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CP Reviewer 2 > Chemistry > Flashcards

Chemistry Flashcards

1
Q

AST is mainly found in what tissues?

A

Cardiac muscle.

Liver.

Skeletal muscle.

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2
Q

A threefold elevation in AST can mean what?

A

Liver disease.

Rhabdomyolysis.

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3
Q

At what time of day are AST and ALT highest?

A

In the afternoon.

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4
Q

Tissues that contain LD1 and LD2.

A

Heart.

Red blood cells.

Kidneys.

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5
Q

Tissues that contain LD4 and LD5.

A

Liver.

Skeletal muscle.

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6
Q

Tissues that contain LD3.

A

Lungs.

Spleen.

Lymphocytes.

Pancreas.

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7
Q

How to establish the hepatobiliary origin of alkaline phosphatase.

A

Measure 5’ nucleotidase or GGT.

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8
Q

Which isoenzyme of alkaline phosphatase is most susceptible to heat and urea?

A

The isoenzyme of bone.

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9
Q

Which isoenzymes of alkaline phosphatase are most susceptible to L-phenylalanine?

A

The isoenzymes of placenta and intestine.

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10
Q

Physiological causes of elevated alkaline phosphatase (3).

A

Pregnancy.

Bone growth.

Postprandial state in group O or group B Lewis-positive secretors.

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11
Q

Medications that can raise the alkaline phosphatase.

A

Oral contraceptives.

NSAIDS.

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12
Q

Main source of 5’ nucleotidase.

A

Biliary epithelium.

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13
Q

Main sources of ammonia.

A

Skeletal muscle and gut.

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14
Q

Hyperammonemia: Causes in adults (3).

A

Liver failure.

Bypass of portal circulation.

Protein overload in the gut.

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15
Q

Hyperammonemia: Pediatric cause.

A

Inborn error of metabolism.

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16
Q

Hyperammonemia: Surgical cause.

A

Ureterosigmoidostomy.

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17
Q

Hyperammonemia: Microbiological cause.

A

Infection with urea-splitting organisms.

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18
Q

Hyperammonemia: Pharmacological causes.

A

Valproic acid.

TPN.

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19
Q

Origin of urobilinogen.

A

Bacterial metabolism of conjugated bilirubin in the gut.

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20
Q

What is δ-bilirubin?

A

Bilirubin that is covalently bound to albumin as a result of prolonged hyperbilirubinemia.

Very slowly cleared from the blood.

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21
Q

How is conjugated bilirubin measured?

A

Directly, i.e. without the use of an accelerator.

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22
Q

How is unconjugated bilirubin measured?

A

Use of an accelerator (alcohol) permits all bilirubin to be measured.

Total bilirubin − conjugated bilirubin = unconjugated bilirubin.

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23
Q

Conditions that increase the delivery of unconjugated bilirubin to the liver.

A

Right heart failure.

Cirrhosis.

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24
Q

Gilbert’s syndrome:

A. Definition.
B. Drugs that cause a similar condition.

A

A. Unconjugated hyperbilirubinemia due to mildly impaired conjugation; uptake of unconjugated bilirubin by the hepatocyte may also be impaired.

B. Rifampin, probenecid.

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25
Q

Crigler-Najjar syndrome:

A. Definition.
B. Cause of secondary disease.

A

A. Unconjugated hyperbilirubinemia due to impaired conjugation within the hepatocytes.

B. Hypothyroidism.

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26
Q

Dubin-Johnson syndrome:

A. Definition.
B. Pharmacological causes.

A

A. Conjugated hyperbilirubinemia due to impaired secretion into the canaliculus.

B. Estrogen, cyclosporine.

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27
Q

Cholestasis leads to what type of hyperbilirubinemia?

A

Conjugated.

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28
Q

Cholestatic vs. hepatocellular jaundice: Which one causes ___?

A. a greater elevation of alkaline phosphatase
B. a greater elevation of AST and ALT
C. elevated cholesterol
D. pruritus

A

A,C,D: Cholestatic.

B: Hepatocellular.

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29
Q

Relation of elevated PT to liver disease.

A

Indicates severe impairment of hepatocellular synthetic function.

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30
Q

Effect on immunoglobulins of

A. Autoimmune hepatitis.
B. Primary biliary cirrhosis.

A

A. Elevated IgG.

B. Elevated IgM.

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31
Q

Effect of liver disease on the ratio of serum albumin to serum immunoglobulins.

A

Decreased due to decreased albumin and increased immunoglobulins.

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32
Q

Physiologic neonatal jaundice:

A. Time of onset.
B. Velocity of rise in total bilirubin.
C. Time of peak of total bilirubin.
D. Usual maximum of total bilirubin.

A

A. About 2-3 days after delivery.

B. No more than 5 mg/dL/day.

C. Usually by day 4 or 5 after delivery.

D. No more than 20 mg/dL.

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33
Q

Pathological neonatal jaundice:

A. Time of onset.
B. Velocity of rise of total bilirubin.
C. Time of peak of total bilirubin.
D. Value of conjugated bilirubin.

A

A. Sometimes within the first 24 hours after delivery.

B. More than 5 mg/dL/day.

C. May continue to rise for more than a week.

D. >2 mg/dL.

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34
Q

Pathologic jaundice: Leading causes.

A

Sepsis.

Hemolytic disease of the newborn.

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35
Q

In uncomplicated pancreatitis, when does serum amylase rise and return to normal?

A

Rise: 2-24 hours.

Return to normal: 2-3 days.

