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Clin Path > Liver Ch 7 D&P > Flashcards

Liver Ch 7 D&P Flashcards

1
Q

Hepatocellular injury is accompanied by what cell changes what else is often seen and why?

A

Cell swelling, inflammation and/or necrosis.

This may alter bile flow > concurrent intrahepatic cholestasis (and increases in cholestatic parameters.)

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2
Q

What are your three leakage enzymes?

A

AST
ALT
SDH

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3
Q

What percentage of the functional hepatocytes must be lost before alterations of hepatic fxn are detectable by serum biochem testing?

A

Approximately 70% or more of fxnl hepatocytes must be lost before alterations of hepatic fxn are detectable by serum biochem testing.

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4
Q

What are the hepatic functions commonly evaluated by laboratory tests?

A
  • Protein synthesis (albumin, alpha and beta globulins, clotting factors)
  • Uptake and excretion of bilirubin and bile acids
  • uptake of ammonia and conversion to BUN
  • glucose homeostasis, glycogen storage
  • Immune fxn of kuppfer cells and Ag’s from the GI
  • Uptake and excretion of exogenous dyes and indycyanine green etc.
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5
Q

Causes of cholestasis - 5 main ones to know.

A
  • Physical obstruction of bile flow
  • Hepatotoxicity
  • fasting horses
  • *sepsis
  • hereditary defects in bile secretion
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6
Q

The two induced enzymes by cholestasis that increase? What else (2) might increase in the blood with cholestasis?

A

GGT(gamma glutamyl transferase) and ALP.

May also see elevations in Bile acids in the blood and bilirubin (secreted in bile).

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7
Q

*What is the effect of cholestasis on the liver and why?

A

Cholestasis can actually cause hepatocellular damage d/t retention of bile acids, which have a detergent action on cellular membranes.

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8
Q

Affect of shunting on the liver?

A

GI blood bypasses the liver, going directly into systemic circulation and concentrations of stuff normally removed by hepatic processing like bile and ammonia increases and you get liver atrophy due to decreased concentrations of intestinal and pancreatic hepatotrophic factors delivered to the liver.

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9
Q

The elevation in serum leakage enzymes after liver injury depends on what three things?

A

Number of hepatocytes injured
Severity of injury
Half life of the enzyme

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10
Q

When may you see decreases in leakage enzymes?

A

Hepatic atrophy.

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11
Q

In what non liver conditions may you see elevations in some of the liver enzymes?

A
  • When it originates in other tissues as in skeletal or cardiac muscle injury or from RBCs (hemolysis) so you would want to measure CK activity to rule this out.
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12
Q

What are commonly elevated hepatocellular leakage enzymes?

A 
ALT
AST
SDH
LDH
GDH
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13
Q

When does ALT increase and what does it stand for?

A

Alanine aminotransferase.
Sublethal hepatocellular injury or necrosis in the dog or cat.
Muscle necrosis.
Steroid or anticonvulsant admin (mild to mod. inc.)
NOT USEFUL in LARGE ANIMALS and NOT INCLUDED ON panel ( if it is it more likely indicates muscle injury).

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14
Q

What causes AST increase and what does it stand for?

A

Aspartate aminotransferase.
Not liver specific, muscle injury and hemolysis may also increase it. (SO YOU NEED TO CHECK MUSCLE CK AND RULE OUT HEMOLYSIS WHEN THIS IS HIGH, in vivo or in vitro.)

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15
Q

What is SDH, when is it elevated?

A
  • Sorbitol dehydrogenase
  • Its liver specific in all species.
  • enzyme of choice for horses, sheep, goats and cattle (more liver specific than ALT and AST)
  • note it has a short clearance half life and should be frozen if not tested right away.
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16
Q

What is LDH and GDH

A
  • Lactate and Glutamate dehydrogenase respectively.
  • LDH > not liver specific, found in many cells, can increase d/t hemolysis, muscle damage or liver injury, similar to AST.
  • GDH is a marker of liver injury in birds but not specific
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17
Q

What are the two induced hepatic enzymes and where are the present in cells and which types of cells?

A

Membrane bound and increase is the result of enzyme induction (cholestasis, drug, hormonal).

  • GGT and ALP
  • In hepatocytes and biliary epithelial cells.
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18
Q

Which is the best induced enzyme for cholestasis in large animals?

A

GGT

ALP not useful in LA

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19
Q

Increased serum ALP may occur in what conditions? 2 main and 6 more.

A 
Cholestatic dz
Bone lysis or remodeling
Corticosteroid txment
Phenobarb txment
Hepatic nodular hyperplasia
Colic in horses
Feline hepatic lipidosis
Hyperthyroid cats
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20
Q

What are the clinically important ALP isoenzymes?

