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Boards.CP.Chemistry > Liver, pancreas, heart > Flashcards

Liver, pancreas, heart Flashcards

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1
Q

Where is AST found? (7)

A
  • Cardiac muscle
  • Liver
  • Skeletal muscle
  • Kidney
  • Brain
  • Lung
  • Pancreas

*In Decreasing order of concentration

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2
Q

Where is ALT found? (2)

A

Liver and Kidney

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3
Q

AST:ALT ratio in alcoholics/cirrhosis

A

> 1

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4
Q

LD1 and LD2 are found where? (3)

A
  • Heart
  • RBCs
  • Kidney
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5
Q

LD3 is found where? (4)

A
  • Lung
  • Spleen
  • Lymphocytes
  • Pancrease
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6
Q

LD4 and LD5 are found where? (2)

A
  • Liver

- Skeletal muscle

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7
Q

Relative concentrations of Lactate Dehydrogenase (LD) isoenzymes in normal serum.

A

LD2>LD1>LD3>LD4>LD5

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8
Q

Conditions associated with “Flipped LD ratio” (LD1>LD2) (3)

A
  • MI
  • Hemolysis
  • Renal infarction
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9
Q

Where is ALkaline Phosphatase concentrated? (4)

A
  • Bone
  • Liver
  • Intestine
  • Placenta
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10
Q

How do you confirm hepatobiliary origin of elevate ALK PHOS?

A

-GGT or 5’-nucleotidase

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11
Q

T/F: Alkaline phosphatase is a SENSITIVE marker for hepatic metastases.

A

True

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12
Q

Decreased Alk Phos is found in what conditions? (2;4)

A
  • Hypophosphatasia (inborn deficiency)
  • Malnutrition

Also reported in:

  • Hemolysis
  • WIlson Dz
  • Theophylline therapy
  • Estrogen therapy
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13
Q

What type of bilirubin in H20 INSOLUBLE?

A

Unconjugated (Indirect)

*Bound to albumin in blood

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14
Q

T/F: Unconjugated bilirubin does NOT appear in urine.

A

True

*Bilirubinuria indicated CONJUGATED hyperbilirubinemia

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15
Q

What type of bilirubin in H20 SOLUBLE?

A

Conjugated (Direct)

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16
Q

What happens to conjugated bilirubin?

A

Excreted in bile into intestine where bacteria convert some of it to URObilinogen.

*Some urobilinogen is reabsorbed and excreted in the urine

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17
Q

What type of bilirubin is measured in direct reaction?

A

Conjugated

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18
Q

What causes Conjugated hyperbilirubinemia?

A

Excretory defect

>30% of serum bilirubin conjugated

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19
Q

What causes Unconjugated hyperbilirubinemia?

A
  • Increased production (Hemolysis)

- Hepatic defect that prevents uptake or conjugation

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20
Q

What is the MCC of conjugated hyperbilirubinemia?

A

Impaired hepatic excretion

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21
Q

DDx of Conjugated Hyperbilirubinemia (Hepatic or Cholestatic):

-Alkaline Phosphatase >3X upper limit normal

A

Cholestatic

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22
Q

DDx of Conjugated Hyperbilirubinemia (Hepatic or Cholestatic):

-Transaminases >3X upper limit of normal

A

Hepatic

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23
Q

DDx of Conjugated Hyperbilirubinemia (Hepatic or Cholestatic):

Which one has Increased Serum Cholesterol?

A

Cholestatic

Hepatic has normal

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24
Q

DDx of Conjugated Hyperbilirubinemia (Hepatic or Cholestatic):

Which one is associated with itching (pruritis)?

A

Cholestatic

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25
Q

What are used as markers of hepatic synthetic function? (2)

A
  • Prothrombin Time (PT)

- Albumin

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26
Q

T/F: Liver disease must be very severe to cause prolonged PT.

A

True

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27
Q

Autoimmune hepatitis is associated with?

A

Polyclonal Increase in IgG

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28
Q

Primary biliary cirrhosis is associated with?

