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Internal Medicine/ Ettinger > Diagnostic Evaluation of the Liver > Flashcards

Diagnostic Evaluation of the Liver Flashcards

1
Q

How can you distinguish between congenital vs secondary copper storage disesae?

A

Location where the copper is stored:
- primary = centrilobular
- secondary = periportal parenchyma

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2
Q

Which breeds are more likely to have intra-hepatic shunts? extra-hepatic shunts?

A

Small/ toy breeds (ex. Yorkie, Havanese, Maltese) = intra-hepatic
large breeds (ex. Irish Wolfhounds, Lab, Golden) = extra-hepatic

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3
Q

In appropriate copper-coloured iris in cats can be an indication of?

A

Portal systemic shunts

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4
Q

What’s the presentation/ prognosis for congenital portal vein hypoplasia (PVH) without a macroscopic shunt? (aka microvascular dysplasia).

A

they usually present later in life, rarely associated with clinical signs, excellent long term prognosis.
- seem in similar breeds as the intra-hepatic PSS

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5
Q

What type of liver disease dose the Scottish Terriers have?

A

Progressive vacuolar hepatopathy

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6
Q

What are the difference types of portal hypertension?

A

Prehepatic, intrahepatic, and post-hepatic
- Prehepatic: increase resistance in extrahepatic portal vein –> young, signs of hepatic encephalopathy
- Intrahepatic: increased resistance in the microscopic portal vein, tributaries, sinusoids, or small hepatic veins –> ex. chronic hepatitis with fibrosis, or cirrhosis
-post-hepatic: secondary to obstruction of larger hepatic vein –> caudal vena cava, R sided heart failure

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7
Q

Which type of portal hypertension is associated with increased protein in the ascites?

A

Post-hepatic, post-sinusoidal, and sinusoidal/intrahepatic

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8
Q

What are the 2 form of hepatic encephalopathy?

A

acute vs chronic

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9
Q

Differentiate between acute vs chronic encephalopathy.

A

Acute - not as common, due to fulminant liver failure –> severe, die in a few days
Chronic - common, due to shunts (acquired multiple or congenital PSS) –> if reversible, can do do better
- most common toxin = ammonia
- the MOA in cats = lack of Arginine. they can’t produce arginine in the liver so relies on dietary intake. Less eating = depletion of arginine = can’t run the urea cycle = back up of ammonia

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10
Q

Is seizure a common clinical sign in hepatic encephalopathy?

A

no

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11
Q

Which liver enzymes represent hepatocyte membrane integrity?

A

ALT, AST

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12
Q

Which liver enzymes are associated with hepatocellular leakage?

A

ALT, AST
ALT = more liver specific
AST = also found in muscle and red blood cells

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13
Q

Which liver enzymes are inducible?

A

ALP, GGT
ALP is not inducible in cats

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14
Q

How is the elevation in liver enzymes classified?

A

mild (<5x upper limit), moderate (5-10x upper limit), and severe (>10x upper limit)

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15
Q

What’s the half life of ALT? AST?

A

ALT T1/2 = 48-60h in dogs, 6h in cats
AST T1/2 = 22h in dogs, 77min in cats

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16
Q

Which liver enzyme has the lowest liver specificity in dogs?

A

ALP; it’s more specific in cats (93%)

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17
Q

What’s the half life of ALP?

A

Dogs = 70h
Cats = 6h

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18
Q

Is it useful to separate C-ALP from L-ALP in dogs?

A

No, because many liver dysfunctions will also lead to an increase in C-ALP

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19
Q

What are some ddx for elevated B-ALP?

A
  • growing animals
  • bone condition: osteomyelitis, OSA, other bone tumours
  • renal secondary hyper-parathryroidism
  • cats: hyperthyroidism
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20
Q

The large elevation is ALP is usually seen with which liver disorder?

A

cholestatic disorder
- massive hepatocellular tumours
- bile duct carcinoma
- glucocorticoid administrations

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21
Q

Which enzyme is more liver specific in dogs, ALP or GGT?

A

GGT (87%, vs ALP = 51%)
but GGT is less sensitive (50%, vs ALP = 80%)

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22
Q

Which enzyme is more liver specific in cats, ALP or GGT?

A

ALP (93%, vs GGT = 67%)
but GGT is more sensitive (86% vs ALP = 50%)

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23
Q

In cats, if there is&raquo_space;GGT but only >ALP, this is most likely indicating what type of hepatitis?

A

necro-inflammatory hepatobiliary disorders

24
Q

Which liver enzymes can be increased in neonatal puppies ingesting colosturm?

A

GGT (not seen in cats)

25
Q

What changes to glucose is expected with liver dysfunction?

A

Hypoglycemia, when 75% of the liver function is lost
- due to lack of gluconeogenesis, glycogen storage, and insulin clearance

26
Q

What changes to BUN is expected with liver dysfunction?

A

Decreased BUN
- blood shunting/ decreased function –> less ammonia converted to urea –> increase ammonia, and decreased BUN

27
Q

What changes to albumin/globulin is expected with liver dysfunction?

A

Hypoalbuminemia, when 70% of liver function is lost
- lack of production but can also be seen with GI loss
- if hypoalbuminemia is due to liver dysfunction, globulin should be normal or increased

28
Q

What changes to cholesterol is expected with liver dysfunction?