A

Hepatic, bone, intestinal and corticosteroid induced forms. (the steroid one is only in dogs)

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21
Q

What causes in increase in the liver ALP isoenzyme?
Cats versus dogs.
Compare to bilirubin.

A

-Intrahepatic or extrahepatic cholestasis. (very sensitive for this and precedes hyperbilirubinemia)
Cats have lower ALP activity than dogs.

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22
Q

In cats with cholestatic dz which enzymes increase (2) and compare their increases to each other, and the one exception to this.

A

ALP increases less than GGT in cats EXCEPT in

FELINE hepatic lipidosis where ALP increases more.

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23
Q

Steroid txment increases which liver enzyme?

A

ALP, endogenous or exogenous steroids.
Its an initial increase in the hepatic enzyme followed by a more slow increase of the steroid isoenzyme until it predominates and it can persist for weeks to months after txment stops.
Levamisole inhibition or heat inactivation can be used to diff the steroid form from the others (its resistant to these two and the others are not).

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24
Q

When is the bone ALP isoenzyme increased?

A

Young, rapidly growing animals and animals with lytic or proliferative lesions or animals with active bone resorption (ie hyperparathyroidism)

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25
Q

What is the significance of the intestinal ALP isoenzyme?

A

Only a small fraction of total ALP in dogs and cats. Does not contribute significantly to serum ALP.
It may increase the serum ALP in horses with colic.

26
Q

What is GGT?

A

Gamma glutamyl transferase.
Like ALP its in the brush border or microvilli of hepatocytes, biliary epi cells, renal tubule epi cells and mammary epi cells.

27
Q

When does GGT increase? It which spp is it superior?

A

Induction involving hepatocytes or biliary epithelial cells.

Cholestasis causes increased serum GGT and its better than ALP in cats, horses and cattle.

28
Q

In what other conditions besides cholestasis may GGT increase?

A
  • Severe hepatic necrosis in horses and cattle
  • Corticosteroid administration in dogs
  • High in neonates cuase its high in colostrum
29
Q

What does GGT in the urine mean?

A

Increased GGT in urine may occur with renal tubular injury, increases in the GGT:creatinine ratio can be early indicator of nephrotoxicity.

30
Q

What is bilirubin, where is it produced and how is it metabolized?

A
  • Pigment produced by degradation of the heme portion of Hgb and myoglobin, and its a component of bile.
  • Most is produced in mononuclear phagocytes
  • Its metabolized to urobilinogen by bacteria in the intestine then MAY BE resorbed and excreted in urine.
31
Q

What are the three types of bilirubin?

A

Unconjugated bilirubin
Conjugated bilirubin
Biliprotein (delta bilirubin)

32
Q

How does unconjugated bilirubin move around in the blood - whats its main characteristic in this regard?

A

Its NOT water soluble so its transported in blood bound to albumin.

33
Q

How is bilirubin conjugated, what affect does this have on the molecule

A
  • Unconjugated bili is dissociated from albumin at the hepatocyte cell membrane and taken into hepatocyte by transporters > CONJUGATED in hepatocyte via GLUCURONIDATION > makes it WATER SOLUBLE > secreted in bile canaliculi.
34
Q

What is biliprotein / delta bilirubin and why is it significant?

A

Conjugated bilirubin that is covalently and irreversibly bound to serum albumin.
Variable quantities formed in hyperbilirubinemic conditions, it has a long half life in serum and high concentrations may account for prolonged bilirubinemia after resolution of hepatic dz.

35
Q

What does direct versus indirect bilirubin refer to?

A

Direct = Conjugated bilirubin.
Indirect = Unconjugated bilirubin.
Total bili = Unconj + Conj. I think.

36
Q

Hyperbilirubinemia results in what clinical condition?

A

Jaundice.

37
Q

What are the causes of hyperbilirubinemia?

A
  • Increased production (pre-hepatic / hemolysis)
  • Decreased hepatic uptake (hepatic, loss of liver fxn, fasting in horses, SEPSIS).
  • Cholestasis (post-hepatic; decreased secretion into bile, physical obstruction, hepatocytes swelling etc, extrahepatic cholestasis - remember bilirubin is secreted into bil.e)
38
Q

Which type of bilirubin is found in the urine?

A

Conjugated, cause both unconj and biliprotein are bound to albumin and therefore too large to go through the glomerulus.
If marked bilirubin crystals may appear in urine sediment.

39
Q

Which occurs first, bilirubinuria or bilirubinemia?

A

Bilirubinuria, esp with hepatic and post hepatic causes

40
Q

What are some of the complications when evaluating conjugated versus unconjugated bilirubin?

