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Anatomic Pathology 2 > Unit 4 - Liver 1 > Flashcards

Unit 4 - Liver 1 Flashcards

1
Q

What are some of the major liver functions?

A

protein metabolism, carbohydrate and lipid metabolism, detoxification, hormone and vitamin metabolism, storage, digestive, hematologic, and immunologic functions

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2
Q

What proteins does the liver create?

A

albumin, carrier proteins, clotting, factors, and many acute phase proteins

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3
Q

How does the liver produce urea?

A

via protein catabolism causing deamination of amino acids leading to urea

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4
Q

What does the liver metabolize?

A

glycogen, ketones, cholesterol

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5
Q

How does the liver create bilirubin?

A

by catabolising heme

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6
Q

What are some clinical signs of hepatic disease?

A

icterus, hepatic encephalopathy, photosensitization, ascites, and hemorrhage

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7
Q

What can cause hepatic encephalopathy?

A

hypoglycemia, increased blood ammonia, increased GABA, toxic amines, aromatic Aas

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8
Q

How can hepatic disease lead to photosensitization?

A

Phylloerythrin is ineffectively removed by the diseased liver and accumulates in the skin

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9
Q

What are the liver causes of ascites?

A

portal hypertension or hypoalbuminemia

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10
Q

How does hepatic disease cause hemorrhage?

A

decreased production of clotting factors or massive necrosis initiating the clotting cascade

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11
Q

What is icterus/jaundice?

A

yellowish discoloration of tissues caused by hyperbilirubinemia

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12
Q

True or False: Icterus is specific for liver disease

A

FALSE

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13
Q

What are the general hepatic causes of icterus/jaundice?

A

pre-hepatic, hepatic, and post-hepatic

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14
Q

What is an example of a pre-hepatic cause of icterus/jaundice?

A

overproduction - ie hemolysis

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15
Q

What can cause hepatic icterus/jaundice?

A

impaired uptake, metabolism, secretion, and/or transport of bile in the liver OR can be due to hepatocellular degeneration, swelling, or necrosis

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16
Q

What can cause post-hepatic icterus/jaundice?

A

biliary duct obstruction typically due to intra-luminal or extra-luminal masses/inflammation

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17
Q

If the liver is not functional what will the bile acids be like in serum?

A

they will be elevated

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18
Q

What are considered the leakage enzymes?

A

ALT, AST, and SDH

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19
Q

What is considered the hepatic induced secreted enzymes?

A

ALP

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20
Q

With liver disease, what may the level of bilirubin look like on serum biochemistries?

A

it may be elevated

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21
Q

In hepatic disease, what will the level of serum bile look like?

A

it will be elevated

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22
Q

What will the levels of BUN and albumin be like in cases of liver disease?

A

it may be decreased since they are produced by the liver

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23
Q

What are some clinical ways to evaluate hepatic disease grossly?

A

radiography, ultrasoumd, contrast studies, or visualize during laparotomy/laparoscopy

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24
Q

What is a common hepatic lesion seen in older dogs?

A

nodular hyperplasia

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25
Q

What are some ways to biopsy a liver (cuts)?

A

wedge or percutaneous core

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26
Q

What is the general structure of the liver?

A

hepatocytes, portal tracts, sinusoids, terminal hepatic venules, bile duct, gall bladder

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27
Q

What are the componenets of the portal triad?

A

hepatic artery, portal vein, bile ductule, and lymphatics

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28
Q

What are the three liver zones?

A

periportal zone (zone 1), Midzonal zone (zone 2), and Centrilobular zone (zone 3)

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29
Q

What proportion of cardiac output does the liver receive?

A

1/4 of total cardiac output

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30
Q

Of the cardiac output that goes to the liver, what percentage of that is delivered via the portal vein?

A

75% (low O2)

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31
Q

What does the portal vein drain blood from?

A

the abdominal organs

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32
Q

What is the livers role in filtering blood?

A

it metabolizes absorbed nutrients and removes absorbed tocins

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33
Q

What is the remaining 25% of the blood that goes to the liver delivered by?

A

the hepatic artery (high O2)

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34
Q

What does reduced hepatic blood flow lead to? Increased blood flow?

A

atrophy, hypertrophy

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35
Q

What are some selected diseases of liver vasculature?

A

passive congestion, portosystemic shunts

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36
Q

What is the cause of passive congestion in the hepatic vasculature?

A

increased pressure in the hepatic veins

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37
Q

What is passive congestion typically due to?

A

right sided heart failure

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38
Q

What is the appearance of acute hepatic passive congestion?

A

the liver is enlarged and dark in color (congested)

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39
Q

What is an example of acute hepatic passive congestion?