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36
Q

Possible meaning of a prolonged rise in serum amylase with pancreatitis.

A

A complication such as a pseudocyst.

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37
Q

Relation of high serum amylase to pancreatitis.

A

Does not correlate with severity of pancreatitis but is more specific for pancreatitis.

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38
Q

Serum lipase:

A. How long it stays elevated in pancreatitis.
B. Advantages over serum amylase.

A

A. Up to 14 days.

B. More specific for pancreatitis; not affected by renal clearance.

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39
Q

Normal serum amylase in pancreatitis:

A. How often?
B. Associated types of pancreatitis.

A

A. In about 10% of cases.

B. Alcoholic; chronic relapsing.

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40
Q

Nonpancreatic causes of elevated serum amylase (9).

A

DKA.
Acute cholecystitis.
Peptic ulcer disease.

Bowel obstruction.
Bowel ischemia.

Ectopic pregancy.
Salpingitis.

Renal insufficiency.
Macroamylasemia.

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41
Q

Ranson’s criteria upon admission:

A

Age: >55 years.

WBC >16,000.

AST >250.

LDH >350.

Glucose >200.

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42
Q

Ranson’s criteria: After admission.

A

48 hours after admission:

Increase in BUN >5 mg/dL.
Calcium less than 8 mg/dL.
PaO₂ less than 60 mmHg.
Base deficit greater than 4 mEq/L.
Fluid sequestration >6 L.
Decrease in hematocrit >10%.
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43
Q

72-hour quantitation of fecal fat:

A. Procedure.
B. Interpretation.

A

A. High-fat diet is given for 3 days before collection and during the 3 days of the collection.

B. Fecal fat >20 g/day suggests exocrine pancreatic dysfunction.

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44
Q

Fluid chemistry: Pancreatic pseudocyst.

A

Elevated amylase and CA 19-9.

Normal CEA.

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45
Q

Fluid chemistry: Serous cystadenoma.

A

Deceased amylase, CA 19-9, CEA.

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46
Q

Fluid chemistry: Mucinous cystic neoplasm.

A

Elevated CEA, CA 19-9.

Normal amylase.

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47
Q

Fluid chemistry: Intraductal papillary neoplasm.

A

Elevated amylase, CEA.

Normal or elevated CA 19-9.

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48
Q

Fluid chemistry: Solid-cystic tumor.

A

Decreased amylase, CA 19-9, CEA.

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49
Q

Isoenzymes of creatine kinase.

A

CK-BB: Brain; fastest migration.

CK-MB: Mostly cardiac muscle; intermediate migration.

CK-MM: Mostly skeletal muscle; slowest.

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50
Q

Relative index:

A. Definition.
B. Interpretation.

A

A. Ratio of CK-MB to total CK.

B. A value >5% implies cardiac origin.

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51
Q

Macro-CK (type 1): Clinical association; migration.

A

Found in healthy elderly women.

Faster than CK-MM but slower than CK-MB.

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52
Q

Macro-CK, type 2:

A. Synonym.
B. Migration.
C. Clinical association.

A

A. Mitochondrial CK.

B. Slower than MM.

C. May be seen in advanced malignancy.

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53
Q

Troponin: Reference value.

A

Everything up to the 99th percentile.

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54
Q

Troponin: Non-ischemic cardiac causes of elevation (3).

A

Pericarditis.

Myocarditis.

Heart failure.

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55
Q

Troponin: Non-cardiac causes of elevation (5).

A

Pulmonary embolism.

Intracranial insults.

Shock.
Sepsis.

Renal insufficiency.

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56
Q

Troponin: Causes of analytical false positives.

A

Heterophile antibodies.

Fibrin.

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57
Q

Diagnosis of myocardial infarction: Abnormal initial troponin value.

A

Requires at least 20% elevation in cardiac TnI at 3 or 6 hours, plus supporting clinical evidence.

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58
Q

Diagnosis of myocardial infarction: Normal initial troponin value.

A

Requires at least a 50% increase in cardiac TnI at 3 or 6 hours, plus supporting clinical evidence.

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59
Q

Indication that elevated troponin may be of non-cardiac origin.

A

Chronic elevation.

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60
Q

Half-lives of BNP and NT-pro-BNP.

A

BNP: 20 minutes.

NT-Pro-BNP: 1-2 hours.

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61
Q

Albumin: Half-life.

A

17 days.

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62
Q

Prealbumin: Half-life.

A

48 hours.

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63
Q

Prealbumin: Functions.

A

Transport of the complex of vitamin A and retinoic-acid-binding protein.

Transport of thyroxine.

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64
Q

Prealbumin: Appearance of band on electrophoresis.

A

Serum: Inconspicuous.

CNS: Prominent.

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65
Q

How acute inflammation affects the serum proteins.

A

Albumin, prealbumin, and transferrin are decreased.

γ-globulins may be normal or decreased.

Everything else is increased.

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66
Q

How chronic inflammation affects the serum proteins.

A

Decreased: Albumin, prealbumin.

Increased: Everything else.

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67
Q

α₁ band of SPEP: Main component.

A

α₁-Antitrypsin.

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68
Q

α₂ band of SPEP: Main components.

A

α₂-Macroglobulin.

Haptoglobin.

Ceruloplasmin.

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69
Q

β₁ band of SPEP: Main component.

A

Transferrin.

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70
Q

β₂ band of SPEP: Main components.

A

IgA, C3.

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71
Q

γ band of SPEP: Main components.

A

Immunoglobulins, CRP.

