Clin Path Flashcards

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1
Q

What is jaundice? (icterus)

A

Yellowing of the skin and other tissues due to deposition of bilirubin

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2
Q

What is cholestasis?

A

Bile w/o motion

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3
Q

What is hyperbilirubinemia?

A

Increased circulating levels of bilirubin in the blood.

  • Retention form refers to increases in unconjugated
  • Regurgitation form refers to increases in conjugated
  • Combined form refers to increases in both
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4
Q

WHat is Hepatic encephalopathy?

A

signs of CN ds related to liver ds. In the dog & cat it is invariable related to congenital or acquired vascular shunting

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5
Q

What are acute phase reactants?

A

refers to altered (mostly increased) levels of specific proteins (mostly globulins) in the blood. They can include clotting proteins e.g. fibrinogen, haptoglobin and C-reactive protein. They occur in response to a variety of acute/active degenerative/inflammatory conditions

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6
Q

Biochemical tests, (liver “function” tests) can detect 3 basic processes that can occur in liver
disease

A

hepatocellular damage, cholestasis and reduced functional mass.

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7
Q

T/F: Biochemical tests cannot differentiate primary and secondary hepatic ds.

A

TRUE

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8
Q

Active liver cell damage tests which enzymes?

A

AST, ALT, LD, ID, ARG, GD, ICD (depending on sp)

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9
Q

Cholestasis tests depend on which enzymes?

A

ALP (ALKP), GGT (both induces enzymes)

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10
Q

Cholestasis and cell damage tests use

A

bilirubin analysis (total; unconjugated; conjugated)

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11
Q

Reduced functional hepatic mass is determined by

A

Bile acids (will detect all 3 processes but more commonly reduced hepatic mass), Bromsulphopthalein (BSP) test ( no longer used, largely replaced by bile acids analysis), blood ammonia/urea, serum proteins

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12
Q

For levels of serum enzymes to be elevated in liver ds, an active damaging process to a significant number of hepatocytes is required. Is this more likely acute/sub-acute or chronic?

A

acute/sub-acute.

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13
Q

What liver enzyme would be elevated if there was hepatocellular damage (hepatocyte damage) in a dog/cat?

A

ALT - also in certain muscle ds in certain breeds (combine with CK). It is present in the cytoplasm, even changes in cell permeability can increase levels.
–> corticosteroids and anti-convulsants may induce ALT

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14
Q

What liver enzyme is used to detect hepatocyte damage commonly for the horse but also the dog.

A

ID - Iditol dehydrogenase

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15
Q

What species is the enzyme OCT used in to determine hepatic disease (hepatocyte damage)?

A

Liver specific in most species. Rarely used except in pigs.

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16
Q

what enzyme would you use to determine cholestasis(hepatic ds) in the dog/cat

A

ALP, lesser so GGT

17
Q

What enzyme would you use to determine in cholestatis (liver ds) was occuring in the horse?

A

GGT, lesser so ALP.

18
Q

What enzyme would you use to determine is cholestasis(hepatic ds) was occuring in the sheep/cattle/pig?

A

GGT.

19
Q

What enzymes would show up if there were cardiac/skeletal damage in any species?

A

CK, AST, KD (esp isoenzyme analysis)

Dogs and cats maybe ALT elevations

20
Q

Which enzyme warrants further investigation in the cat in regards to cholestasis and why?

A

ALP, irrespective of the magnitude in change as cats have lower levels in hepatocytes and biliary epithelium and shorter plasma T1/2 in the cat (6 hours compared to 72hrs in the dog).

21
Q

What does the Van den Bergh’s test measure?

A

Serum bilirubin

22
Q

Why might bilirubin levels in the male dog need to be interpreted with care?

A

THe dog has a low renal threshold to conjugated bilirubin. The male dog’s kidney has good ability to break down haemoglobin and to conjugate bilirubin.

23
Q

Icterus of the tissues due to the presence of significant hyperbilirubinemia has been divided into 3 types:

A
  1. Retention hyperbilirubinemia -> unconjugated bilirubin predominant in the blood (haemolytic crises are the main cause; extrahepatic and hepatic ds can interfere with hepatic uptake and conjugation e.g. anorexia )
  2. Regurgitation (cholestatic) hyperbilirubinemia -> conjugated is predominant form. Bilirubinuria is usually present. Both intra and extrahepatic pbstruction to bile flor produce regurgitation hyperbilirubinemia
  3. Combined hyperbilirubinemia -> develops both due to retention and regurgitation methods -> both conjugated and unconjudated bilirubin levels in the blood are increased. Bilirubinuria usually present. Can occur in both acute/chronic hepatic ds.
24
Q

How are bile acids synthesised?

A

by hepatocytes from cholesterol and then conjugated prior to excretion in the bile. Stored and concentated in the gall bladder during the interdigestive period.

25
Q

What is serum protein estimation useful in deterimine?

A

Serum protein estimation (total and types of protein) can be useful in detecting a chronic
hepatopathy. It is rarely of use in early hepatopathies (but there may be increased levels of
globulins in acute hepatic disease. These increased proteins are usually acute phase reactants.

26
Q

What is significant about cholesterol in determining ds?

A

Cholesterol is utilised for the synthesis of bile acids. Hypercholesterolemia can occur in
cholestatic conditions but may also occur in the nephrotic syndrome, acute pancreatitis,
congenital hyperlipidemias and certain endocrinopathies (DM, hyperadrenocorticism,
hypothyroidism). Increases may also occur post prandially. Increased blood levels of cholesterol
alone will not cause gross turbidity of the serum or plasma. Decreased serum cholesterol can
occur in hepatic shunting and in gut problems (Exocrine Pancreatic Insufficieancy,
malabsorption, Protein Losing Gastroenteropathy).

27
Q

What is malassimilation?

A

Collective for maldigestion and malabsorption.

28
Q

What is maldigestion? and malabsorption?

A

maldigestion = abnormality in the failure of normal digestive processes

malabsoroption = abnormality resulting in the failure of normal absorptive processes

29
Q

What are the types of exocrine pancreatic disorders?

A

acute pancreatic necrosis (necrotizing pancreatitis) and pancreatic insufficiency.

30
Q

What enzymes can be used to confirm acute bouts of pancreatic necrosis in the dog and other sp. ?

A

Elevation of serum enzymes. In the dog and cat elevations of AMS and LPS.

along with other supportive lab findings - haematology (stress leuk with left shift); hyperlipidemia (fasting); fluid imbalance (due to emesis and loss of HCl); pre-renal azotemia; non-septic exudate in peritoneal cav; transient, mild hyperglycemia; transient hypocalcemia.

NOTE: Hepatocellular necrosis and cholestasis may occur secondarily to the acute pancreatic
necrosis and need to be investigated appropriately.