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Clinical Pathology Exam 4 > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

What three things must happen for an enzyme to be able to accumulate in the blood?

A

The enzymatic activity in the target cell must be greater than in the blood

It must have a long enough half life that it can accumulate in the blood

It must have access to the blood stream directly or through lymphatics

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2
Q

Why would an enzyme increase in the blood?

A

Leakage from damaged cells

Increased synthesis of the enzyme

Decreased inactivation or clearance

Absorption of maternal enzymes in colostrum

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3
Q

What does a high sensitivity mean?

Specificity?

A

High true positives and low false negatives

High true negatives and low false positives

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4
Q

When would increased enzymes be significant?

A

When it is 2 to 3 fold increase over upper RI

2-3= mild
3-6= moderate
>6= marked
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5
Q

What are the exceptions to the “>2-3x RI” rule?

A

ALP in cats, GGT, and SDH

Low-grade inflammatory lesion

Decreased number of target cells due to necrosis or fibrosis

Inhibitors of enzyme activity

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6
Q

What does low enzymes mean?

A

Not clinically significant

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7
Q

What type of enzymes come from muscles?

A

Only leakage

CK, AST, LDH

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8
Q

What do muscle enzymes tell you?

A

Correlates with number of injured cells, not injury type

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9
Q

Can you determine the cause of a myopathy from a chem panel?

A

No

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10
Q

What type of enzyme is CK? Where does it come?

A

Muscle leakage

Skeletal muscle mainly

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11
Q

Describe the half life of CK

A

Very short- goes up and comes down quickly following muscle injury

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12
Q

What might cause interference in measuring CK?

A

Hemolysis

Difficult blood draw

Young animals, post exercise

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13
Q

What type of enzyme is AST? Where does it come from?

A

Leakage

Muscle, hepatocytes, other cells

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14
Q

Describe the half life of AST in comparison with CK?

A

Much longer than CK

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15
Q

ALT in muscle damage?

A

May see mild elevation in dogs and cats, but not usually the main cause

may see in young dogs and cat with muscular dystrophy

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16
Q

What blood changes might you see with MASSIVE rhabdomyolysis

A

Hyperkalemia
Hyperphosphatemia
Increased creatinine

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17
Q

Other than chem panel, what else might you see with a myelopathy?

A

Myoglobin in the urine

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18
Q

What type of enzyme is AST?

Where does it come from?

A

Leakage from skeletal muscle and hepatocytes

*low sensitivity

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19
Q

What type of enzyme is ALT?
Where does it come from?
Who is it not used in?
What artifactually increases the values?

A

Leakage from hepatocytes
Not used in large animals
Hemolysis increases the value in cats and pigs

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20
Q

What type of enzyme is SDH?
Where does it come from?
Who is it used in?

A

Leakage from hepatocytes

Horses, pigs, ruminants

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21
Q

What leakage enzymes increase in myopathies?

Liver injury? Both?

A

Myopathies- CK
Liver injury- ALT, SDH
Both- AST

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22
Q

What enzymes are inducible in the liver?

A

ALP, GGT

23
Q

What is cholestasis? What enzymes are markers of cholestasis?

A

Impaired biliary flow

ALP and GGT

24
Q

What are other markers besides enzymes of cholestasis?

A

Tbili, cholesterol, bile acids

25
Q

What is extrahepatic cholestasis?

Intrahepatic cholestasis?

A

Extrahepatic- gall bladder and common bile duct affected

Intrahepatic- canaliculi and hepatic biliary duct affected

*can’t tell difference without imaging

26
Q

What type of enzyme is ALP?

Where does it come from?

A

Hepatocytes, biliary epithelium, osteoblasts, colostrum

Inducible

27
Q

Describe the half life for ALP

A

3 days in dog, 6 hours in cat

28
Q

What is it important to take note of small increases in ALP in cats

A

Because ALP has such a short half life in cats

29
Q

What species is ALP most sensitive in?

A

Dog>cattle>cat>horse

*Increases in ALP will precede hyperbilirubinemia in dog

30
Q

What can cause increased ALP activity?

A

Cholestasis (dog>cattle>cat>horse)

Glucocorticoids (dog) (drugs, Cushings, chronic stress, phenobarbitol)

Less than one year old/bone pathology

Colostrum ingestion

31
Q

What type of enzyme is GGT?

