Lecture 4: Liver 1 Flashcards

1
Q

Portal hypertension can be prehepatic, intrahepatic or post-hepatic. Of these, one is more common than the other two. Which one?

A

Intrahepatic causes are most common (the other two are rare).

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2
Q

What are some of the clinical signs and gross lesions seen in a puppy
with a congenital portosystemic shunt?

A
  1. Stunting, relative to littermates; 2. Hepatic encephalopathy (manifesting as mental dullness); 3. Small liver size.
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3
Q

Which types of equids are prone to development of hepatic lipidosis?

A

Ponies, mini horses & donkeys

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4
Q

What is the characteristic histologic lesion of hepatic lipidosis?

A

Clear cytoplasmic vacuoles within hepatocytes.

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5
Q

What is the cause of the fibrous tags or plaques found on the diaphragmatic surface of the liver of horses?

A

unknown

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6
Q

What is the significance of tension lipidosis in cattle?

A

None; it’s incidental and insignificant.

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7
Q

Where, precisely, in the liver is amyloid deposited in cases of amyloidosis?

A

The spaces of Disse

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8
Q

What is the underlying cause of excessive glycogen accumulation in the liver?

A

Excessive glucocorticoids [either exogenous (iatrogenic) or endogenous (hyperadrenocorticism)]

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9
Q

What is hepatic telangiectasia? What does it look like grossly?

A

Randomly scattered areas of dilation of hepatic sinusoids by blood where hepatocytes have been lost. Grossly, it appears as dark red “dit-dots” and patches throughout hepatic parenchyma.

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10
Q

What histologic changes would you expect in the liver of an anemic animal?

A

Centrilobular hepatocyte degeneration and necrosis with dilation and congestion of centrilobular sinusoids by blood. [Note that “enhanced reticular pattern” is a gross, not a histologic change and is not an acceptable answer, sorry.]

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11
Q

In which phases or periods are cattle most susceptible to developing hepatic lipidosis, and why?

A

Fat cows in late gestation, immediately post partum or in peak lactation. Excessive mobilization of body fat stores to cope with demand overwhelms liver’s ability to process and export it –> accumulation.

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12
Q

What is the characteristic histologic lesion of hepatic lipidosis?

A

Clear cytoplasmic vacuoles within hepatocytes.

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13
Q

What is the underlying pathogenesis of hepatic lipidosis?

A

The rate of accumulation of triglycerides within hepatocytes exceeds the rate of their removal

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14
Q

What is the most common reason for chronic passive congestion in the liver?

A

Chronic right-sided heart failure (for a variety of reasons)

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15
Q

Excessive administration of glucocorticoids by veterinarians can cause what substance to accumulate in the liver? What is the term for this condition?

A

Glycogen. “Steroid hepatopathy”

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16
Q

What is tension lipidosis?

A

Areas of pallor in hepatic parenchyma where the liver is suspended by ligaments.

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17
Q

You are performing a necropsy on a bird euthanized for chronic foot infections and notice that the liver is swollen, pale, waxy and friable. What is the most likely cause of the liver lesion?

A

Hepatic amyloid accumulation (amyloidosis)

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18
Q

What is the characteristic signalment and scenario for a cat that develops hepatic lipidosis?

A

Obese cat –> stressed (disease, change of environment etc.) –> goes off food for several days –> idiopathic accumulation of lipids in hepatocytes.

19
Q

What is the gross appearance of a liver with acute passive congestion (give 3 gross findings)?

A
  1. Slight hepatomegaly; 2. Enhanced reticular pattern / centrilobular congestion; 3. Oozes blood from cut surfaces
20
Q

In what type of animal is the edge of the liver fimbriated or “frilly”?

A

Camelids (llamas etc.)

20
Q

In which domestic species are fibrous tags or plaques often found on the diaphragmatic surface of the liver?

A

Horses

21
Q

What is the most common reason for an INTRAhepatic congenital portosystemic shunt?

A

Intrahepatic congenital PSSs are generally due to failure of closure of the ductus venosus at birth. [The ductus venosus is a normal fetal vessel that conducts blood from the umbilical vein to the caudal vena cava.]

22
Q

Describe the gross appearance of a liver affected by hepatic lipidosis.

A

Enlarged, friable, pale, greasy, may float in formalin

23
Q

Explain the difference between the terms “nutmeg liver,” “enhanced lobular pattern” and “enhanced reticular pattern.”

