Hepatobiliary System, Pt. 3 Flashcards

1
Q

What 6 insults commonly cause hepatocyte death?

A
  1. hypoxia
  2. toxins (centrilobular zone)
  3. microorganisms (miliary)
  4. immunological events and inflammation
  5. severe metabolic disturbances
  6. trauma
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2
Q

What are the main patterns of necrosis an their cause?

A
  1. massive (panlobular) - toxic and nutritional
  2. zonal (zone 3) - toxic or hypoxia
  3. multifocal random (miliary) - infectious agents, like viruses, bacteria, and protozoa
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3
Q

What is a common cause of massive (panlobular) necrosis of pig liver?

A

hepatosis dietetica from a deficiency in vitamin E and/or selenium

  • bright/dark red marbled necrosis affecting all lobes
  • ACUTE massive mecrosis
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4
Q

What is the most common form of zonal necrosis of the liver? What is it caused by? How does it look grossly?

A

centrilobular area (zone 3)

hypoxia or toxins

linear trabecular pattern of pallor necrosis affecting one zone

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5
Q

What is the most common cause of multifocal random necrosis of the liver? How does it look grossly?

A

infectious agents, including viruses, bacteria, and certain protozoa

multifocal, small, miliary, pallor spots of necrosis randomly distributed throughout the liver

(equine herpesvirus infection, foal)

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6
Q

What is the most common sequelae to massive chronic hepatic injury? What does it look like grossly?

A

cirrhosis, end-stage liver

multifocal nodules of regeneration after parenchymal death with fibrosis between nodules —> liver will not completely regenerate and will be smaller

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7
Q

How much can the liver regenerate after damage/surgical removal?

A

70% of normal liver can be regenerated without clinical insufficiency

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8
Q

What are the 3 steps to hepatic regeneration?

A
  1. hepatocellular loss is replaced by proliferation of bipotential progenitor cells with the ability to mature into hepatocytes or biliary epithelium, resulting in ductular reactions and biliary hyperplasia
  2. endothelial buds establish sinusoidal channels
  3. hepatic stellate (Ito) cells replicate and synthesize extracellular matric rich in collagen, leading to fibrosis
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9
Q

Hepatic injury and development of fibrosis:

A

damage to reticulin framework = no regeneration

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10
Q

What 4 things happen during cirrhosis (end-stage liver)?

A
  1. loss of hepatic parenchyma
  2. nodular regeneration
  3. bridging fibrosis
  4. biliary hyperplasia
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11
Q

What is the consequence of cirrhosis in dogs? How does this happen?

A

acquired portosystemic shunts

  • hepatic fibrosis causes portal hypertension
  • blood vessels unable to make it to the liver redirect to the caudal vena cava, bypassing liver sinusoids
  • decrease in liver function due to decreased nutrition causes ascites
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12
Q

How can nodular regeneration and nodular hyperplasia be differentiated?

A

REGENERATION = response to a loss of hepatocytes and contains fibrosis

HYPERPLASIA = common incidental finding in older dogs lacking fibrosis

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13
Q

What are 6 causes of cirrhosis?

A
  1. chronic toxicity
  2. chronic cholangitis and/or obstruction
  3. chronic congestion (right-sided heart failure)
  4. inherited disorders of metal metabolism
  5. chronic hepatitis
  6. idiopathic
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14
Q

Cirrhosis, histology:

A

n = regenerative nodules surrounded by fibrosis + loss of hepatic structure

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15
Q

What is happening in the histology of this cirrhotic liver?

A
  • ductular reaction of disassociated hepatocytes
  • blue cells = hyperplastic biliary epithelium (usually only seen in portal triad bile duct)

+ cytokeratin 7 stain, an epithelial marker for biliary epithelium

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16
Q

What are the 2 most common causes of circulatory disturbances of the liver? What are 3 other causes?

A
  1. congestion
  2. portosystemic shunts/vascular anomalies
  • portal vein hypoplasia
  • portal thrombi
  • infarction
17
Q

Acute passive liver congestion:

A
  • due to right-sided heart failure causing fluid back up into the liver
  • dark red
18
Q

What is the most common gross presentation of chronic passive congestion of the liver?

A

nutmeg liver - central vein surrounded by a reticular pattern of pale necrosis and congestion

19
Q

What is a common cause of passive congestion in cattle? What is the pathogenesis?

A

high-altitude disease, brisket disease

  • high altitude causes hypoxia and pulmonary arterial vasoconstriction
  • this causes right-sided heart failure and hepatic congestion (nutmeg liver!)
  • this further causes increased intravascular hydrostatic pressure, leading to ascites and peripheral edema in the brisket area
20
Q

What does the development of a portosystemic shunt cause? What are the 2 types of congenital portosystemic shunts?

A

portal blood bypasses the liver and its sinusoids

  1. INTRAHEPATIC: large breed dogs; patent ductus venosus
  2. EXTRAHEPATIC: cats and small breed dogs; portocaval, portoazygos
21
Q

What is a common sign of extrahepatic congenital portosystemic shunt?

A

hepatic encephalopathy due to an accumulation of ammonium —> ammonium biurate crystals in urine

(portal vein takes GI nutrients/toxins to liver, if it bypasses it, the contents of the blood directly reach systemic circulation)

22
Q

How do congenital and acquired portosystemic shunts compare?

A

CONGENITAL
- usually affects a single large caliber vessel
- NO portal hypertension or ascites (just bypassing liver, no resistance)
- early onset in young animals

ACQUIRED
- involves multiple small vessels
- associated with portal hypertension and ascites

23
Q

Congenital portosystemic shunts:

A

portal vein connects to vena cava and bypasses liver sinusoids

24
Q

How does congenital portosystemic shunts appear grossly?

A

small liver and abnormal singular vascular anastomosis

v = single anomalous vessel connecting portal circulation with systemic circulation

25
Q

What do ammonium biurate crystals look grossly?

A

thorny apple crystals in urine

  • result of portosystemic shunts
  • protein from diet is broken down into ammonium, but cannot react the liver to be metabolized into urea
  • ammonia bypasses the liver and reaches systemic circulation (crystals and CNS signs)
26
Q

What causes acquired portosystemic shunts? What does this result in?

A

portal hypertension - external compression of vessels by tumors or abscesses, severe hepatic diseases, cirrhosis, etc.

increased hydrostatic pressure causes ascites

27
Q

How do acquired portosystemic shunts appear grossly?

A

multiple, small, tortuous anastomosing vessels, usually extrahepatic (unable to reach liver in the first place) to find its way to systemic circulation

28
Q

What are the main 2 causes of hepatic rupture?

A
  1. blunt or sharp force trauma (HBC, high drops, gunshot injury)
  2. predisposing hepatic disease, like hepatitis, neoplasia, fatty liver, or amyloidosis increases the fragility of the liver
29
Q

What are common causes of hepatic lobar torsion?

A
  • trauma
  • idiopathic

infarct of lobe leads to necrosis

30
Q

Hepatic rupture with hemorrhage:

A

fissures on lobe

31
Q

Amyloidosis with hepatic rupture and hemorrhage:

A