A
  • Unconj generally dominates in hemolytic dz UNLESS the secretory capacity of the hepatocytes is excedded and then conjugated bili may increase.
  • In horses and cattle hyperbilirubinemia from any cause is typically predominantly unconjugated bilirubin
  • Post hepatic biliary obstruction should just increase conj bili but may also increase unconj bili cause cholestasis (the bile) damage hepatocytes.
41
Q

Which type of bilirubin increases in hepatic dz and why?

A

BOTH
Unconj > decreased bili uptake and conj by damaged hepatocytes.
Conj > Intrahepatic cholestasis from hepatocyte swelling.

42
Q

Other parameters to look at to determine type of hyperbilirubinemia?

A

Anemia that would suggest hemolytic dz

Increased GGT or ALP that would suggest cholestatic dz.

43
Q

Where do bile acids come from adn what do they do?

A
  • Made in liver from cholesterol, secreted into bile and solubilize lipids and aid in fat digestion in the intestine.
  • Most is recyclied thru the portal circulation, ‘enterohepatic circ.’ Hepatocytes remove the bile from portal blood.
  • bile acids can damage hepatocytes in cholestasis thru detergent action on cell membranes.
44
Q

How is bile acid testing performed? What about in horses?

A

-Baseline fasting and postprandial are measured. Feeding induces release of bile so two hour post prandial test increases overall sensitivity of test.
In horses a single test is performed b/c they have to gall bladder so there is no advantage to doing a post sample

45
Q

Four causes of increased bile acid concentration.

A
  • Portosystemic shunt (portal blood bypasses liver and goes into systemic circulation so BA are not removed,and shunting causes atrophy of the liver, reducing functional mass, decreasing the ability of the liver to remove BA from blood.
  • Liver failure
  • Cholestasis with refulx of BA into bloodstream
  • Inappropriate contraction of the GB
46
Q

When may you see decreased BA concentration?

A
  • Small intestine disease (ileal malabsorption).

- Not generally observed in hepatic failure, probably due to reutilization and recirculation

47
Q

Where does Ammonia come from and what happens to it?

A
  • Produced in the GI tract via breakdown of AA and urea by gut microbes and txported via portal blood to liver and converted to UREA by HEPATIC UREA CYCLE ENZYMES.
48
Q

When may hyperammonemia occur?

A
  • Hepatic insufficiency (decreased liver uptake and conversion to urea - may see decreased BUN with this and may take loss of 70% of fxnl mass before hyperammonemia is observed.)
  • PSS, ammonia directly enters systemic circulation.
  • Ruminants fed excessive urea or ammoniated feed additives as a non protein nitrogen source; urea > ammonia via rumen microflora > absorbed to systemic circulation.
49
Q

Clin Path findings with hyperammonemia?

A
  • Ammonium biurate crystals in the urine.
  • Baseline ammonia values (volatile and hard to measure) well above normal, OR may require ammonia tolerance test to detect if normal ammonia and PSS is highly suspected. p223
50
Q

How does hepatic photosensitivity occur?

A

Phylloerythrin is a porphyrin produced from bkdown of chlorophyll by the GI flora of herbivores. > absorbed via portal circulation > removed by hepatocytes > excreted in bile.
- With hepatic insufficiency, phylloerythrin enters the systemic circulation and accumulates in skin where it reacts with sunlight causing free radical formation, inflammation and necrosis. (THIS IS TYPE III) in unhaired or unpigmented areas.- Type I is they eat a naturally photosensitive plant and type II is a defect in porphyrins, which are also a byproduct of RBC metabolism involved in heme synthesis.

51
Q

Three main non liver specific tests or parameters affected by alterations in hepatic synthesis/hemostasis?

A
  • Glucose > reduced hepatic glycogen stores and decreased insulin clearance = hypoglycemia.
    May also see hyperglycemia post prandial d/t decreased hepatic uptake of Glc from portal blood.
  • hypoAlbumin (only if liver dz is chronic but its a non specific indicator cause it can be low in many other conditions like starvation, malabsortpoin, inflammation, PLE, PLN etc.)
    -Alpha and beta globulins decrease
    -Hemostasis, as the vitamin K dependent clotting factors II, VII, IX, X and fibrinogen are produced in liver (have a short half life so def. may show up in acute dz)
52
Q

Multifocal hepatic necrosis typically is associated with what kind of process and what are the lab findings?

A
  • infectious diseases
  • hepatocellular leakage enzymes increase
  • hepatic function tests (or those associated with cholestasis) may be normal or decreased
53
Q

Centrilobular hepatic lesions are generally associated with what process and what are the typical lab findings?