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72
Q

Proteins found at the interfaces between bands on SPEP.

A

Albumin-α₁: HDL.

α₁-α₂: GC globulin, α₁-antichymotrypsin, α₁-acid glycoprotein.

α₂-β₂: Hemoglobin if there is hemolysis.

β₁-β₂: LDL.

β₂-γ: Fibrinogen if there is incomplete clotting.

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73
Q

Significance of α₂-macroglobulin (2).

A

Elevated in renal disease and liver disease.

Retained in the nephrotic syndrome.

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74
Q

Transferrin: Appearance on CSF electrophoresis.

A

Double peak due to partial asialation (to form the tau protein).

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75
Q

CRP: Analytic sensitivity of highly sensitive assays.

A

Detect as little as 0.5 mg/L.

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76
Q

CRP: Stratification of values.

A

3-10 mg/dL: Associated with low-level chronic inflammation and poor outcomes from cardiovascular events.

Greater than 10 mg/dL: Associated with inflammation and collagen-vascular diseases.

Less than 3 mg/dL: Normal.

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77
Q

SPEP: Nephrotic syndrome.

A

Fading of all bands except that of α₂-macroglobulin.

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78
Q

SPEP pattern: Acute inflammation.

A

Increased α₁ and α₂ bands.

Normal or decreased γ-globulins.

Everything else is decreased.

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79
Q

SPEP pattern: Cirrhosis.

A

Decreased albumin.

β-γ bridging.

Blunting of α₁ and α₂ bands.

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80
Q

Biclonal gammopathy:

A. Incidence.
B. Most common with which immunoglobulin?

A

A. 3-4% of M proteins.

B. IgA (because of monomers and dimers).

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81
Q

Pseudo-M spike: Causes (7).

A 
Hemoglobin.
Fibrin.
Excess transferrin.
Excess CRP.
Excess of tumor markers, esp. CA 19-9.
Certain antibiotics.
Radiocontrast agents.
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82
Q

SPEP: Typical location of

A. IgG.
B. IgA.
C. IgM.

A

A. γ region.

B. β₂ region.

C. β-γ interface.

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83
Q

UPEP pattern: Glomerular proteinuria.

A

Bands at albumin and α₁ regions.

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84
Q

UPEP pattern: Tubular proteinuria.

A

Loss of small proteins that are normally filtered by the tubules, e.g. β₂-microglobulin, α₁-microglobulin, and light-chain immunoglobulins.

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85
Q

Causes of overflow proteinuria.

A

Hemoglobinuria.

Myoglobinuria.

Bence Jones proteins.

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86
Q

Type I cryoglobulins:

A. Definition.
B. Clinical associations.

A

A. Monoclonal immunoglobulins.

B. Multiple myeloma, Waldenström’s macroglobulinemia.

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87
Q

Type II cryoglobulins:

A. Definition.
B. Clinical association.

A

A. Monoclonal IgM + polyclonal IgG.

B. Rheumatoid arthritis: The monoclonal IgM often has specificity for the Fc portion of IgG.

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88
Q

Type III cryoglobulins:

A. Definition.
B. Clinical association.

A

A. Polyclonal IgG and polyclonal IgM.

B. Rheumatoid arthritis.

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89
Q

Which cryoglobulins are considered mixed?

A

Types II and III.

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90
Q

Mixed cryoglobulinemias: Clinical associations (5).

A

Hepatitis C.
Chronic liver disease.
Chronic infections.

Lymphoproliferative disorders.

Autoimmune diseases.

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91
Q

Mixed cryoglobulinemias: Manifestations of the systemic immune-complex disease (7).

A 
Palpable purpura (LCV).
Arthralgias.
Hepatosplenomegaly.
Lymphadenopathy.
Anemia.
Sensorineural deficits.
Glomerulonephritis.
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92
Q

Mixed cryoglobulinemias:

A. Most common type of renal disease.
B. How this disease appears on EM.

A

A. Membranoproliferative glomerulonephritis, type II.

B. Subendothelial electron-dense deposits in a fingerprint-like pattern.

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93
Q

SPEP: Usual pH.

A

8.6.

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94
Q

Immunofixation electophoresis: Steps.

A
  1. Patient’s sample is placed in 6 wells.
  2. Electric current is applied.
  3. Antisera for IgG, IgA, IgM, and κ and λ light chains are added.
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95
Q

Steps of immunophenotyping (immunofixation).

A
  1. Patient’s sample is added.
  2. Microspheres with bound antibodies to IgG, IgA, IgM, and κ and λ light chain are added.
  3. Electric current is applied.
  4. Where the abnormal spike disappeared, one can see which bead took it away.
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96
Q

Cause of spurious hyponatremia.

A

Drawing the sample proximal to an intravenous or central line.

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97
Q

Pseudohyponatremia:

A. Type of analyzer affected.
B. Causes.

A

A. Any that uses the indirect method, in which the sample must be diluted first.

B. Hyperproteinemia, hypertriglyceridemia, hypercholesterolemia.

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98
Q

Pseudohyponatremia: Effect on osmolality and osmolality gap.

A

Osmolality is normal, but there is an increased osmolality gap.

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99
Q

Hypertonic hyponatremia: Causes.

A

Hyperglycemia.

Mannitol.

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100
Q

Hyponatremia due to hyperglycemia: Correction factor.

A

ΔNa = [1.6 × (serum glucose - 100)] / 100.

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101
Q

In the setting of true hypo-osmotic hyponatremia, what suggests that renal disease may be the cause?