A

Polyclonal Increase in IgM

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29
Q

Benign Vs. Pathologic Neonatal Jaundice:

-Appears within first 24 hours

A

Pathologic

30
Q

Benign Vs. Pathologic Neonatal Jaundice:

-Rises quickly (>5 mg/dL/day)

A

Pathologic

31
Q

Benign Vs. Pathologic Neonatal Jaundice:

-Peaks by day 4-5

A

Benign

*Pathologic persists past 10 days

32
Q

Benign Vs. Pathologic Neonatal Jaundice:

-Total bilirubin exceeds 12 mg/dL

A

Pathologic

*Bening rarely exceeds 20

33
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Physiologic

A

Unconjugated

34
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Breast Milk

A

Unconjugated

35
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Sepsis or TORCH infection

A

Conjugated

36
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Inherited disorders of bilirubin metabolism (Gilbert syndrome, Crigler-Najjar syndrome)

A

Unconjugated

37
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Biliary obstruction (extrahepatic biliary atresia)

A

Conjugated

38
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Metabolic disorders (galactosemia, fructose intolerance, glycogen storage disease)

A

Conjugated

39
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Wilson disease, alpha1-antitrypsin diefiiency

A

Conjugated

40
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Hemolysis

A

Unconjugated

41
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Hirshsprung, CF, Ileal atresia

A

Unconjugated

42
Q

Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated):

-Dubin-Johnson, Rotor syndrome

A

(inherited disorders of bilirubin transport)

Conjugated

43
Q

In uncomplicated Acute Pancreatitis, when do Amylase levels return to normal?

A

2-3 days

44
Q

If elevated Amylase levels persist beyond 5 days, what does this suggest?

A

Psuedocyts

45
Q

T/F: Higher Amylase levels do NOT correlate with greater severity, but is more specific for pancreatitis.

A

True

46
Q

What percentage of cases of Acute pancreatitis are associated with normal levels of amylase?

A

10%

47
Q

What conditions is Amylase sensitivity Lowest?

A

Chronic relapsing and alcoholic

48
Q

Which is more SPECIFIC, Amylase or Lipase?

A

Lipase

49
Q

How long does Lipase remain elevated?

A

14 days

50
Q

Which is less dependent on renal clearance, Amylase or LIipase?

A

Lipase

51
Q

Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9):

  • Pseudocyst
A

Amylase - Increase
CEA - Normal
CA19-9 - Increase

52
Q

Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9):

  • Serous Cystadenoma
A

Amylase - Decrease
CEA - Decrease
CA19-9 - Decrease

53
Q

Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9):

  • Mucinous Cystic Neoplasm
A

Amylase - Normal
CEA - Increase
CA19-9 - Increase

54
Q

Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9):

  • IPMN
A

Amylase - Increase
CEA - Increase
CA19-9 - Normal to Increase

55
Q

Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9):

  • Solid Pseudopapillary
A

Amylase - Decrease
CEA - Decrease
CA19-9 - Decrease

56
Q

Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9):

  • All three DECREASED levels
A
  • Serous Cystadenoma

- Solid-Pseudopapillary

57
Q

Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9):

  • Only one with Normal Amylase
A

Mucinous Cystic Neoplasm

58
Q

What are the 3 Creatine Kinase (CK) isoenzymes?

A
  • BB (CK1; fast migrating)
  • MB (CK2)
  • MM (CK3)
59
Q

Where is CK-BB (CK1) found?

A

Brain

60
Q

Where is CK-MB (CK2) found?

A
  • Cardiac Muscle (30%)

- Skeletal Muscle (1%)

61
Q

Where is CK-MM (CK3) found?

A
  • Skeletal Muscle (99%)

- Cardiac Muscle (70%)

62
Q

What improves the specificity of CK-MB for myocardial infarction?

A

Ratio or CK-MB to total CK (the “relative index”)

- >5% is suggestive of cardiac source

63
Q

What population may Macro CK (macro CK type 1) be found?

A

healthy elderly women

64
Q

What population may Mitochondrial CK (macro CK type 2) be found?

A

Patients with advanced malignancy

65
Q

T/F: Troponin (Tn) is Highly cardiospecific.

A

True (replaced CK for MI diagnosis)

66
Q

What are causes of Elevated Troponin in Nonischemic states? (9)

A
  • PE
  • Myocarditis
  • Pericarditis
  • Heart failure
  • Intracranial insults
  • Rhabdo
  • Sepsis
  • Shock
  • Renal insufficiency
67
Q

What are the causes for analytical false positive troponin elevation?

A

Interferences (eg. fibrin, heterophilie Abs)

68
Q

What is the main source of B type natriuretic peptide (BNP)?

A

Ventricular myocytes

69
Q

T/F: Synthesis of BNP correlates directly with ventricular wall tension.

A

True

70
Q

What is the T1/2 of BNP?

A

20 minutes (rapidly degraded)

71
Q

what is the T1/2 of NT-proBNP?

A

1-2 hours

Boards.CP.Chemistry (17 decks)

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