A

“Enhanced lobular pattern” and “enhanced reticular pattern” mean the same thing and are interchangeable terms. Both refer to any repeating lesion within all hepatic lobules, including (for example) periportal inflammation or cancer, centrilobular necrosis, and midzonal glycogen accumulation (i.e., anything that causes a repeating dark-light pattern at the level of every hepatic lobule). “Nutmeg liver” is a form of enhanced lobular pattern reserved for the chronic passive congestion associated with chronic right sided heart failure.

24
Q

In which breeds of dogs (large or small) are INTRAhepatic congenital portosystemic shunts more common?

A

Large breeds

25
Q

In what form is glucose stored in the liver?

A

As glycogen

26
Q

What is the definition of a portosystemic shunt?

A

An abnormal vascular channel that allows portal blood to bypass the liver and enter the systemic circulation.

27
Q

What accumulates in the cytoplasm of hepatocytes in so-called “steroid hepatopathy”?

A

Glycogen (NOT steroids!)

28
Q

In which two domestic species is hepatic telangiectasia most commonly seen?

A

Cats and cattle

29
Q

Portal hypertension caused by intrahepatic disease is far more common that that caused by prehepatic or posthepatic disease. What are two common, underlying mechanisms for intrahepatic portal hypertension?

A
  1. Chronic liver disease with loss of architecture & fibrosis; 2. Hepatic accumulations e.g., amyloid. [Both cause increased resistance to blood flow through liver.]
30
Q

You are performing a necropsy examination on a cat and find dozens of dark red foci throughout its liver parenchyma and over the capsular surface of the liver. What are these lesions most likely to be?

A

Hepatic telangiectasia

31
Q

Describe 3 key histologic findings in a liver with chronic passive congestion

A
  1. Centrilobular congestion; 2. Centrilobular hepatocyte atrophy and/or necrosis; 3. Periportal hepatocyte lipid accumulation. To summarize: the centres of lobules are dark because of accumulation of “stagnant” blood and loss or compression of hepatocyte plates, while the peripheral areas of lobules are pale because hypoxic hepatocytes have accumulated lipid. This repeating dark-light pattern is called “nutmeg liver.”
32
Q

In which domestic species is tension lipidosis most commonly seen?

A

Cattle, and less commonly in horses (i.e., large animals with heavy livers).

33
Q

What is the most common reason for acute passive congestion in the liver?

A

Acute right-sided heart failure (for a variety of reasons)

34
Q

Explain how toxic or hypoxic damage to hepatocytes can cause hepatic lipidosis.

A

Hepatocellular injury –> Reduces ability to process, transform & export lipids –> Accumulation within cytoplasm of hepatocytes.

35
Q

Anemia can cause an enhanced lobular pattern grossly and centrilobular hepatocyte degeneration and necrosis microscopically. Explain the pathogenesis of this pattern of injury.

A

Centrilobular hepatocytes receive blood last and so receive the least oxygenated blood in the liver. Therefore, hypoxia caused by anemia hits the centrilobular hepatocytes the hardest –> degeneration or death of centrilobular hepatocytes, while periportal hepatocytes may be spared.

36
Q

What is the significance of several biliary cysts in the liver parenchyma?

A

None; they are incidental and insignificant.

37
Q

What are 2 histologic lesions are seen in the liver of a puppy with a congenital portosystemic shunt?

A
  1. Small or absent portal veins in portal areas; 2. “Arteriolar reduplication” in portal areas
38
Q

What is the significance of fibrous tags or plaques found on the diaphragmatic surface of the liver of horses?

A

None; they are incidental and insignificant.

39
Q

What is the pathogenesis of tension lipidosis in cattle?

A

Tension on liver by suspensory ligaments –> impedes blood flow –> localized hypoxia –> localized lipid accumulation –> areas of pallor

40
Q

What is the gross appearance of a liver with chronic passive congestion (give 3 gross findings)?

A
  1. Hepatomegaly; 2. Rounded edges to liver; 3. Enhanced reticular pattern (“nutmeg liver”)
41
Q

What is the most common underlying reason for development of an acquired (not congenital) portosystemic shunt?

A

Portal hypertension. [Portal blood can’t pass through the liver and so creates an “escape valve” to give itself some way back into the systemic circulation.]

42
Q

In what key way do congenital biliary cysts differ from the cysts in the liver associated with polycystic kidney disease?

A

In number. Congenital biliary cysts are few, whereas those associated with PKD are much more numerous.

43
Q

In which breeds of dogs (large or small) are EXTRAhepatic congenital portosystemic shunts more common?

A

Small breeds