A

Urine Na >30 mEq/L.

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102
Q

Hypovolemic hypo-osmotic hyponatremia: Causes (8).

A

Urine Na below 30: Vomiting, diarrhea, third-spacing.

Urine Na above 30: Diuretics, renal insufficiency, adrenal insufficiency, renal tubular acidosis, cerebral salt-wasting syndrome.

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103
Q

Euvolemic hypo-osmotic hyponatremia: Causes (5).

A

Urine Na below 30: Psychogenic polydipsia.

Urine Na above 30: SIADH, hypothyroidism, adrenal insufficiency, drugs (desmopressin, SSRIs, TCAs, MDMA, chlorpropamide).

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104
Q

Hypervolemic hypo-osmotic hyponatremia: Causes (4).

A

Cirrhosis.

Nephrosis.

CHF.

Renal failure.

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105
Q

Hypernatremia: Basic etiologies.

A

Inability to drink water.

Iatrogenic.

Diabetes insipidus.

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106
Q

Central diabetes insipidus: Causes.

A

Mass or trauma affecting the neurohypophysis and/or the hypothalamus.

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107
Q

Nephrogenic diabetes insipidus: Causes (6).

A 
Renal medullary disease.
Hypercalcemia.
Hypokalemia.
Renal tubular acidosis.
Fanconi's syndrome.

Drugs: Demeclocycline, lithium, gentamicin, amphotericin B.

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108
Q

Hypokalemia is associated with which types of renal tubular acidosis?

A

Types 1 and 2.

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109
Q

Hypokalemia: Five eponymous diseases that can cause it.

A

Bartter’s syndrome.

Gitelman’s syndrome.

Liddle’s syndrome.

Cushing’s syndrome.

Conn’s syndrome.

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110
Q

Hypokalemia can result from what other electrolyte abnormality?

A

Hypomagnesemia.

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111
Q

Hypokalemia: How to recognize a possible renal cause.

A

Urine K >30 mEq/day.

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112
Q

Hypokalemia: Nonrenal causes (3).

A

GI losses: Vomiting, diarrhea, villous adenoma, nasogastric suction.

Metabolic alkalosis.

Correction of diabetic ketoacidosis.

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113
Q

Hyperkalemia: Artifactual causes in vitro.

A

Leukocytosis.

Clotting.

Hemolysis.

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114
Q

Hyperkalemia: Artifactual causes during phlebotomy.

A

Blood draw proximal to infusion of potassium.

Excessive fist clenching.
Prolonged use of tourniquet.
Use of small-bore needle.
Traumatic blood draw.

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115
Q

True hyperkalemia: Causes (6).

A

Acidosis.
Addison’s disease.

Iatrogenic.
Potassium-sparing diuretics.

Renal failure.
Rhabdomyolysis.

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116
Q

Relation between hyperkalemia and acidosis.

A

Acidosis is nearly always associated with hyperkalemia.

Exception: Renal tubular acidosis, types 1 and 2.

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117
Q

How much of calcium is bound to albumin?

A

About 50%.

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118
Q

How does pH affect the amount of free calcium?

A

Acidosis increases it.

Alkalosis decreases it.

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119
Q

Hypercalcemia: Finding on EKG.

A

High-peaked T waves.

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120
Q

Hypercalcemia: Neurological manifestations.

A

Lethargy.

Slowed mentation.

Depression.

Hyporeflexia.

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121
Q

Hypercalcemia: Possible gastroenterological complications.

A

Peptic-ulcer disease.

Pancreatitis.

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122
Q

Primary hyperparathyroidism: Laboratory findings (4).

A

Hypercalcemia.

Hypophosphatemia.

Increased ratio of chloride to phosphate.

Increased urinary cAMP.

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123
Q

Humoral hypercalcemia of malignancy: Causes (6).

A 
SCC.
HCC.
RCC.
T-ALL.
Breast carcinoma.
Hypercalemic variant of small-cell carcinoma of the ovary.
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124
Q

Familial hypocalciuric hypercalcemia: Gene and its location.

A

CASR (calcium-sensing receptor) on 3q21.1.

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125
Q

Type of diuretic associated with hypercalcemia.

A

Thiazide.

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126
Q

Endocrinological causes of hypercalcemia (3).

A

Addison’s disease.

Acromegaly.

Hyperthyroidism.

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127
Q

Forms of parathyroid hormone: Biological activities and half-lives.

A

Intact and N-terminal: Active; 5 minutes.

C-terminal and mid-portion: Inactive; longer half-life.

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128
Q

Hypocalcemia: Findings on EKG.

A

Low-voltage T waves.

Prolonged QT interval.

Dysrhythmias.

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129
Q

Leading cause of primary hypoparathyroidism.

A

Iatrogenic.

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130
Q

Relationship between hypomagnesemia and PTH secretion.

A

Transient or mild hypomagnesemia may stimulate secretion.

Prolonged or severe hypomagnesemia may suppress it.

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131
Q

Hypocalcemia: Genetic cause.

A

DiGeorge’s syndrome.

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132
Q

Classes of diuretics that may cause hypocalcemia.

A

Loop diuretics.

Osmotic diuretics.

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133
Q

How renal failure can lead to hypocalcemia.

A

The excess serum phosphate chelates the calcium.

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134
Q

Acidemia vs. acidosis.

A

Acidemia: Acidic pH of the blood.

Acidosis: A condition that will lead to acidemia unless there is compensation.

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135
Q

Henderson-Hasselbalch equation.

