Diagnostic Evaluation of the Liver Flashcards

(55 cards)

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
What changes to glucose is expected with liver dysfunction?
Hypoglycemia, when 75% of the liver function is lost - due to lack of gluconeogenesis, glycogen storage, and insulin clearance
26
What changes to BUN is expected with liver dysfunction?
Decreased BUN - blood shunting/ decreased function --> less ammonia converted to urea --> increase ammonia, and decreased BUN
27
What changes to albumin/globulin is expected with liver dysfunction?
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
What changes to cholesterol is expected with liver dysfunction?
Variable - end stage liver = hypocholesterolemia - cholestatic disease = hypercholesterolemia
29
What are the 3 main categories of hyperbilirubinemia?
1. prehepatic = hemolysis 2. hepatic = inadequate uptake, conjugation and/or excretion of bilirubin 3. post-hepatic = abnormal biliary excretion of bilirubin
30
Is hyperbilirubinemia a feature of PSS?
No, hyperbilirubinemia is not affected by abnormal liver perfusion
31
How does sepsis lead to hyperbilirubinemia?
cytokines involved in sepsis inhibits expression of hepatic transporters necessary for bilirubin transport - liver disease does not need to be present
32
How like is a feline hepatolipidosis to have hyperbilirubinemia?
95%
33
How can one distinguish between hepatic vs post-hepatic hyperbilrubinemia?
AUS - can't use direct (conjugated) vs indirect (unconjugated)
34
What changes to bile acids is expected with liver dysfunction?
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
What diseases are associated with increased bile acids?
portal systemic shunts, cholestasis, parenchymal hepatic disease
36
Pre- and post-prandial bile acids are useful in diagnosing which hepatic disordres?
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
What changes to ammonia is expected with liver dysfunction?
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
Which clotting factors are produced by the liver?
All except for von Willebrand factor subfactor of factor VIII
39
How can cholestasis lead to coagulopathy?
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
Deficiency in vitamin K dependent coagulation factors will cause in a prolongation in PT or PTT?
PT
41
What's the most common liver disorder in cats that can lead to coagulopathy?
Cholestasis
42
What's hypersplenism? What's the cause?
Prolonged pooling of platelets in the spleen --> thrombocytopenia - due to portal hypertension
43
How can fibrinogen be depleted in liver disease?
Fibrinogen is an acute phase protein that's produced by the liver in excess with inflammatory or neoplastic disease --> leading to increased consumption
44
What changes to red blood cells is expected with liver dysfunction?
microcytosis - anemia - poikilocytosis - Heinz body formation
45
What U/A abnormalities in cats can indicate liver dysufnciton?
Bilirubinuria in cats = always abnormal! - hepatobiliary or hemolytic disease
46
What U/A abnormalities can indicate liver disease in dogs and cats?
Ammonia biurate crystals - can be normal in Dalmatians and English bulldogs
47
Which imaging modality is the most accurate for liver size measurement?
R lateral radiographs Liver length should be around 5.5x length of T11
48
How sensitive is ultrasound at diagnosing hepatic disease?
The liver can still look normal even with severe underlying disease
49
How useful is ultrasound at diagnosing hepatic extrahepatic biliary duct obstruction (EHBDO)?
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
What are some causative agents for emphysematous cholecystitis?
E coli, C perfringens, DM
51
How sensitive is ultrasound at detecting multiple acquired portal systemic shunts vs congenital portal systemic shunts?
MAPPS = 67% CPSS = 90-100%
52
Which type of shunts is more commonly associated with ascites?
multiple acquired portal systemic shunts
53
What other abdominal changes can be noted with PSS?
uroliths and renomegaly
54
How is protein C used in diagnosing liver disease?
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
What are some changes that can falsely decrease the post-prandial bile acids level?
- lack of CCK/ diet not fatty enough - severe ilea disease (less bile acid reabsorption) - lipemia can lead to increase in bile acids