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Path 2 > E1. Liver > Flashcards

E1. Liver Flashcards

1
Q

look at slides/skipped 19-22, 34, 38-41, 45, 53-54, 60, 62-63, 71-74, 78, 92-93, 97-98, 103, 108-109, 114-116, 118-138, 141-142, 146-163, 168-174, 177-181, 183-184, 190, 192, 195-197, 203-204, 214, 216-217, 219

pics slide: 10-14, 26, 29-33, 36, 42-43, 46-48, 50-52, 55-57, 66, 70, 76-77, 79-80, 84-88, 94-96, 106-107, 110, 117, 140, 144-145, 173, 180, 185, 191, 193-194, 198-201, 205, 218, 220-221

A

look at them

____ = Specific dz.’s sure to be on exam LOOK AT!!!!!!!!!!!!!!!!!!!

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2
Q

What is the percent body weight that the liver accounts for in carnivores, omnivores, and herbivores?

A

Carnivores: 3 to 4%

omnivores: 2%
herbivores: 1%

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3
Q

What percent of cardiac output does the liver get?

A

25% (67% portal vein, 33% hepatic artery)

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4
Q

Of the three zones which zone gets the most blood? Which gets the least?

A

Zone one

zone three

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5
Q

What is approximately 80% of the liver mass?

A

Hepatocytes

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6
Q

What are other names for stellate cells? What do they do?

A

Lipocytes, Ito cells.

produce and maintain intracellular matrix and store vitamin A.

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7
Q

What are Kupfer cells, and what do they do?

A

They are regional macrophages, and participate in immune and regenerative response.

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8
Q

What are the functions of the liver? (7)

A

– Bilirubin metabolism

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9
Q

What percent of the parenchyma in the liver needs to be injured before you see clinical signs?

A

Approximately 75%

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10
Q

What liver enzymes can be used as biomarkers for liver injury?

A

(AST, ALT, LDH, alkaline phosphatase, gamma-glutamyl transpeptidase)

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11
Q

What can cause liver atrophy? (4)

A

– Increased catabolism

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12
Q

What percent of the liver can regenerate within a week?

A

60%

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13
Q

What can differentiate into hepatocytes or bile duct epithelium?

A

Oval (stem) cells

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14
Q

What are the three things needed for liver regeneration?

A

Intact framework, good blood supply, patent bile ducts.

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15
Q

What are the three general responses of liver to injury?

A

Regeneration parenchyma, replacement of fibrosis, or biliary hyperplasia.

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16
Q

What happens to the liver with fibrosis?

How significant is this?

A

You’ll see an increased amount of connective tissue within it.

Significance depends upon the facts on normal hepatic function and type of collagen.

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17
Q

What can cause white spotted the liver in a pig? (slide 31)

A

Ascaris suum

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18
Q

What is cirrhosis?

A

Is regeneration that can result in hepatocellular nodular proliferation, fibrosis and impaired blood and bile flow. Usually seen in chronic injury.

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19
Q

What are the three types of liver degeneration and necrosis?

A

Random (single cell, multifocal piecemeal necrosis)
Zonal
Massive

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20
Q

Define zonal necrosis. Give some examples. (4)

A 
Areas within hepatic lobule or acini are affected.
– centrilobular 
– midzonal
–periportal
–bridging
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21
Q

What is one of the most common causes of the massive hepatic necrosis?

A

Hepatosis dietetica of swine.

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22
Q

What is Hepatitis dietetica associated with?

A

Generation of free radicals and deficiency of vitamin E/selenium.

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23
Q

What breeds are predisposed to congenital polycystic liver disease?
What is this disease?
Why might an animal die?

A

The breeds are:cair Terriers, West Highland White Terriers, and Persian cats.
The disease is multiple cysts located on the liver and kidney.
Animals may die due to liver or renal failure.

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24
Q

What are the five types of circulatory disturbances?

A

Congestion, infarction/ischemia (very rare), thrombosis, congenital portosystemic shunts, telangiectasis.