A

pH = pKa + log([base]/[acid]).

7.4 = 6.1 + log[(24)/(0.03 × 40)].

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136
Q

Clue that a given acid-base disorder may be metabolic (or respiratory).

A

Metabolic: pH and bicarbonate move in the same direction.

Respiratory: pH and bicarbonate move in opposite directions.

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137
Q

Anion gap: Formula.

A

AG = [Na] − [Cl] − [bicarbonate].

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138
Q

Why is the anion gap normal in some forms of metabolic acidosis?

A

Because the chloride is elevated.

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139
Q

Causes of a decreased anion gap.

A

Hypoalbuminemia.

Paraproteinemia.

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140
Q

Osmolal gap: Formula and normal value.

A

OG = Measured osmolality − (2[Na] − [glucose]/18 − [BUN]/2.8).

Normal value: <10.

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141
Q

Causes of metabolic acidosis with an increased anion gap.

A 
Methanol.
Uremia.
Diabetic ketoacidosis.
Paraldehyde.
Alcoholic ketoacidosis.
Lactic acidosis.
Ethylene glycol.
Salicylates.
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142
Q

Causes of metabolic acidosis with a normal anion gap.

A 
Diarrhea.
Renal tubular acidosis.
Ureterosigmoidostomy.
NH₄Cl.
Carbonic anhydrase inhibitors.

TPN.
Recovery from diabetic ketoacidosis.

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143
Q

Causes of an increased osmolal gap with metabolic acidosis.

A

Ethylene glycol, propylene glycol.

Methanol.

Paraldehyde.

Ethanol (sometimes).

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144
Q

Causes of increased osmolal gap without metabolic acidosis.

A 
Isopropanol.
Mannitol.
Acetone.
Glycerol.
Ethanol (sometimes).
Sorbitol.
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145
Q

How to tell whether metabolic alkalosis will respond to chloride.

A

Urine Cl less than 10 mEq/L: Responsive.

Urine Cl greater than 10 mEq/L: Resistant.

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146
Q

Causes of chloride-responsive metabolic alkalosis.

A 
Diuretics.
Vomiting.
Villous adenoma.
Nasogastric suction.
Carbenicillin.
Contraction alkalosis.
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147
Q

Causes of chloride-resistant metabolic alkalosis.

A 
Bartter's syndrome.
Milk-alkali syndrome.
Cushing's syndrome.
Hyperaldosteronism.
Exogenous corticosteroids.
Licorice.
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148
Q

Relationship between BUN and GFR.

A

The BUN underestimates the GFR, especially at higher concentrations of BUN.

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149
Q

Azotemia vs. uremia.

A

Azotemia: Elevated BUN.

Uremia: Azotemia with toxic effects.

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150
Q

Relationship between creatinine and GFR.

A

The creatinine overestimates the GFR, especially at higher concentrations of creatinine.

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151
Q

Creatinine clearance: Formula, typical reference range (including units).

A

CrCl = (urine creatinine ÷ plasma creatinine) × (urine volume ÷ time).

80-120 mL/minute.

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152
Q

At what point does the relationship between creatinine and GFR become linear?

A

When GFR is about half normal.

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153
Q

Nonglomerular influences on creatinine.

A

Muscle mass.
Muscle activity.
Muscle injury.

Protein intake.

Age, race, gender.

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154
Q

Ratio of BUN to creatinine: Normal.

A

About 10 to 1.

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155
Q

Ratio of BUN to creatinine: Causes of high value.

A

Prerenal azotemia.

Early postrenal azotemia.

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156
Q

Ratio of BUN to creatinine: Types of renal failure with a normal value.

A

Intrarenal azotemia.

Late postrenal azotemia.

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157
Q

Cystostatin C: Utility.

A

Estimates the GFR.

Strongly predicts cardiovascular mortality in patients with chronic renal disease.

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158
Q

Proteinuria:

A. Normal value.
B. Definition of “significant proteinuria”.

A

A. 150 mg/day.

B. >300 mg/day.

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159
Q

Value of a random urine sample in screening for proteinuria.

A

A random urine protein and a concurrent urine creatinine are as good as a 24-hour urine protein in screening for proteinuria.

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160
Q

Proteinuria:

A. Sensitivity of the urine dipstick.
B. Sensitivity of the microalbuminuria screen.

A

A. 30 mg/dL.

B. 0.3 mg/dL.

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161
Q

Significant microalbuminuria:

A. Type of specimen.
B. Measured analytes and their units.

A

A. Random urine.

B. Albumin and creatinine in mg/g.

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162
Q

β₂-microglobulin and lysozyme.

A. Handling by the nephron.
B. Clinical utility.

A

A. Freely filtered by the glomerulus and completely reabsorbed by the tubules.

B. Their presence in the urine suggests renal tubular dysfunction.

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163
Q

Who should be testing annually for chronic kidney disease (according to the National Kidney Foundation)?

A

Those with diabetes, hypertension, or a family history of renal disease.

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164
Q

Chronic kidney disease: Recommended screening tests.

A

Microalbuminuria screen.

Estimated GFR.

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165
Q

Chronic kidney disease: Definition.

A

Estimated GFR <60

  • or -

Microalbuminuria for 3 consecutive months.

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166
Q

Chronic kidney disease: Stages.

A

Stage 1: GFR >90 but with microalbuminuria.

Stage 2: GFR between 60 and 89.

Stage 3: GFR between 30 and 59.

Stage 4: GFR between 15 and 29.