A

Mullberry Heart Disease in swine

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40
Q

What is chronic hepatic passive congestion also known as?

A

nutmeg liver

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41
Q

What is the appearance of chronic hepatic passive congestion?

A

the liver is speckled, dark red areas represent dilated and congested central sinusoids and venules, the pale areas are intact periportal region with fatty change

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42
Q

What is chronic hepatic passive congestion often accompanied by?

A

ascites

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43
Q

What microscopic lesions are associated with hepatic passive congestion?

A

degeneration/necrosis of centrilobular hepatocytes, central veins, hepatic veins, and sinusoids are dilated

44
Q

What is a portosystemic shunt?

A

an abnormal communication between the portal vein and systemic circulation, bypassing the liver

45
Q

What are some results of a portosystemic shunt?

A

reduced hepatic circulation leading to microhepatica (small liver) and bacteria, toxins, and ammonia are not removed by the liver and enter the circulation

46
Q

What is the most common cause of hepatic encephalopathy in young dogs and cats?

A

portosystemic shunts

47
Q

When do clinical signs from congenital portosystemic shunts show up?

A

at 6-18 months of age

48
Q

What clinical signs are associated with congeintal portosystemic shunts?

A

small body size, vomitting and/or diarrhea, polyuria/poydyspsia, anesthetic intolerance, and behavioral abnormalities

49
Q

What behavioral abnormalities are associated with congenital portosystemic shunts?

A

ataxia, seizures, blindness, and head pressing

50
Q

When are clinical signs due to congenital portosystemic shunts more noticeable?

A

after eating

51
Q

What is the severity of clinical signs due to a congenital portosystemic shunt dependent on?

A

the size of the shunt

52
Q

What are the types of congenital portosystemic shunts?

A

intrahepatic, extrahepatic, and hepatic microvascular dysplasia

53
Q

When do clinical signs from congenital intrahepatic shunts show?

A

6-18 months

54
Q

What breeds/species is congenital intrahepatic shunts observed in?

A

large and giant breed dogs and cats

55
Q

What are the types of congenital intrahepatic shunts?

A

failure of ductus venosus to close at birth or arise from 1 of the 3 main branches of the portal vein and enter the caudal vena cava directly or via a large branch of the hepatic vein

56
Q

What breeds/species are congenital extrahepatic shunts observed in?

A

young small and toy breeds (signs 6-18 months) and cats

57
Q

What do extrahepatic shunts arise from?

A

the main trunk of the portal vein or one of its major tributaries and typically empty into the caudal vena cava or azygos vein

58
Q

What is a portocaval shunt?

A

a shunt between the portal vein and vena cava

59
Q

What is a portoazygos shunt?

A

a shunt between the portal vein and azygos vein

60
Q

What is hepatic microvascular dysplasia?

A

when the microvasculature of the liver is abnormally formed impairing blood flow through the liver

61
Q

What clinical signs are observed with hepatic microvascular dysplasia?

A

clinical signs similar to those seen with portosystemic shunts

62
Q

What is the average age of presentation of hepatic microvascular dysplasia?

A

3 years of age

63
Q

What breeds are most commonly affected with hepatic microvascular dysplasia?

A

small and toy breeds

64
Q

What is liver failure?

A

the inability to adequately perform normal functions due to insufficient functional hepatic mass

65
Q

What is acute liver failure?

A

abrupt loss of hepatic function

66
Q

What are some potential causes of acute liver failure?

A

acute toxic hepatitis or acute infectious hepatitis

67
Q

What can cause acute toxic hepatitis?

A

poisonous mushrooms or blue-green algae

68
Q

What can cause acute infectious hepatitis?

A

canine adenovirus 1, Tyzzer’s disease, or Leptospira

69
Q

What is chronic liver failure?

A

progressive loss of hepatic function

70
Q

What lesions are associated with chronic liver failure?

A

chronic inflammation, fibrosis, nodular regeneration, bile ductule proliferation, acquired vascular shunts

71
Q

What can cause hepatocellular degeneration?

A

vacuolar change, necrosis and apoptosis, inflammation, fibrosis, hepatocellular regeneration, bile ductule proliferation, and neoplasia

72
Q

What are the three types of vacuolar change?

A

hydropic change, glycogenn accumulation, and lipidosis

73
Q

What is vacuolar degeneration?

A

injured hepatocytes that respond by swelling and become vacuolated

74
Q

What may vacuoles distending the cytoplasm contain?

A

lipid, glycogen, intracellular water (edema), other metabolic wastes or intermediates

75
Q

Is vacuolar degeneration reversible?