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25
Q

What would you expect to see with the liver in acute congestion?

A

Slight enlargement, and prominent reticular pattern due to congestion of centrilobular areas.

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26
Q

What will your liver look like with chronic passive congestion?

A

Nutmeg liver

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27
Q

What is another name for hepatic vein thrombosis?

A

Budd-chiari syndrome

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28
Q

What characterizes hepatic vein thrombosis?

A

Hepatomegaly, ascites, and abdominal pain.

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29
Q

What are the probable causes for hepatic vein thrombosis?

A

Conditions producing thrombotic tendencies or sluggish flow such as myeloproliferative disorders, infections, trauma and neoplasia.

*It is caused by thrombosis of the hepatic vein and the adjacent inferior vena cava

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30
Q

Why is the liver small with a Portosystemic shunt (congenital)?

A

It has been deprived of primary perfusion by portal hepatic trophic factors such as insulin, glucagon and amino acids.

31
Q

What is the definition of Telangiectasis?

What is their gross appearance?

A

Presence of focal areas in which sinusoids are dilated and filled with blood.

Irregular, circumscribed, dark red foci of cavernous ectasia of sinusoids.

32
Q

What are the mechanisms of hepatic lipidosis? (5)

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.
  3. Increased esterification of fatty acids to triglycerides.
  4. Decreased apoprotein synthesis and subsequent decreased
    production and export of lipoprotein from hepatocytes.
  5. Impaired secretion of lipoprotein from the liver.
33
Q

What does the liver look like with hepatic lipidosis?

A

Enlarged, heavy, uniform light yellow or orange that cuts with ease and is greasy when severed. The edges are rounded and the surface is smooth the tissue will float in water or fixative.

34
Q

What is the significance of hepatic lipidosis?

A

*depends on the cause, severity and duration.
– Lesion is reversible in mild cases, but could lead to hepatic necrosis, fatty cysts, fat embolism and liver rupture with internal hemorrhage.
– Fatty livers are also more susceptible to toxic damage and traumatic injury.

35
Q

When are you more likely to see a fatty liver?

A

In late pregnancy, heavy lactation, or simple dietary excess. Fasting in obese animals is followed by a heavy demand on that source, since the liver must provide lipoproteins to other tissues. The synthesis and transport of low-density lipoprotein acts as a bottleneck in the movement of lipid through hepatocytes and triglyceride accumulates.

36
Q

When would you expect to see ketosis?S

A

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.

37
Q

Name the three causes of glycogen accumulation in the liver.

A

Diabetes mellitus,hyperadrenocorticism (steroid induced hepatopathy), glycogen storage disease.

38
Q

How do you distinguish a fatty liver from one that has glycogen accumulation?

A

Use a PAS stain.

Also the liver with glycogen accumulation won’t float.

39
Q

What is the cause of Hepatic amyloidosis?

Which animals are predisposed to this? T

A

Is a consequence of prolonged antigenic stimulation such as chronic infection or repeated inoculations of an antigen.

Abyssinian and Siamese cats, and also in Chinese Shar-Pei dogs.

40
Q

What are the causes of copper toxicosis?(5)

A
  • Dietary excess in ruminants
  • Grazing on pasture low in molybdenum
  • Hepatic (cholestatic) disease
  • Chronic liver disease
  • Hereditary disorders
41
Q

What breeds are predisposed to copper toxicosis? (3)

A

Bedlington and West Highland terriers, Dalmatians.

42
Q

What are the two stains needed to detect copper?

A

Rubeanic acid, or Rhodanine

43
Q

What are the classifications of hepatitis according to time?(5)

A

Percute, subacute, cute, chronic, chronic active.

44
Q

What are the classifications of hepatitis according to location? (2)

A
45
Q

What are liver abscess is a result of?

What is the most common animal this is seen in?

A

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

Cattle as a complication of chemical rumenitis or traumatic reticulitus.

46
Q

What bacterial flora can cause abscesses, and which lobe is more frequently affected?

A

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.

47
Q

What does granulomataus hepatitis occurs secondary to?