A

Variable
- end stage liver = hypocholesterolemia
- cholestatic disease = hypercholesterolemia

29
Q

What are the 3 main categories of hyperbilirubinemia?

A
  1. prehepatic = hemolysis
  2. hepatic = inadequate uptake, conjugation and/or excretion of bilirubin
  3. post-hepatic = abnormal biliary excretion of bilirubin
30
Q

Is hyperbilirubinemia a feature of PSS?

A

No, hyperbilirubinemia is not affected by abnormal liver perfusion

31
Q

How does sepsis lead to hyperbilirubinemia?

A

cytokines involved in sepsis inhibits expression of hepatic transporters necessary for bilirubin transport
- liver disease does not need to be present

32
Q

How like is a feline hepatolipidosis to have hyperbilirubinemia?

A

95%

33
Q

How can one distinguish between hepatic vs post-hepatic hyperbilrubinemia?

A

AUS
- can’t use direct (conjugated) vs indirect (unconjugated)

34
Q

What changes to bile acids is expected with liver dysfunction?

A

Increases.
Bile acids are produced in the liver exclusively from cholesterol
- goes into bile, excreted into the duodenum due to stimulation by cholecystokinin –> helps with fat digestion
- then it’s reabsorbed in the ileum –> portal vein –> >95% goes back to the liver = enterohepatic circulation

35
Q

What diseases are associated with increased bile acids?

A

portal systemic shunts, cholestasis, parenchymal hepatic disease

36
Q

Pre- and post-prandial bile acids are useful in diagnosing which hepatic disordres?

A

portal systemic shunts and cirrhosis in dogs (99% sensitive, 95-100% specific for PSS in dogs and cats)
vacuolar hepatopathy would have significantly elevated bile acids

37
Q

What changes to ammonia is expected with liver dysfunction?

A

Increases, but at that point, it means 70% of liver function is lost, as it has a high capacity for detoxification
- it’s more common with shunts
- highly sensitive (98%) and specific (89%) for PSS in dogs

38
Q

Which clotting factors are produced by the liver?

A

All except for von Willebrand factor subfactor of factor VIII

39
Q

How can cholestasis lead to coagulopathy?

A

decrease absorption of fats, including fat soluble vitamin, such as vitamin K
- Vitamin K dependent clotting factors: II, VII, IX, X, protein C, and protein S (protein C and S = inhibitory clotting protein)
- but it’s NOT usually clinical

40
Q

Deficiency in vitamin K dependent coagulation factors will cause in a prolongation in PT or PTT?

A

PT

41
Q

What’s the most common liver disorder in cats that can lead to coagulopathy?

A

Cholestasis

42
Q

What’s hypersplenism? What’s the cause?

A

Prolonged pooling of platelets in the spleen –> thrombocytopenia
- due to portal hypertension

43
Q

How can fibrinogen be depleted in liver disease?

A

Fibrinogen is an acute phase protein that’s produced by the liver in excess with inflammatory or neoplastic disease –> leading to increased consumption

44
Q

What changes to red blood cells is expected with liver dysfunction?

A

microcytosis
- anemia
- poikilocytosis
- Heinz body formation

45
Q

What U/A abnormalities in cats can indicate liver dysufnciton?

A

Bilirubinuria in cats = always abnormal!
- hepatobiliary or hemolytic disease

46
Q

What U/A abnormalities can indicate liver disease in dogs and cats?

A

Ammonia biurate crystals
- can be normal in Dalmatians and English bulldogs

47
Q

Which imaging modality is the most accurate for liver size measurement?

A

R lateral radiographs
Liver length should be around 5.5x length of T11

48
Q

How sensitive is ultrasound at diagnosing hepatic disease?

A

The liver can still look normal even with severe underlying disease

49
Q

How useful is ultrasound at diagnosing hepatic extrahepatic biliary duct obstruction (EHBDO)?

A

Quite useful
- the bile duct can remain dilated in dogs for quite some time even after resolution - so it’s not a reliable indicator for disease
- gallbladder can still be normal in size
- cannot distinguish between cholecystitis from cholangiohepatitis on AUS

50
Q

What are some causative agents for emphysematous cholecystitis?

A

E coli, C perfringens, DM

51
Q

How sensitive is ultrasound at detecting multiple acquired portal systemic shunts vs congenital portal systemic shunts?

A

MAPPS = 67%
CPSS = 90-100%

52
Q

Which type of shunts is more commonly associated with ascites?

A

multiple acquired portal systemic shunts

53
Q

What other abdominal changes can be noted with PSS?

A

uroliths and renomegaly

54
Q

How is protein C used in diagnosing liver disease?

A

Protein C is produced by the liver
- Protein C activity of <70% was common in patients with PSS (88%) but uncommon with patients with microvascular dysplasia (5%).

55
Q

What are some changes that can falsely decrease the post-prandial bile acids level?

A
  • lack of CCK/ diet not fatty enough
  • severe ilea disease (less bile acid reabsorption)
  • lipemia can lead to increase in bile acids

Internal Medicine/ Ettinger (93 decks)

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