Where does it come from?

A

Induced from biliary epithelium, hepatocytes, mammary gland/colostrum, renal tubules in urine

32
Q

What can cause increased GGT?

A

Cholestasis (more specific than ALP) (more specific in cat, horse, cattle)

Colostrum ingestion

Drug induction in the dog

33
Q

What are enzymes not a test of?

A

Function!

34
Q

What does the liver do?

A

Makes most proteins (except gamma globulins), coag factors, glucose, cholesterol, urea, and bilirubin

Processes RBCs and hemoglobin

Filters bacteria from portal blood

35
Q

Which enzymes tell you there is hepatocyte injury

A

Leakage- ALT, AST, SDH

36
Q

Which enzymes/markers tell you there is cholestasis

A

ALP, GGT, bilirubin, bile acids, cholesterol

37
Q

What markers/tests tell you about liver function

A

Bile acids, ammonia, bilirubin, albumin, glucose, BUN, cholesterol, coag factors

38
Q

What tests, when increased, show you the liver is having problems excreting?

A

Bilirubin, bile acids, ammonia

39
Q

Which tests, when decreased, show you the liver is having problems synthesizing?

A

Albumin, urea (BUN), cholesterol, glucose, coag factors

40
Q

What is the metabolic pathway of bilirubin?

A

Hemoglobin degraded to unconjugated bilirubin —> in plasma, unconjugated bilirubin binds to albumin —> uptake by hepatocytes —> hepatic conjugation —> excretion through biliary tract into intestine

41
Q

What type of bilirubin will you see if you have pre-hepatic hyperbilirubinemia?

Hepatic hyperbilirubinemia?

Post-hepatic hyperbilirubinemia?

A

Mostly unconjugated

Mix of conjugated/unconjugated

Mostly conjugated

42
Q

What things would cause hyperbilirubinemia?

A

Increased production of unconj bilirubin (hemolytic disease)

Defective uptake of unconjugated bilirubin (hepatic dysfunction, anorexia in horse)

Defective conjugation/excretion of bilirubin (hepatic dysfunction, functional cholestasis)

Cholestasis

43
Q

Who would be the best candidate for using the split bilirubin test?

A

Anorectic horse with suspected liver disease

44
Q

Describe the metabolism of bile acids

A

Synthesized from cholesterol in hepatocytes, conjugated and excreted into the bile
Stored in gall bladder
CCK causes it to be released into intestine to aid in fat digestion
Reabsorbed in ileum and enters portal circulation to be recycled

45
Q

What does bile acid testing test for?

A

Hepatocellular dysfunction
Cholestasis
Hepatic circulation disorder

*all of these are necessary for bile acids to be synthesized and cleared

46
Q

What does increased bile acids mean?

A

Decreased hepatic clearance (portovascular anomalies, shunts, microvascular dysplasia)

Hepatocellular dysfunction

Decreased hepatic biliary excretion (intra- and extra- hepatic cholestasis, functional cholestasis)

47
Q

What may falsely increase bile acid? Falsely decrease?

A

Lipemia may falsely increase

Hemolysis may falsely decrease

48
Q

What are you thinking if your bile acids are decreased in a postprandial sample compared to fasted sample?

A

Animal not truly fasted
Spontaneous gallbladder contraction
Delayed gastric emptying
Animal vomited before postprandial draws

49
Q

What breed has naturally high bile acids?

A

Maltese dogs

50
Q

What are some problems with bile acid assays?

A

Excess fat can induce lipemia that interferes with measurement

Intestinal disease like PLE can falsely decrease

*therapeutic use of bile acids doesn’t affect measurement

51
Q

When would ammonia be increased?

A

When more than 60% of liver is dysfunctional

Portosystemic shunts

Hepatic enphalopathy

52
Q

What are some problems of ammonia testing?

A

Hemolysis increases ammonia
Improper handling decreases ammonia
In vitro issues in the test tubes

53
Q

What are causes of hyperammonemia caused by decreased blood clearance?

A

Hepatocellular dysfunction (decreased uptake)
Hepatic vascular shunts (PSS)
Urea cycle disorders (rare)

54
Q

What are causes of hyperammonemia cause by increased production or intake?

A

Physiologic (post prandial, post exercise)

Urea toxicosis (cattle)

Intestinal disease (horses)

Clinical Pathology Exam 4 (4 decks)

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