Liver Disease in SA Flashcards

1
Q

Evaluation of the Liver

(3)

A
  • can look at these different aspects and any changes
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2
Q

Enzymes Indicating Hepatocellular Damage

(4)

A
  • these are the classic ones- leakage enzymes
  • tell us there is damage to the hepatocytes
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3
Q

Hepatocellular damage - “leakage”

A
  • these enzymes are readily available from the cytosol of the hepatocytes
  • if there is damage to hepatocytes and it dies, the enzymes in hte cytoplasm will be released
  • or some degree of damage to hepatocyte causes wall to release a little bit of cytoplasmic material
  • blebosome: will have a bit of cytoplasmic material in it
  • if you even just have a lot of blebbing from a large amount of hepatocytes, will still see an increase of these specific enzymes
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4
Q

Hepatocellular Enzymes: ALT and GLDH

A
  • will increase about 12 hours after injury
  • last for about 1-2 days
  • more common in SA
    large animals: ALT activity is very low!
    *
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5
Q

Hepatocellular Enzymes: AST and ALT

A
  • if you have marked muslce damage, you may see increase in AST
  • need to differentiate if it is liver damage or liver damage
  • CCK can help in this
  • (echo)
  • need to factor in how specific certain enzymes are to a tissue
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6
Q

Liver vs. Muscle

A
  • CK can be a good indicator of muscle cell damge, but has a very short half life
  • so the measurement of this parallel is not full proof
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7
Q

Enzymes Indicating Cholestasis

(2)

A
  • we have lots and lots of hepatocytes, can see increases with little or large damage
  • key enzymes of cholestasis: ALP and GGT
    *
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8
Q

Alkaline Phosphatase

(ALP)

A

Derived from bile duct epithelium

  • cholestasis will irritate bile duct epithelial cells and this ALP will be released
  • but it also comes from other places too (young dogs- bone isoform of ALP) –> need to be aware
  • any dog that is stressed or given prednisolone over time will likely have a notable ALP increase (steroid induced isoform)
  • in cats it has a VERY short half life, any increase is significant (could be hepatic lipidosis, or if not yellow- hyperthyroidism) –> the dynamic of the changes can be very important in cats
  • dogs can get an increase for stress and other things
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9
Q

Induction vs. Leakage

A

ALP is an induction enzyme: they are present on some of the biliary epithelium but can also have induced production of these enzymes –> trascription and translation induced

  • different to the leakage enzymes which are present in the cytoplasm
  • may see these enzymes 6 or 7 days later after the induction process occurs and then are released –> ex: steroid induced
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10
Q

Gammaglutamyltransferase (GGT)

A
  • other cholestetic enzyme we look at
  • nursing animals will have a high GGT as it is in colostrum
  • If renal tubular cells get damaged, they will release this into the urine, BUT NOT THE BLOOD, need to be aware
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11
Q

Measures of Hepatic Function

(7)

A
  • key enzymes
  • leakage: dmaage to hepatocytes
  • cholestasis: blockage present
  • these are generally on biochem panel
  • these are measure of liver FUNCTION where as other enzymes show damage
  • can have damage but the functional capacity of the liver is rather large
  • damage and function of the hepatocyte does not have to coincide but can also go hand in hand
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12
Q

Bilirubin Metabolism

A
  • we have a regular turnover of RBC’s (110 days) and we want to conserve ironand conserve Hb –>happening in spleen
  • bilirubin is not solube in water- trafficked using albumin
  • conjugated in the hepatocyte –> makes it water soluble (can then float in fluid without carrier)
  • conjugated bilrubin will be converted urobilin or stercobilin or can be excreted in the urine
  • WATCH THE VIDEO
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13
Q

Bilirubin

A
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14
Q

Bilirubinemia- Hemolysis

A
  • if you have excess break down of RBC’s
  • the hepatocytes can only conjugate so much
  • the key limiting step though is the EXCRETION INTO THE BILE
  • there will be back up into the system, you will start to leak out the conjugated bilirubin which is soluble and you will see it being released in urine
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15
Q

Bilirubinemia - Cholestasis

A
  • Break down of RBCs is normal, the hepatocytes will conjugate the bilirubin
  • there is blockage: bilirubin in the blood and in the urine
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16
Q

Bilirubinuria

A
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17
Q

Ammonia and Urea

(what is ammonia converted into?)