A
  • Hypoxic injury
  • With evidence of cardiovascular dz or anemia is present
  • High protein ascites may occur
  • Mild to Mod increase in leakage enzymes
  • Cholestatic test results WNL as bile canaliculi are at periphery of hepatic lobule, unaffected by centrilobular lesion
  • May be hyperbilirubin if hypoxia d/t anemia
  • Liver fxn tests usually normal
54
Q

Acute submassive or massive hepatic necrosis usually caused by what and what are the typical lab findings?

A
  • Usually due to toxic insult
  • Leakage enzymes markedly increased
  • +/- concurrent cholestasis
  • Hepatic function tests often impaired (Alb WNL cause of long half life but hemostasis abnormalities occur)
55
Q

Large focal hepatic lesions are usually caused by what and what are the typical lab findings?

A
  • Abscesses, infarcts or neoplasms in a small portion of the liver.
  • Acutely there is increase in leakage enzymes but chronically they return to normal
  • Hepatic abscesses in ruminants may only have polyclonal gammopathy as the only laboratory abnormality
56
Q

IN what conditions may you see hepatic lipidosis?

A
  • DM, acute pancreatitis in cats, hepatotoxicity, inflammatory bowel dz, hyperthyroid, starvation and anorexia, esp in obese cats.
  • Triglycerides accumulate in hepatocytes faster than they can be secreted as lipoproteins causing hepatocellular swelling and membrane damage.
57
Q

What are the typical lab findings in hepatic lipidosis?

A
  • Liver leakage enzymes are increased d/t increased membrane permeability.
  • Cell swelling causes intrahepatic cholestasis so bilirubin and bile acids as well as ALP and possible GGT may increase. (esp in cats, ALP increases).
  • Albumin WNL
  • Hyperammonia may occur
  • Prolonged coag tests may occur
58
Q

What causes steroid hepatopathy, what do the hepatocytes look like? What are the lab findings?

A
  • Steroid txment or hyperadrenocorticism
  • Diffuse indistinct vacuolar swelling of hepatocytes with glycogen
    Lab: INcreased leakage (I think they mean induced enzymes).
    ALP is very high, the corticosteroid isoenzyme or if recent the hepatic ALP isoenzyme.
  • Cholestasis occurs to due hepatocyte swelling and compression of bile canaliculi
  • Alb, ammonia, bile acids, hemostasis are unaffected.
59
Q

What are the features and lab findings with cholangitis, cholangiohepatitis and extrahepatic biliary dz?

A

Extrahepatic obstructions with little hepatic infolvement or intrahepatic dz affecting the biliar tract. May see hepatomegaly and icterus.
Lab findings:
- Increased bile acids, bilirubin, ALP, GGT
- Mild to Mod increase in hepatocellular leakage enzymes
- If obstruction is complete may cause malabsorption of fat soluble vitamin K and hemostasis disorders.
- Ammonia is WNL as it has nothing to do with the biliary tract.

60
Q

What are the causes, histo features and lab findings in Chronic progressive liver dz?

A
  • Chronic inflammation, toxicosis, accumulation of metals like Cu and Fe and progressive subtle damage to the liver.
  • Cirrhosis, bile duct hyperplasia with disruption of normal portal circulation and biliary drainage.
  • Lab findings: Increased leakage enzymes ALT, AST, SDH (may actually decline at the end).
  • Indicators of cholestasis (bili, ALP, GGT, BA) increased
  • **ACQUIRED portosystemic shunts may develop d/t restriction of portal blood flow from fibrosis so as blood bypasses liver plasma ammonia and bile acids increase
  • Once greater than 70% lost > hypoalbuminemia, fasting hypoglycemia and abnormal hemostasis may be observed.
  • Polyclonal gammopathy d/t decreased numbers of kuppfer cells so there is reduced clearance of antibodies and/or removal of Ag’s from portal blood.
61
Q

What are the two types of portosystemic shunts and why does liver atrophy occur with these?

A
  • Extra or intrahepatic
  • Hepatic microvascular dysplasia (microscopic shunting) may occur as separate dz or in combination with macroscopic shunts (micro is usually less severe).
  • Atrophy occurs d/t reduced delivery of intestinal and pancreatic hepatotrophic factors
62
Q

What are the typical lab findings with PSS?

A
  • Baseline ammonia and bile acids increased (may actually require post prandial measure to detect abnormality).
  • Leakage enzymes and cholestatic indicators normal
  • Liver may atrophy enough to cause low Alb or decreased BUN
  • Microcytic anemia
  • Acquired PSS is similar but may have increased hepatic enzymes depending on the primary cause of the shunt

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