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Equine Medicine > Unit 3 - Hepatic > Flashcards

Unit 3 - Hepatic Flashcards

1
Q

Where is the liver located in the horse?

A

It is located to the right of midline, entirely within the rib cage

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2
Q

True or False: Horses do not have a gall bladder.

A

True

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3
Q

Where does the common bile duct open into?

A

The proximal duodenum

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4
Q

What does the equine liver synthesize?

A

Proteins, coagulation factors. and glucose

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5
Q

What does the equine liver deaminate?

A

amino acids for energy and ammonia into urea

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6
Q

What does the equine liver do to fatty acids?

A

Uptake, esterification, and oxidization

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7
Q

What does the equine liver metabolize?

A

toxins

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8
Q

What clinical signs are associated with hepatic disease in the horse?

A

Weight loss, decreased appetite, fever, icterus, colic signs, edema, ascites, photosensitization, and abnormal behavior/mentation

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9
Q

What liver leakage enzymes will be elevated in cases of hepatic disease in the horse?

A

SDH, LDH, and AST

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10
Q

What membrane bound enzymes will be elevated on serum chemistry in a horse with hepatic disease?

A

GGT and ALP

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11
Q

What are some non-specific markers of hepatic disease on serum chemistry in the horse?

A

Albumin, BUN, glucose, and bilirubin

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12
Q

At what level do leakage enzymes become a significant concern?

A

At least 2-3x within the reference range

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13
Q

What is the most liver specific leakage enzyme in horses?

A

SDH

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14
Q

What do elevations in SDH indicate?

A

That there is active or ongoing liver damage because the half life is short

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15
Q

What is AST a leakage enzyme for?

A

The liver and skeletal and cardiac muscle

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16
Q

Why is AST less sensitive than SDH?

A

Because its half-life is 2-10 days - it is slow to rise and slow to fall

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17
Q

What is LDH a leakage enzyme for?

A

The liver and skeletal muscle

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18
Q

What non-hepatic disease process will elevate LDH?

A

hemolysis

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19
Q

Where are hepatic membrane bound enzymes found?

A

in the biliary tract

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20
Q

What are hepatic membrane bound enzymes a marker for?

A

hepatobiliary disorders and cholestasis

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21
Q

When do membrane bound enzymes become concerning?

A

When they are elevated at 2-3x their reference range

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22
Q

What enzyme is the best indicator for biliary disease in the horse?

A

GGT

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23
Q

Typically, when is albumin decreased in relation to hepatic disease?

A

In end-stage liver disease

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24
Q

What is BUN produced by?

A

The liver when processing/detoxifying ammonia

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25
Q

When is glucose decreased in relation to hepatic disease?

A

In end-stage liver disease

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26
Q

What is the most common reason for elevated unconjugated bilirubin?

A

Anorexia

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27
Q

What causes elevated unconjugated bilirubin?

A

Decreased hepatic uptake or decreased conjugation of bilirubin

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28
Q

What causes conjugated bilirubin elevations?

A

Intrahepatic cholestasis or extrahepatic bile duct obstruction

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29
Q

What may a CBC show in patients with hepatic disease?

A

Leukocytosis and hyperfibrinogenemia

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30
Q

What additional diagnostic tools are good for evaluation of hepatic disease in horses?

A

Transcutaneous abdominal ultrasound, percutaneous liver biopsy, bile acids, and ammonia

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31
Q

Where is the liver best visualized during a transcutaneous abdominal ultrasound?

A

On the right side of the horse between the lungs/diaphragm and large colon

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32
Q

What does a normal liver look like on transcutaneous abdominal ultrasound?

A

Homogenous echogenicity, crisp edges, subjective size, few bile ducts with hypoechoic contents, unable to see the portal vein, and no shadowing effects

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33
Q

What does an abnormal liver look like on transcutaneous abdominal ultrasound?

A

Heterogenous echogenicity, subjective size, many dilated bile ducts with hyperechoic sludge contents or shadowing, able to identify the portal vein, and shadowing effects

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34
Q

If the liver is readily findable on the left, everywhere on the right, and with round edges, what does that indicate?

A

It is swollen and enlarged

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35
Q

If you are unable to locate the liver on the right or the left, what does that indicate?

A

The liver is small and fibrotic

36
Q

If the liver extends past the costochondral junctions, what does that indicate?

A

The liver is enlarged

37
Q

If you are able to identify the portal vein in the horse, what does that indicate?

A

it is enlarged due to portal hypertension

38
Q

If there are shadowing effects that indicate gas, what is the likely cause?

A

abscess

Note: shadowing effects can also be due to choleliths

39
Q

When doing a percutaneous liver biopsy, what structures should you make sure to avoid?

A

The diaphragm and the large colon

40
Q

When should you not do a percutaneous liver biopsy?

A

If there are hepatic abscesses or coagulopathies

41
Q

What can you use your liver biopsy for?

A

Histopathology, culture, and hepacivirus testing

42
Q

What are the pros to the percutaneous liver biopsy?

A

Rule in or out specific disease
May get a tangible answer
Will at least get some information

43
Q

What are the cons to the percutaneous liver biopsy?

A

Small piece of a big organ - may over or under estimate damage
Could sample something else
Could bleed afterwards

44
Q

Why do you not need to take pre and post-prandial samples when doing bile acids in a horse?

A

because they do not have a gall bladder

45
Q

When are ammonia levels typically evaluated?

A

When horses are mentally inappropriate - obtunded and manic

46
Q

Why do ammonia levels and bile acid levels typically need to be run in house?