Stage 5 (renal failure): GFR below 15, or dialysis dependent

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167
Q

Acute renal failure: Three basic types.

A

Prerenal, intrarenal, postrenal.

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168
Q

Intrarenal acute renal failure: Leading causes.

A

Acute glomerulonephritis.

Acute tubular necrosis.

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169
Q

Acute tubular necrosis: Leading causes.

A

Ischemia, toxins.

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170
Q

Urinary sediment: Glomerulonephritis.

A

Dysmorphic red cells, red-cell casts.

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171
Q

Urinary sediment: Acute tubular necrosis.

A

Tubular casts.

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172
Q

Urinary sediment: Pyelonephritis.

A

White-cell casts.

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173
Q

Urinary sediment: Allergic interstitial nephritis.

A

Eosinophils.

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174
Q

Drugs that cause acute tubular necrosis.

A

Contrast agents, aminoglycosides, amphotericin B.

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175
Q

Drugs that cause acute glomerular injury.

A

Cyclosporine, penicillamine.

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176
Q

Drugs that cause acute tubulointerstitial nephritis.

A

NSAIDs.

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177
Q

Fraction excretion of sodium: Formula.

A

FENa = (urine Na × plasma Cr) / (urine Cr × plasma Na).

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178
Q

Prerenal vs. intrarenal acute renal failure:

A. Ratio of BUN to creatinine.
B. Fractional excretion of sodium.
C. Fractional excretion of urea.

A

A. Prerenal: >10 to 1; intrarenal: about 10 to 1.

B. Prerenal: Less than 1%.

C. Prerenal: Less than 35%.

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179
Q

Hepatorenal syndrome: Frequent cause.

A

Profound fluids shifts resulting from treatment of ascites.

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180
Q

Bilirubin: Maximal absorbance by scanning spectrophotometry.

A

450 nm.

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181
Q

Oxyhemoglobin: Maximal absorbance.

A

About 410 nm.

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182
Q

Amniotic-fluid bilirubin: Range at which absorbances are measured.

A

340 to 560 nm.

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183
Q

What is the ΔOD450?

A

The difference between the measured absorbance at 450 nm and the theoretical absorbance based on the assumption that amniotic fluid contains no pigment.

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184
Q

What is a Liley chart used for?

A

To estimate the severity of fetal hemolysis. The ΔOD450 is plotted against the gestational age.

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185
Q

hCG: Molecular structure.

A

α subunit: Shared with FSH, LH, and TSH.

β subunit: Unique.

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186
Q

hCG: Leading cause of false positives.

A

Heterophile antibodies.

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187
Q

hCG: Conditions associated with pituitary production.

A

Pituitary tumor.

Postmenopausal state.

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188
Q

hCG: When it becomes detectable in a normal gestation.

A

At about 6-8 days after conception.

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189
Q

hCG: Phase and frequency of doubling.

A

About every 48 hours during the first trimester.

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190
Q

hCG: Peak during normal gestation.

A

About 100,000 mIU/mL near the end of the first trimester, followed by a slight decline and a plateau early in the 2nd trimester.

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191
Q

hCG: Causes of high value in an intrauterine pregnancy (4).

A

Multiple gestation.

Polyhydramnios.

Eclampsia.

Hemolytic disease of the fetus.

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192
Q

hCG: Clue to an ectopic pregnancy.

A

Failure to rise at least 66% within 48 hours.

However, this can be seen in up to 20% of normal pregnancies, and up to 20% of ectopic pregnancies show a normal rise in hCG.

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193
Q

hCG: Level after removal of

A. Ectopic pregnancy.
B. Uncomplicated molar pregnancy.

A

A. Can remain elevated for several weeks.

B. Can remain elevated for up to 10 weeks.

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194
Q

hCG: Schedule of monitoring after removal of uncomplicated molar pregnancy.

A

hCG is measured weekly until undetectable for 3 weeks, and then monthly for 1 year.

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195
Q

“Quad” screen:

A. Components.
B. When performed.
C. Sensitivity for detection of Down’s syndrome.

A

A. hCG, AFP, unconjugated estradiol, dimeric inhibin A.

B. At 18 weeks of gestation.

C. 78%.

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196
Q

“First trimester” test:

A. Components.
B. When performed.
C. Sensitivity for Down’s syndrome.

A

A. hCG, pregnancy-associated plasma protein A, thickness of nuchal fold as estimated by ultrasonography.

B. At 10-13 weeks.

C. 83%.

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197
Q

Integrated screens:

A. Components of the “serum integrated screen”.
B. Components of the “full integrated screen”.
C. Sensitivity of the latter for Down’s syndrome.

A

A. hCG, AFP, uE, DIA, PAPP-A.

B. All of the above plus nuchal-fold thickness.

C. 88%.

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198
Q

How are serum gestational markers expressed for purposes of calculation?

A

As multiples of the mean (MoM).

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199
Q

What makes the cutoff between “positive” and “negative” in prenatal screening for Down’s syndrome?

A

The theoretical risk for Down’s syndrome in a child born to a healthy 35-year-old mother, i.e. 1 in 270.

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200
Q

Serum markers: Down’s syndrome.

A

Elevated hCG, DIA.

Decreased AFP, uE.

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201
Q

Serum markers: Edwards’ syndrome.

A

hCG, AFP, and uE are all decreased.

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202
Q

Serum markers: Neural-tube defect.

A

Elevated AFP.

Normal hCG.

Decreased uE.

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203
Q

Use of test for fetal fibronectin.

