Test 2- Liver Flashcards

1
Q
A

Metastatic carcinoma.

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2
Q
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Atrophy of right liver lobe due to colonic impaction. AVC

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3
Q
A

Fibrosis due to parasitic migration

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4
Q
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“White-spotted” liver in a pig: due to parasitic migration

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5
Q
A

End stage liver in a dog. From: Mc Gavin and Zachary

 In cases of chronic injury, regeneration can result in hepatocellular nodular proliferation, fibrosis and impaired blood and bile flow. This condition is commonly known as cirrhosis.

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6
Q
A

Capsular hepatic fibrosis. Equine liver.

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7
Q
A

Capsular fibrosis/perihepatitis filamentosa and atrophy of right liver lobe in a horse with colonic impaction.

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8
Q
A

Incidental lesions: tension lipidosis

Focal areas of pale discoloration

Adjacent to mesenteric attachment

Seen occasionally in cattle and horses

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9
Q
A

Liver Autolysis

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10
Q
A

Bile Inhition

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11
Q
A

Multifocal liver necrosis

Size: <1mm to1cm.
Etiology: Infections= bacterial, viral, parasitic.

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12
Q
A

Centrilobular or Zone 3/ periacinar or Centrilobullar necrosis is commonly due to hypoxia. Pig liver. C = central vein

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13
Q
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Midzonal necrosis. Pig liver. C = central vein, P = portal area. This pattern of degeneration and necrosis is rarely seen.

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14
Q
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Zone 1, Periportal necrosis. Horse liver P = portal area. Etiology is often toxic

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15
Q
A

Patterns of hepatocellular degeneration and necrosis

Massive hepatic necrosis

 Involves entire lobule or contiguous lobules

 Although this type of necrosis is commonly severe, the name massive indicates involvement of the whole lobule.

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16
Q
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One of the most common causes of massive hepatic necrosis is the condition known as hepatosis dietetica of swine.

 Hepatosis dietetica has been associated with generation of free radicals and deficiency of Vitamin E/Selenium.

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17
Q
A

MASSIVE HEPATIC NECROSIS IN HEPATOSIS DIETETICA OF SWINE. CUT SURFACE

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18
Q
A

Congenital cysts

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19
Q
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CONGENITAL POLYCYSTIC LIVER DISEASE

 Multiple cysts are located in the liver and kidney

 Cair terriers, West Highland white terries, and Persian cats are predisposed to the disease. Also described in other species

 May result in mortality due to liver or renal failure

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20
Q
A

Moose liver with a parasitic cyst

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21
Q
A

Dog liver with congenital liver cysts

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22
Q
A

Hepatic chronic passive congestion

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23
Q
A

Chronic passive congestion

 “Nutmeg appearance”

 Reticulated pattern due to zonal congestion

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24
Q
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 Hepatic vein thrombosis: also known as Budd-chiari syndrome is characterized by hepatomegaly, ascites, and abdominal pain. It is caused by thrombosis of the hepatic vein and the adjacent inferior vena cava.

 Probable causes include conditions producing thrombotic tendencies or sluggish flow such as myeloproliferative disorders, infections, trauma and neoplasia.

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25
Q
A

CIRCULATORY DISTURBANCES D. Portosystemic shunts (congenital)

  • Blood within the portal venous system bypass the liver and drain into the posterior vena cava, or the azygous vein.
  • Hepatic encephalopathy and ascites are seen in congenital cases in dogs and cats.
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26
Q
A

E. Telangiectasis

 Definition: presence of focal areas in which sinusoids are dilated and filled with blood.

 Gross appearance: irregular, circumscribed, dark-red foci of cavernous ectasia of sinusoids.

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27
Q
A

Telangiectasis is common in cattle and old cats

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28
Q
A

HEPATIC LIPIDOSIS

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29
Q

Mechanisms of hepatic lipidosis

A
  1. Excessive entry of fatty acids into the liver: as a consequence of excessive dietary intake of fat or increased mobilization of fat from adipose tissue due to increased demand (lactation, starvation, and endocrine abnormalities).
  2. Decreased oxidation of fatty acids within hepatocytes that arises as a consequence of abnormal hepatocyte function and leads to accumulation of triglycerides within hepatocytes.
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30
Q
A

Ketosis

 Occurs following excessive fat metabolism during peak lactation in cattle or twin pregnancy in ewes.

 Also related to the added stimulus for fatty acid oxidation caused by the drain of heavy pregnancy or lactation.

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31
Q
A

Equine hyperlipemia

 Especially in obese ponies of Shetland breed.

 The pathogenesis is unknown.

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32
Q
A

Morphologic diagnosis: Multifocal hepatitis, moderate to severe Etiologic diagnosis: Viral hepatitis.

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33
Q
A

METABOLIC DISTURBANCES C. Amyloidosis

 Hepatic amyloidosis usually occurs as a consequence of prolonged antigenic stimulation such as chronic infection or repeated inoculations of an antigen.

 Familial predisposition to hepatic amyloidosis has been detected in Abyssinian and Siamese cats, and also in Chinese Shar-Pei dogs.