A
  • when you eat a proteinaceous meal, there is ammonia present and will be detoxified in the liver into urea (still toxic but not as toxic) and then can excrete urea into the kidneys
  • If you have a filing liver, you will have a decrease in urea in the blood
  • ammonium will increase
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18
Q

Ammonia and Urea

(role of urea and what is seen in hepatic disease?)

A
  • bilirubin will increase in the blood if the liver is failing because the liver cant process it and get it into the biliary ducts
    *
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19
Q

Glucose

A
  • If the liver is fialing you may see a decrease in glucose as the liver cant synthesize it
  • but glucose is so important that this is not an early sign as it is conserved until desparate
  • failing liver–> would see decrease in albumin
20
Q

Cholesterol

(synthesis and increase/decrease)

A
21
Q

Cholesterol

A
  • If the liver fails to build cholesterol, it will go down in the blood
  • If there is blockage there may be an increase
  • or you can have both happening and not really see a change (could still be liver failure)
  • essentially cholesterol levels are not PARTICULARLY helpful
  • post prandial- post meal (be aware of cholesterol increase there)
    *
22
Q

BIle Acids

A
  • echo
  • why do we need bile acids? emulsify fat in digestion, need to have it coming into the gut
  • liver builds bile acids and excretes into bile ducts, but it is expensive to build bile acid!
  • NEED TO RECYCLE
    once bile does its job, it is reabsorbed by portal vein and is taken up by hepatocytes to be excreted again
  • in healthy animal: should see bile acids in duct or bile
  • but shouldnt see in circulation!
23
Q

BIle Acid Concentration [BA]

A
  • want to feed the animal after initial reading
  • will cause the gall bladder to contract, can see if the liver is not uptaking the bile acid correctly
24
Q

increase [BA] in serum or plasma

A
  • either a decrease in clearance from portal blood or lower excretion via bile
  • portosystemic shunt: abnormal vessel that connects the portal blood to a vessel –> can be congenital or acquired (hepatocytes are functioning well but the blood might be channeled away from the hepatocyte)
  • Obstructive cholestasis: bile acids cannot be excreted (backed up toilet effect)
  • If bilirubin is high due to cholestasis then you know bile acids are high, but only do the bile acid test when necessary (if they arent really icteric)
25
Q

Bile Acid Challenge Test

A

*

26
Q

Ammonium (NH4+) concentration

A
  • we are going to have ammonium in the intestine and ideally want to channel to hepatocyte and then be excreted
27
Q

Ammonium Concentration

(analytical concepts and samples)

A
  • not really a good thing to sample and it is very unstable
  • needs to be on ice and analyzed in 30 min
  • cant have smoke or sweat on hands as it may increase levels in the sample
28
Q

Hyperammonemia

A
  • ammonia can have access to large circulation
  • or can have a post prandial increase after meal (protein)
29
Q

Other lab findings to consider - CBC

(Acanthocytosis, Anemia, Codocytosis, Microcytosis)

A
30
Q

Other lab findings to consider - UA

A
31
Q

Other lab findings to consider -others

(PTT or PT, Fecal Exam Results, Peritoneal Fluid analysis)

A
  • all of the COAGUALTION ENZYMES are built in the liver- can be another way to indicate the liver
32
Q

Liver

(diagnosing a lesion)

A
  • what causes the damage? - you will need to do imaging
  • aspirate
  • biopsy
  • gives a more morphological idea of what is happening
33
Q
A
  • portal triad=P
  • C= central vein
  • hexagon = liver lobule
34
Q
A
35
Q
A
  • PSS
36
Q

Neurological signs in a case of Liver Failure

A
37
Q
A

NUTMEG LIVER

  • can be caused by RHS heart failure by venous congestion
38
Q

Describe the lesion

A
  • orange/yellow color
  • capsular
  • swollen
39
Q
A

fatty liver

40
Q
A
  • Immunochemistry or Immunohistology
  • immunoperoxidase to demonstrate cells containing viral antigen
41
Q

Equine Herpes Virus

A
42
Q
A
  • Multifocal haemorrhage
43
Q
A
  • Intracellular viral inclusion body
44
Q

Describe the lesion

A
  • white
  • multifocal
  • encapsulated
  • distributed throughout parenchyma
45
Q
A
  • neutrophils
46
Q
A
  • malignant
  • secondary
  • haemangiosarcoma
47
Q

Why would pancreatic hypoplasia lead to emaciation?

A