A

Absence of FF has a strong NPV, but its presence does not have a high PPV for imminent preterm birth.

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204
Q

Use of transvaginal ultrasound to predict imminent preterm birth.

A

High NPV but not a high PPV.

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205
Q

Fetal-lung maturity.

A. Accelerating factor.
B. Impeding factor.

A

A. Stressful pregnancy, i.e. corticosteroids.

B. Maternal diabetes mellitus.

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206
Q

Fetal-lung maturity: When testing becomes relevant.

A

At 32-38 weeks of gestation.

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207
Q

Fetal-lung maturity: Best specimen for testing.

A

Uncontaminated amniotic fluid.

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208
Q

Fetal-lung maturity: When a confirmatory test is indicated.

A

When the screening test yields a result below the cutoff for maturity.

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209
Q

Normal ratio of lecithin to sphingomyelin.

A

At least 2.5 to 1.

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210
Q

Ratio of lecithin to sphingomyelin: Confounding factors and their effects.

A

Meconium falsely decreases the ratio.

Blood normalizes it to 1.5.

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211
Q

Fetal-lung maturity: Preferred method of testing in diabetic mothers.

A

Phospatidylglycerol concentration.

212
Q

Phospatidylglycerol concentration:

A. Advantage of this method.
B. Disadvantage.

A

A. Not affected by blood or meconium.

B. Cannot be used until 35-36 weeks of gestation.

213
Q

Lamellar-body count:

A. Value that indicates fetal-lung maturity.
B. Limitations.

A

A. At least 50,000/mL.

B. Blood and meconium.

214
Q

Fluorescence-polarization method: What is measured?

A

The ratio of surfactant to albumin, in mg/g.

215
Q

Fluorescence-polarization method: Cutoffs for maturity and immaturity.

A

Maturity: Above 55 mg/g.

Immaturity: Below 40 mg/g.

216
Q

How do the following analytes change during pregnancy?

A. Albumin.
B. Calcium.
C. Creatinine.

A

A. Decreases.

B. Decreases, but ionized calcium remains the same.

C. Decreases.

217
Q

How do the following analytes change during pregnancy?

A. Fibrinogen.
B. BUN.
C. Urine protein.

A

A. Increases.

B. Decreases by about half.

C. Roughly doubles.

218
Q

How do hematocrit and hemoglobin change during pregnancy?

A

Hematocrit: -4 to -7%.

Hemoglobin: -1.5 to -2 mg/dL.

219
Q

What happens to responsiveness to insulin during pregnancy?

A

Human placental lactogen, secreted early in the third trimester, imparts relative insulin resistance.

220
Q

How does the half-life of a drug affect the timing of doses?

A

A dose is given at the completion of each half-life.

221
Q

By what kinetics are most drugs eliminated in the body?

A

By first-order (exponential) kinetics.

Elimination of ethanol follows zero-order kinetics.

222
Q

Steady state:

A. Definition.
B. When it typically occurs.

A

A. The state in which the amount of drug entering the body equals the amount of drug leaving it.

B. After 4-5 half-lives.

223
Q

How does the chemical composition of a drug influence its volume of distribution?

A

Lipophilic drugs have a large volume of distribution.

Hydrophilic drugs have a smaller volume of distribution.

224
Q

Volume of distribution: Units and formula.

A

Volume of distribution =

Dose (mg) / concentration in plasma (mg/L) / body weight (kg).

225
Q

What value of ___ would suggest alteration of urine to be tested for drugs of abuse?

A. creatinine
B. nitrite

A

A. Less than 20 mg/dL.

B. Greater than 500 mg/dL.

226
Q

Window of detection: Cannabinoids.

A

Single use: 3 days.

Chronic use: Up to 30 days.

227
Q

Window of detection: Benzodiazepines.

A

2-10 days, depending on the drug.

228
Q

Window of detection: Amphetamines.

A

2-3 days.

229
Q

Window of detection: Barbiturates.

A

3-15 days, depending on the drug.

230
Q

Window of detection: Opiates.

A

2-3 days.

231
Q

Window of detection: Ethanol.

A

One day.

232
Q

Window of detection: Cocaine.

A

2-3 days.

233
Q

Ethanol: Metabolism.

A

Converted by alcohol dehydrogenase to acetaldehyde, which is then converted by aldehyde dehydrogenase to acetic acid.

234
Q

Ethanol: Ratio of concentration in breath to concentration in whole blood.

A

1 to 2100.

235
Q

Ethanol: Correlation of concentration in the blood to clinical manifestations.

A 
>0.05%: Sobriety.
0.05-0.1%: Euphoria.
0.1-0.2%: Excitement.
0.2-0.3%: Confusion.
0.3-0.4%: Stupor.
>0.4%: Coma and death.
236
Q

Ethanol: Use of GGT to monitor consumption.

A

A normal GGT suggests abstinence for at least 4 weeks.

237
Q

Ethanol: Use of carbohydrate-deficient transferrin to monitor consumption.

A

At least as sensitive and probably more specific than GGT.

238
Q

Class of drugs associated with hyperthermia, dry skin, flushing, mental-status changes.

A

Anticholinergics.

239
Q

Class of drugs associated with hypertension, mydriasis, tachycardia, anxiety.

A

Adrenergics.

240
Q

Class of drugs associated with increased secretions, vomiting, gastrointestinal cramps, miosis.

A

Cholinergics / organophosphates.

241
Q

Oxygen-saturation gap: Definition, normal value.