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34
Q
A

Etiologic diagnosis: Parasitic hepatitis. Etiologic agent: Fascioloides magna

35
Q
A

VIRAL HEPATITIS
Equine serum hepatitis (Theiler’s disease)

  • Idiopathic until 2013, when in was linked to newly discovered Pegivirus (Flaviviridae family).
  • Disease usually occurs 1-2 months after injection with a biological products of equine serum origin e.g. pregnant mare serum or tetanus antitoxin, but can occur without any such inoculation.
  • Grossly: “dish rag liver”
36
Q

Bacterial infections of the liver

A

Usual pattern is: Multifocal necrotizing hepatitis

37
Q
A

Bacillary hemoglobinuria

 Caused by Clostridium haemolyticum which produces a B toxin.

 Disease of cattle and sheep and occurs when the liver is injured.

 Migrating liver flukes create an anaerobic environment for latent spores of the organism to germinate and elaborate the toxins.

38
Q
A

Tyzzer’s disease

 Caused by Clostridium piliforme (previously known as Bacillus piliformis).

 Seen especially in rodents and immunocompromisedor very young animals (foals, calves, kittens, puppies.

39
Q
A

Demonstration of Leptospira sp. Organisms in tissues requires special (silver) stain such as Warthin Starry.

40
Q
A

Liver abscesses

 Seen in many species as a result of hematogenous infection or secondary to omphalophlebitis

 Commonly seen in cattle as a complication of chemical rumenitis or traumatic reticulitis.

 Abscesses may be few or many and are usually caused by mixed bacterial flora including Fusobacterium necrophorus, Trueperella pyogenes (formerly known as Arcanobacter pyogenes), Streptococci and Staphylococci. The left lobe is more frequently affected.

41
Q
A
  1. Granulomatous hepatitis

 Occurs secondary to fungal infections (Blastomycosis, Histoplasmosis), and some bacterial diseases such as tuberculosis.

Note: Specific conditions are discussed in the fungal hepatitis subsection.

42
Q
A

HEPATIC GRANULOMAS: AVIAN TUBERCULOSIS

43
Q
A
  1. NEMATODES

Ascaris suum

 Ascaris suum larvae cause “milk spots” in pig livers.

 Migration of other parasitic larvae can cause similar changes

 These are multiple areas of fibrosis following migration of larvae through the liver.

44
Q
A

Fasciola hepatica

 Lesions occur in the liver due to migration of larvae.

 The mature fluke resides within bile ducts

45
Q
A

Fascioloides magna.

 The adult trematod resides in cysts within the liver parenchyma

46
Q

Fasciola hepatica matures

A

Fasciola hepatica matures in bile ducts causing chronic fibrosing cholangitis (top photo)

47
Q

Fascioloides magna resides in

A

Fascioloides magna resides in cysts within liver parenchyma.

48
Q
A

Cysticercus tenuicollis in a sheep

49
Q
A

Cestodes

Ecchinonoccus granulosus (Hydatidosis)

  • Cysts (INTERMEDIATE STAGE) in multiple species (moose liver in top photo; camel liver and lung- bottom photo)
  • Adultsareincarnivores
50
Q
A

HYDATID CYSTS

51
Q
A

COCCIDIOSIS IN RABBITS

 Etiology: Eimeria stiedae

 Gross appearance: multiple, raised, off-white nodules scattered throughout the liver

 Histologically: Proliferative cholangitis with intralesional organisms.

52
Q
A

HISTOMONIASIS. Condition also known as “Black head”.

Histomoniasis in a peacock
Etiology: Histomonas meleagridis
Pathogenesis associated to Heterakis gallinarum
MDX: Multifocal granulomatous hepatitis and Diffuse granulomatous typhilits

53
Q
A

HISTOMONIASIS: Multifocal granulomatous hepatitis (so-called “target lesions)

54
Q

The liver is the most common site of toxic injury because:

A

The liver is the most common site of toxic injury because:

 any toxic substance ingested and absorbed through the gastrointestinal tract is carried to the liver.

 liver is capable of biotransformation of various endogenous and exogenous substances for excretion.

55
Q

HEPATOTOXIC PLANTS: Blue-green algae

A

Toxin present in microscopic algae related to bacteria (Microcystis, Anabaena, Aphanizomenon)

 Algae grow as blooms on lakes and ponds, usually in late summer or early fall

 Microcystin is the main preformed toxin

56
Q

What are the lesions of Blue-green algae?

A

Lesions include:
• Acute hemorrhagic gastro-enteritis

  • Acute centrilobular to massive hepatic necrosis
  • Chronicliverdiseaseinsurvivors
57
Q

HEPATOTOXIC PLANTS: Pyrrolizidine alkaloid toxicity

A

Worldwide distribution
 Common genera are Senecio, Crotalaria, Tichodesma and

Heliotropium

 The disease is due to a variety of alkaloids which are converted to toxic pyrrolic esters by hepatic cytochrome p450 system

 Pigs, cattle, horses, goats and sheep are affected

58
Q

Pyrrolizidine alkaloid toxicity.

