads

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24
Q

What is periportal necrosis seen most commonly with?

A

direct-acting hepatotoxins

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25
Midzonal necrosis is uncommon. What species is it seen in and why?
it is seen in pigs and horses with aflatoxicosis and cats with hexachlorophene
26
What can cause massive hepatic necrosis?
toxins, infectious agents, and nutrition
27
What are some examples of causes of massive hepatic necrosis?
hepatosis dietetica (swine), blue-green algae, poisonous mushrooms
28
Can the liver regenerate itself?
yes, when needed it has remarkable regenerative abilities by replicating mature hepatocytes and progenitor cells
29
What are some consequences of severe and/or chronic injury to the liver?
fibrosis, biliary proliferation, or nodular regeneration
30
What does fibrosis result from?
repetitive injury or massive necrosis with damage to ECM scaffold
31
What is the process of fibrosis in the liver?
the activated hepatic stellate cells proliferate and produce increased extracellular matrix
32
What does hepatic fibrosis represent?
a wound healing response to liver injury from a wide variety of etiologies
33
What gross changes are associated with hepatic fibrosis?
irregular surface, shrunken/smaller in size, firm (fibrotic), and pale
34
How does injury lead to bile duct proliferation?
the release of cytokines at injured limiting plates causes the bile duct to proliferate
35
What can cause biliary hyperplasia?
biliary obstruction, periportal inflammation and fibrosis, sustained attempts at regeneration, and toxins (phomopsin, pyrrolizidine alkaloids, and aflatoxin)
36
What is nodular regeneration due to?
the loss of the extracellular matrix and the presence of fibrosis, regeneration is typically nodular
37
Why does nodular regeneration lead to diminished functional capacity?
regenerative nodules + fibrosis leads to an abnormal blood flow in and abnormal bile flow out
38
What is cirrhosis?
the combination of fibrosis, biliary proliferation, and nodular regeneration
39
What do the changes in a cirrhotic liver lead to?
distortion of the liver parenchyma, altered blood flow, and the potential development of liver failure
40
What clinical issues are associated with cirrhosis?
ascites and hypoproteinemia
41
What gross changes are seen with cirrhosis?
livers are smaller than normal with an irregular surface, pale in color, firm and fibrotic, and numerous nodules throughout the parenchyma
42
What microscopic changes are associated with cirrhosis?
bridging fibrosis, nodular regeneration, biliary proliferation, +/- chronic inflammation
43
What can cause cirrhosis?
chronic toxicity, chronic cholangitis and/or obstruction, chronic congestion, chronic inherited disorders of copper or iron metabolism, chronic hepatitis
44
What agents are potentially associated with cirrhosis?
toxins, drugs, copper, infectious agents
45
What canine breeds are predisposed to chronic hepatitis?
American and English cocker spaniel, West Highland white terrier, Laborador retriever, doberman pinscher, and scottish terriers
46
What age dog is cirrhosis commonly found in?
8 year old dogs
47
What are some lesions that can happen to the gall bladder?
cystic hyperplasia, mucocele, cholelithiasis, cholecystitis, and gall bladder distention
48
What is cystic hyperplasia of the gall bladder?
hyperplasia of the mucosal epithelium in the gall bladder with multilobular gelatinous mucosal cysts due to the dilation of deep invaginations of surface epithelium
49
What is a mucocele?
an abnormal, intraluminal accumulation of inspissated bile and/or mucous within the gallbladder
50
What is cholelithiasis?
formation of stones from inspissated bile
51
What is cholecystitis?
inflammation of gall bladder (mucosa/wall)
52
What species does gallbladder cystic mucosal hyperplasia occur in?
dogs and sheep
53
True or False: Gallbladder cystic mucosal hyperplasia is a commoon incidental aging change in dogs
TRUE
54
Is gallbladder cystic mucosal hyperplasia a significant finding in dogs?
no
55
What dogs seem to be predisposed to gallbladder mucoceles?
older, small to medium breed dogs
56
What clinical signs are associated with gallbladder mucoceles?
vomiting, lethargy, anorexia, abdominal pain, icterus, and polyuria-polydipsia
57
In the case of a gallbladder mucocele, what does serum biochemistry usually reveal?
increased liver enzymes
58
What are some predisposing factors to mucoceles?
hyperlipidemias, hypothyroidism, hyperadrenocorticism, and poor gallbladder motility
59
What can rupture of a gallbladder mucocele lead to?
peritonitis
60
What is the pathogenesis of cholelithiasis?
bile causing supersaturation leading to precipitate leading to stones
61
What is the clinical significance of cholelithiasis?
stones may migrate down the biliary tree and obstruct the bile duct causuing post-hepatic jaundice
62
What may bile stones be made up of?
cholesterol, bilirubin, CaPO4, or CaCO3
63
What can cause cholecystitis?
ascending infection from duodenum or bacteremia
64
What is cholecystitis a sequela to?
cholelithiasis
65
How does cholecystitis benefit bacteria residing in the gall bladder?
they allow the bacterium to escape the host immune system and allow them to be released into the intestine in bile
66
What is biliary obstruction due to?
cholangitis, gall stones, stenosis due to scarring of the dugs, and space occupying masses compressing the common bile duct
67
What is a frequent gall bladder lesion associated with anorexia?
distended gallbladders with viscous bile
68
What are tumors and tumor like lesions are associated with the liver and biliary system?
nodular hyperplasia, primary neoplasms, and secondary neoplasia
69
What are the more frequent/common tumors of the liver?
metastatic neoplasias - 2.5 times more frequent
70
What primary neoplasms affect the liver and biliary systems?
hepatocellular neoplasms, biliary tract neoplasms, and hemangiosarcomas
71
What are some primary hepatocellular neoplasms?
adenomas and carcinomas
72
What are some primary biliary tract neoplasms?
adenoma (cystadenoma), and carcinoma
73
What are some metastatic neoplasias of the liver and biliary system?
intestinal carcinoma, exocrine pancreatic carcinoma, islet cell carcinoma, splenic hemangiosarcoma, lymphosarcoma, and leukemia
74
What species is nodular hyperplasia common in?
the dog
75
What is the consistency of nodules in nodular hyperplasia?
they feel the same as the adjacent liver
76
What do nodules from nodular hyperplasia that are lighter in color indicate?
they are made up of fat and glycogen
77
What do nodules from nodular hyperplasia that are darker in color indicate?
congestion
78
True or False: Nodular hyperplasia causes livers to be reduced in size
FALSE