A

generally yes

76
Q

What are some synonyms to hydropic degeneration?

A

cellular edema or vacuolar degeneration

77
Q

Is hydropic degeneration reversible?

A

yes

78
Q

What can cause hydropic degeneration?

A

ischemia, toxins, and metabolic disease

79
Q

What is the pathogenesis of hydropic degeneration?

A

there is an accumulation of water in the mitochondria and cytocavitary network due to an inability of cells to maintain ionic and fluid homeostasis

80
Q

What gross changes are seen with hydropic degeneration?

A

the liver is slightly enlarged and pale tan in color

81
Q

What microscopic changes are associated with hydropic degeneration?

A

the hepatocytes are swollen and have clear to flocculent, eosinophilic cytoplasm

82
Q

What does flocculent mean?

A

resembling tufts of wool

83
Q

What species does glycogen accumulation occur most commonly in?

A

dogs

84
Q

What can glycogen accumulation in the liver result from?

A

glucocorticoids, diabetes mellitus, or glycogen storage diseases

85
Q

What is glycogen accumulation in the liver most commonly due to?

A

elevated endogenous or exogenous glucocorticoids (steroid hepatopathy)

86
Q

What microscopic changes are associated with glycogen accumulation in the liver?

A

hepatocelluar vacuolation due to glycogen accumulation

87
Q

Dogs with increased ALP and evidence of vacuolar hepatopathy should be investigated for __________.

A

hyperadrenocorticism

88
Q

What is another term for hepatic lipidosis?

A

fatty liver

89
Q

What is hepatic lipidosis?

A

intracytoplasmic accumulation of triglyceride within hepatocytes

90
Q

When does hepatic lipidosis occur?

A

when the rate of intrahepatic triglyceride accumulation exceeds degradation and/or release as lipoproteins

91
Q

What are the primary causes of hepatic lipidosis?

A

excessive delivery of fatty acids to liver, decreased oxidation of fatty acids due to mitochondrialinjury, or impaired lipoprotein synthesis and release

92
Q

What can cause mitochondrial injury leading to decreased oxidation of fatty acids?

A

toxins and hypoxia

93
Q

What can cause impaired lipoprotein synthesis and release?

A

toxicity and protein-calorie malnurition

94
Q

What gross changes are associated with hepatic lipidosis?

A

Liver is enlarged, pale, tan to yellow in color, friable, greasy on cut surface, has rounded edges, may float in formulin and may be icteric

95
Q

What is the microscopic appearance seen in hepatic lipidosis?

A

multiple small or a few large clear, well-defined vacuoles within hepatocytes, large vacuoles compress the nucleus to the perifery of the cell

96
Q

An obese cat with a history of stress leading to prolonged anorexia shows up on your necropsy table. The cat has hepatic lipidosis. What is the pathogenesis of this lesion?

A

the anorexia leads to fat mobilization to the liver thus there is a slow rate of triglyceride exported as lipoprotein which causes the fatty liver

97
Q

What is a common liver disease that sheep get during pregnancy?

A

pregnancy toxemia

98
Q

What clinical signs are associated with pregnancy toxemia?

A

depression, lethargy, head droop and grinding teath, loss of appetite, and swollen distal limbs

99
Q

You take a urine sample from an ovine suffering from pregnancy toxemia. What do you expect the urine dipstick to show?

A

it is positive for ketones which are produced by liver from fatty acids during times of negative calorie balance

100
Q

At necropsy, what will the liver look like from an animal suffering from preganncy toxemia?

A

the liver is enlarged, pale, tan to yellow in color, friable, greasy on cut surfacem has rounded edges, and floats in formalin

101
Q

What can cause pregnancy toxemia?

A

inadequate caloric intake, increased caloric demand, source of lipid

102
Q

What is the difference microscopically between steroid hepatopathy and hepatic lipidosis?

A

steroid hepatopathy - clear to flocculent eosinophilic cytoplasm with a central nucleus
Hepatic lipidosis - well-demarcated clear vacuoles. Nucleus frequently compressed to the periphery of the cell

103
Q

What are the routes by which the liver can become infected?

A

via the bloodstream, ascending infection via the biliary tree, seeded from adjacent structures/tissues, or parasite infection/migration/encystment

104
Q

How can the liver become infected via the bloodstream?

A

systemic infection or infected via the portal circulation

105
Q

What ascending infection up the biliary tree can infect the liver?

A

suppurative cholangiohepatitis

106
Q

What pattern do you expect to see in the liver when there is a systemic infection?

A

small, multifocal, random liver lesions - lesions in other tissues are anticipated

Anatomic Pathology 2 (48 decks)

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