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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
What are used as markers of hepatic synthetic function? (2)
- Prothrombin Time (PT) | - Albumin
26
T/F: Liver disease must be very severe to cause prolonged PT.
True
27
Autoimmune hepatitis is associated with?
Polyclonal Increase in IgG
28
Primary biliary cirrhosis is associated with?
Polyclonal Increase in IgM
29
Benign Vs. Pathologic Neonatal Jaundice: -Appears within first 24 hours
Pathologic
30
Benign Vs. Pathologic Neonatal Jaundice: -Rises quickly (>5 mg/dL/day)
Pathologic
31
Benign Vs. Pathologic Neonatal Jaundice: -Peaks by day 4-5
Benign *Pathologic persists past 10 days
32
Benign Vs. Pathologic Neonatal Jaundice: -Total bilirubin exceeds 12 mg/dL
Pathologic *Bening rarely exceeds 20
33
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Physiologic
Unconjugated
34
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Breast Milk
Unconjugated
35
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Sepsis or TORCH infection
Conjugated
36
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Inherited disorders of bilirubin metabolism (Gilbert syndrome, Crigler-Najjar syndrome)
Unconjugated
37
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Biliary obstruction (extrahepatic biliary atresia)
Conjugated
38
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Metabolic disorders (galactosemia, fructose intolerance, glycogen storage disease)
Conjugated
39
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Wilson disease, alpha1-antitrypsin diefiiency
Conjugated
40
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Hemolysis
Unconjugated
41
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Hirshsprung, CF, Ileal atresia
Unconjugated
42
Causes of Neonatal Hyperbilirubinemia (Conjugated Vs. Unconjugated): -Dubin-Johnson, Rotor syndrome
(inherited disorders of bilirubin transport) Conjugated
43
In uncomplicated Acute Pancreatitis, when do Amylase levels return to normal?
2-3 days
44
If elevated Amylase levels persist beyond 5 days, what does this suggest?
Psuedocyts
45
T/F: Higher Amylase levels do NOT correlate with greater severity, but is more specific for pancreatitis.
True
46
What percentage of cases of Acute pancreatitis are associated with normal levels of amylase?
10%
47
What conditions is Amylase sensitivity Lowest?
Chronic relapsing and alcoholic
48
Which is more SPECIFIC, Amylase or Lipase?
Lipase
49
How long does Lipase remain elevated?
14 days
50
Which is less dependent on renal clearance, Amylase or LIipase?
Lipase
51
Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9): - Pseudocyst
Amylase - Increase CEA - Normal CA19-9 - Increase
52
Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9): - Serous Cystadenoma
Amylase - Decrease CEA - Decrease CA19-9 - Decrease
53
Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9): - Mucinous Cystic Neoplasm
Amylase - Normal CEA - Increase CA19-9 - Increase
54
Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9): - IPMN
Amylase - Increase CEA - Increase CA19-9 - Normal to Increase
55
Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9): - Solid Pseudopapillary
Amylase - Decrease CEA - Decrease CA19-9 - Decrease
56
Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9): - All three DECREASED levels
- Serous Cystadenoma | - Solid-Pseudopapillary
57
Pancreatic Cyst Fluid Evaluation (Amylase, CEA, CA19-9): - Only one with Normal Amylase
Mucinous Cystic Neoplasm
58
What are the 3 Creatine Kinase (CK) isoenzymes?
- BB (CK1; fast migrating) - MB (CK2) - MM (CK3)
59
Where is CK-BB (CK1) found?
Brain
60
Where is CK-MB (CK2) found?
- Cardiac Muscle (30%) | - Skeletal Muscle (1%)
61
Where is CK-MM (CK3) found?
- Skeletal Muscle (99%) | - Cardiac Muscle (70%)
62
What improves the specificity of CK-MB for myocardial infarction?
Ratio or CK-MB to total CK (the "relative index") | - >5% is suggestive of cardiac source
63
What population may Macro CK (macro CK type 1) be found?
healthy elderly women
64
What population may Mitochondrial CK (macro CK type 2) be found?
Patients with advanced malignancy
65
T/F: Troponin (Tn) is Highly cardiospecific.
True (replaced CK for MI diagnosis)
66
What are causes of Elevated Troponin in Nonischemic states? (9)
- PE - Myocarditis - Pericarditis - Heart failure - Intracranial insults - Rhabdo - Sepsis - Shock - Renal insufficiency
67
What are the causes for analytical false positive troponin elevation?
Interferences (eg. fibrin, heterophilie Abs)
68
What is the main source of B type natriuretic peptide (BNP)?
Ventricular myocytes
69
T/F: Synthesis of BNP correlates directly with ventricular wall tension.
True
70
What is the T1/2 of BNP?
20 minutes (rapidly degraded)
71
what is the T1/2 of NT-proBNP?
1-2 hours

Boards.CP.Chemistry (17 decks)

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