 Lesions include:

A

Lesions include:
 Acute: periacinar necrosis

 Hepatic veno-occlusive disease

 Chronic with fibrosis (most common form)

59
Q
A

Senecio toxicity. Chronic form in an ovine.

60
Q
A

Pyrrolizidine alkaloid toxicity: Histological appearance

  • Portal fibrosis: may also be perivenous or extensive
  • Biliary hyperplasia: Proliferation of bile ducts and ductules

 Megalocytosis: Giant hypertrophic hepatocytes (as the toxin has an antimitotic effect)

• Parenchymal regeneration is absent.

61
Q
A

Megalocytosis – Seneciosis (pyrrolizidine alkaloid hepatotoxicity).

62
Q

Alsike clover

A

 Trifolium hybridum found in North America

 Toxic principle unknown  Lesions:

 Horses - chronic liver disease and photodynamic dermatitis.

 Histological features:
• Fibrosis, bile duct hyperplasia,

portal hepatitis
• NO megalocytosis

63
Q

Mycotoxins. A. Aflatoxins

A

 Four major aflatoxins (B1, B2, G1 and G2)

 B1 is the most common and potent (carcinogen)

 Ingested in mouldy feed (corn, peanuts, cottonseed)

 Converted to toxic intermediates in hepatocytes

 Occurrence:
• Warm humid temperatures

64
Q
A

Chronic intoxication - more common than acute form and characterized by:

 Severe fatty degeneration  Fibrosis
 Biliary hyperplasia
 Megalocytosis

 Aflatoxins are carcinogenic and predispose to formation of:

  • Hepatomas
  • Cholangiocellulartumours
65
Q

Sporidesmin

A

 Toxin from fungus Pithomyces chartarum

 Found on dead ryegrass in warm climates (New Zealand and Australia)

 Liver pathology due to excretion of unconjugated sporidesmin in bile

(Toxic to bile duct epithelium)

 Lesions:
• Acute to chronic

• Photosensitization in sheep (due to retention of phylloerythrin)

66
Q
A

Sporidesmin toxicity (facial eczema) in sheep

Chronic cholangiohepatitis and bile lakes in sheep with sporidesmin toxicity

67
Q

Copper toxicosis

A

 Sheep are particularly susceptible.

 Cu accumulates in the liver within lysosomes.

 Stored Cu is released as a consequence of stress, causing lipid peroxidation and massive hepatic necrosis

68
Q
A

Cholelithiasis in a bovine

69
Q
A

Canaliculi are distended with bilirubin. Canine liver. Etiology: Babesiosis

70
Q
A

Acquired portosystemic shunt in a dog with chronic liver disease.
Fibrosis causes resistance to portal blood flow

71
Q
A

Acquired Portosystemic shunt

72
Q
A

Photosensitization

Activation of photodynamic pigments by UV light of 290 to 400 nm

 Primary
 St John’s wort (Hypericum perforatum)

 Chlorpromazine  Phenothiazine

 Secondary (hepatogenous)
• Occurs in herbivores with impaired

excretion of phylloerythrin • Isthemostcommonform

73
Q
A

Hepatocutaneous syndrome

 Rare disease in dogs

Crustingerosionsand scaling especially at mucocutaneous junctions and footpads

74
Q
A

NODULAR HYPERPLASIA

 Only common in dogs

 Age-related change

 Hepatocellular adenoma is the main differential diagnosis

75
Q
A

Diffuse hepatic lymphosarcoma compared to normal. Calf liver.

76
Q
A

Hepatocellular Adenoma

  • Benign neoplasm of hepatocytes
  • Seen in young ruminants
  • Single, non-encapsulated, red to brown nodule, which may be pedunculated.
  • Composed of well differentiated hepatocytes
  • Portal areas are not seen in neoplastic area
  • Not easy to differentiate from nodular hyperplasia in old dogs
77
Q
A

Hepatocellular tumors

Hepatocellular Carcinoma

  • Malignant
  • Most often seen in dogs
  • Most differentiate from hyperplasia and adenoma
78
Q
A

Hepatocellular Carcinoma

  • Gross features:
  • Solitary and involves an

entire lobe

  • Cut surface is multilobulated and grey-white to yellow- brown
  • Histologic features:
  • Cells arranged in a trabecular pattern (3 or more cells thick)
  • Individual hepatocytes exhibit atypical and bizarre forms
79
Q
A

Cholangiocellular carcinoma

  • Relatively common (described in all species)
  • Multilobulated,firm,raised, with central areas of depression (umbilicated
80
Q
A

Cholangiocellular carcinoma in a dog.

81
Q
A

LIVER METASTASIS

 A number of tumors metastasize to the liver.

 Metastasis is the most common malignant tumor of the liver.

 Grossly, they are characterized by multifocal nodules resembling the colour and consistency of the primary neoplastic site.

82
Q
A

HEMANGIOSARCOMA

83
Q
A

Metastatic melanoma. Goat liver.