A

Because they are unstable at room temperature

47
Q

What are the poor prognostic indicators for hepatic disease in horses?

A 
Bile acids >50 mg/dl
Hyperammonia
Hypoalbuminemia
Low BUN
Hypoglycemia
48
Q

True or False: You should treat the blood work, not the horse.

A

No

49
Q

What is the general treatment for hepatic disease in horses?

A

Anti-inflammatories, antimicrobials if infectious component, nutrition, and time

50
Q

What do you want your antimicrobial to do? What do you want to avoid with your antimicrobial?

A

You want the antimicrobial to concentrate in the bile

You want to avoid an antimicrobial that requires cytochrome p450 or other hepatic metabolism

51
Q

What are the common causes of hepatic disease in the horse?

A

Tyzzer’s disease, pyrrolizadine alkaloid toxicity, Theiler’s disease, ascending cholangiohepatitis, cholelithiasis, chronic active hepatitis, hepatic lipidosis, and hepatic abscesses

52
Q

What causes Tyzzer’s disease?

A

Clostridium piliforme

53
Q

What is the signalment of Tyzzer’s disease?

A

5-30 days of age

54
Q

What clinical signs are associated with Tyzzer’s disease?

A

Acute onset - icterus, lethargy, weakness, pyrexia, and tachycardia

55
Q

What will you see on CBC and chemistry in a patient with Tyzzer’s disease?

A

Leukopenia, hypoglycemia, and a marked elevation in AST, bilirubin, and SDH

56
Q

How is Tyzzer’s disease treated?

A

Parenteral nutrition, antimicrobials, and supportive care

57
Q

How do you diagnose Tyzzer’s disease?

A

Necropsy - multifocal hepatic necrosis, intracellular bacilli +/- culture

58
Q

What is the signalment for Pyrrolizidine alkaloid (PA) toxicity?

A

Any age able to graze

59
Q

What are the causative plants for PA?

A

Ragwort, heliotrope, common groundsel, and aslike/red clover

60
Q

What is the pathophysiology of PA?

A

Pyrrolizidine alkaloid creates pyrrole derivatives that alkylate nucleic acids and protein. This prevents cell division, hepatocytes then enlarge and die resulting in fibrosis and liver failure

61
Q

What clinical signs are associated with PA toxicity?

A

Signs associated with liver failure

62
Q

How is PA diagnosed?

A

Liver biopsy - fibrosis and megalocytosis

Finding plants in pasture/hay

63
Q

How is PA treated?

A

remove the feed source and supportive care

64
Q

What patient history is associated with Theiler’s disease?

A

Typically 1-3 months after administering a equine biologics product

65
Q

What are the causative agents of Theiler’s disease?

A

Theiler’s disease associated virus, equine parvovirus, nonprimate hepacivirus, and equine pegivirus

66
Q

How is Theiler’s disease diagnosed?

A

History of receiving equine origin product and PCR testing of serum +/- liver biopsy

67
Q

What clinical signs are associated with Theiler’s disease?

A

Clinical signs associated with liver failure

68
Q

How is Theiler’s disease treated?

A

time and supportive care

69
Q

What signalment/history is associated with ascending cholangiohepatitis?

A

Intermittent fevers, may be associated with recent colic or ileus

70
Q

What is the pathophysiology of ascending cholangiohepatitis?

A

Suspect that bacteria ascend into the liver via the common bile duct. Ileus may increase the risk of this occuring

71
Q

What physical exam findings will you see in horses with ascending cholangiohepatitis?

A

General liver failure and fevers

72
Q

How is ascending cholangiohepatitis diagnosed?

A

Liver biopsy - culture or histopath (neutrophilic inflammation +/- bacteria)

73
Q

How is ascending cholangiohepatitis treated?

A

Antimicrobials - target gram negatives, concentrate in the bile, do not require hepatic metabolism, and long-term

74
Q

What is the signalment for cholelithiasis?

A

Typically middle aged to older horses

75
Q

What clinical signs are associated with cholelithiasis?

A

Liver failure CS, fevers, and intermittent colic

76
Q

What is the pathogenesis of cholelithiasis?

A

Secondary to ascending cholangiohepatitis and calcium bilirubinate stones

77
Q

How do you diagnose cholelithiasis?

A

Ultrasound

78
Q

What will cholelithiasis look like on ultrasound?

A

Acoustic shadowing from the liver/bile ducts and dilated bile ducts

79
Q

How is cholelithiasis treated?

A

Long term antimicrobial treatment, IV DMSO to possibly dissolve choleliths (will not work with Ca-bilirubinate stones

80
Q

What is the signalment for hepatic lipidosis?

A

overweight horses, miniature horses and ponies, and donkeys

81
Q

What history is pertinent to hepatic lipidosis?

A

Typically off-feed for several days (may be as few as one)

82
Q

What is the pathophysiology of hepatic lipidosis?

A

It is a viscous cycle: Decreased caloric intake leads to mobilization of fat stores, which makes the liver unable to process the lipids. There is then hyperlipidemia which causes nausea, and inappetence and then there is more decreased caloric intake… the cycle continues

83
Q

What clinical signs are associated with hepatic lipidosis?

A

Cloudy serum (if triglycerides are >500), persistent anorexia, and signs of liver failure if it progresses to true hepatic lipidosis

84
Q

How is hepatic lipidosis treated?

A

Break the cycle of anorexia - IV dextrose or PO if the GI tract works

85
Q

When should chronic active hepatitis be a differential?

A

Once all other causes of hepatitis are ruled out

86
Q

How is chronic active hepatitis treated?

A

Long tapering dose of steroids

Equine Medicine (27 decks)

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