A

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

48
Q

Why is the liver the most common site for toxic injury?(2)t

A
49
Q

What can influence the effect of a hepatotoxic gents?

A

dosage, duration of exposure, nature of agents and host susceptibility (influenced by age, sex, diet, endocrine function, genetic constitution and diurnal factors).

50
Q

Name the four types of the hepatotoxic agents.

A

Plants, mycotoxins, chemicals, therapeutic agents.

51
Q

List the types of hepatotoxic plants.

A

Blue – green algae, Pyrrolizidine alkaloid toxicity, Alsike clover, .

52
Q

What plants cause Pyrrolizidine alkaloid toxicity?

What happens to create this toxicity?

What animals are affected?

A

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

53
Q

What lesions are associated with Pyrrolizidine alkaloid toxicity? (3)

A
54
Q

What is Pyrrolizidine alkaloid toxicity histological appearance?

A
  • Portal fibrosis: may also be perivenous or extensive

* Biliary hyperplasia: Proliferation of bile ducts and ductules

55
Q

What are the four major aflatoxins?

Which is the most common and potent?

How are these toxins obtained by an animal?

What animals is most common to find this in?

A

B1, B2, G1 and G2

B1

ingested in moldy feed (corn, peanuts, cottonseed)

pigs, poultry, cattle and the

56
Q

True or false:Aflatoxins are not carcinogenic.

A

False, they are carcinogenic.

57
Q

What can aflatoxins predispose an animal to the formation of?(2)

A

Hepatomas, cholangiocellular tumours

58
Q

What are the four had a toxic chemical?

A
59
Q

When will you see manifestations of hepatic failure?

A

Clinical signs occur after severe liver disease or secondary to obstruction of biliary outflow.

60
Q

List the six manifestations of liver dysfunction and failure.

A
  1. Hepatic encephalopathy
  2. Disturbances of bile flow and icterus/ jaundice
  3. Metabolic disturbances
  4. Vascular and hemodynamic alterations
  5. Cutaneous lesions
  6. Impaired immune functions – detoxification and phagocytosis
61
Q

What can cause hepatic encephalopathy? (3)

List some clinical signs.

A

acute liver disease (horses and permanence), Portosystemic shunts (dogs and cats), chronic liver disease (any animal)

62
Q

What animal(s) is ascites most common in?

A

Dogs and cats

63
Q

What is ascites secondary to? (5)

A
64
Q

With the two cutaneous problems in liver disease?

A

– Photosensitization

– the hepatocutaneous syndrome (superficial necrolytic dermatitis)

65
Q

What are the primary causes of photosensitization? (3)

A

– St. John’s wort(hypericum perforatum)
–chlorpromazine
– phenothiazine

66
Q

What are the secondary causes of photosensitization?

A

• Occurs in herbivores with impaired
excretion of phylloerythrin
Is the most common form

67
Q

What is the hepatocutaneous syndrome?

A

Trusting erosions and scaling especially at mucocutaneous junction and footpads.
*rare disease in dogs

68
Q

What are the two categories of growth disturbances of the liver?

A

Non-neoplastic and neoplastic

69
Q

What are the non-neoplastic growth disturbances of the liver? (3)

A

Hepatocellular nodular hyperplasia, regenerative nodules, bile duct hyperplasia

70
Q

What are the neoplastic growth disturbances of the liver? (2)

A

Benign and malignant (primary, metastatic)

71
Q

In what animal will you see nodular hyperplasia? What is it related to?S

A

Only common in dogs, and is an age-related change. Hepatocellular adenoma is the main differential diagnosis

72
Q

How do most malignant end up in the liver?

A

They metastasize from other organs

73
Q

Where do primary liver tumors arise from? (3)

A

Hepatocytes, bile ducts, mesenchymal tissue.

74
Q

What type of tumor is an hepatocellular carcinoma? What animal is it seen?

A

It is malignant, and most often seen in dogs.

*must differentiate from hyperplasia and adenoma.

Path 2 (7 decks)

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