A

The difference between the oxygen saturation measured by co-oximetry and that measured by pulse oximetry.

Normally <5%.

242
Q

Causes of abnormally high venous oxygen content.

A

Carbon monoxide.

Cyanide.

Hydrogen sulfide.

Azides.

243
Q

Causes of increased oxygen-saturation gap.

A

Carbon monoxide.

Cyanide.

Hydrogen sulfide.

Methemoglobin.

244
Q

How can one determine whether ethanol is responsible for an increased osmolal gap?

A

Modified calculated osmolality =

2*[Na] + [glucose]/18 + [BUN]/2.8 + [ethanol]/4.6.

245
Q

Metabolites of each of the following alcohols:

A. Methanol.
B. Ethylene glycol.
C. Isopropanol.

A

A. Formaldehyde, formic acid.

B. Glycolic acid, oxalic acid.

C. Acetone.

246
Q

Lead: Tissues in which it gets distributed.

A

Erythrocytes, bones, kidneys.

247
Q

Lead toxicity: Mechanisms.

A

Binding to sulfhydryl groups.

Direct toxicity to mitochondria.

248
Q

Lead toxicity: Affected enzymes of heme synthesis.

A

δ-ALA dehydratase.

Ferrochelatase.

249
Q

Lead toxicity: Metabolites of heme synthesis that accumulate.

A

Zinc protoporphyrin.

Free erythrocyte protoporphyrin.

250
Q

Lead toxicity: Other affected enzymes of erythrocytes.

A

5’ nucleotidase.

ATPase of sodium channel.

251
Q

Lead toxicity: Relationship to iron deficiency.

A

Both conditions increase the ZPP and the FEP.

Iron deficiency exacerbates lead toxicity.

252
Q

Lead toxicity: Classical neurological sign.

A

Bilateral wrist drop.

253
Q

Lead toxicity: Renal effects.

A

Glycosuria.

Aminoaciduria.

Phosphaturia.

254
Q

Lead toxicity: Gastrointestinal effect.

A

Abdominal pain.

255
Q

Lead toxicity: Diagnostic concentration.

A

At least 10 μg/dL in venous blood (by atomic-absorption spectrophotometry).

256
Q

Carbon monoxide: Normal source; normal value of carboxyhemoglobin.

A

From the breakdown of heme.

<1%.

257
Q

Carbon monoxide toxicity: Mechanisms.

A

Binding to hemoglobin.

Inhibition of cellular oxidative pathways.

258
Q

Carbon monoxide toxicity: Nonspecific tests.

A

Anion gap.

Lactate level.

Cyanide level.

Cardiac enzymes.

259
Q

Carbon monoxide toxicity: Specific test.

A

Co-oximetry.

260
Q

Carbon monoxide toxicity: Correlation of level of carboxyhemoglobin to clinical manifestations.

A

> 2%: Normal smoker.

2-6%: Normal nonsmoker.

10-20%: Dyspnea on exertion.

20-50%: Headache, lethargy, syncope.

> 50%: Coma and death.

261
Q

Acetaminophen toxicity: Phases.

A
  1. Mild nausea and abdominal pain that abate within hours.
  2. Progressive liver injury beginning after 24 hours.
  3. Fulminant hepatic failure.
  4. Recovery, transplant, or death.
262
Q

When can one use the Rumack-Matthew nomogram?

A

No sooner than 4 hours after ingestion of acetaminophen.

263
Q

Acetaminophen: Potentially toxic dose in healthy individuals.

A

150 mg/kg.

264
Q

Acetaminophen: Nontoxic metabolism.

A

Conjugation with sulfate or glucuronide.

265
Q

Acetaminophen: Toxic metabolite and its effect.

A

N-Acetyl-p-benzoquinoneimine.

Causes necrosis in zone 3 (centrilobular).

266
Q

Cyanide toxicity: Mechanism.

A

Inhibits cytochrome a3, thus uncoupling the electron-transport chain.

267
Q

Cyanide toxicity: Laboratory findings.

A

Anion gap with lactic acidosis.

Hyperglycemia.

Increased venous oxygen content.

268
Q

Cyanide toxicity: Treatment.

A

Sodium nitrite and amyl nitrite convert hemoglobin to methemoglobin, which binds cyanide.

Sodium thiosulfate converts cyanide to nontoxic thiocyanate.

269
Q

Salicylate toxicity: Associated acid-base abnormalities.

A

Respiratory alkalosis due to direct stimulation of medulla.

Metabolic acidosis, at first compensatory and then due to inhibition of oxidative pathways.

Respiratory acidosis due to CNS depression.

270
Q

Arsenic toxicity: Distribution of arsenic in body fluids and tissues.

A

Skin, hair, nails, urine.

271
Q

Arsenic toxicity: Mechanism.

A

Inhibits oxidative production of ATP.

272
Q

Acute arsenic toxicity: Affected body systems.

A

Gastrointestinal tract: Nausea, vomiting, abdominal pain, bloody diarrhea.

Hematopoietic system: Basophilic stippling, cytopenias.

273
Q

Chronic arsenic toxicity: Affected tissues.

A 
Nerves (peripheral neuropathy).
Kidneys (nephropathy).
Skin (hyperpigmentation, hyperkeratosis).
Nails (transverse lines).
Marrow (myelodysplasia).
274
Q

Arsenic toxicity: Best and worst tests.

A

Best: 24-hour urinary arsenic excretion.

Worst: Blood arsenic concentration.

275
Q

Tricyclic antidepressants: Toxic effects.

A

Anticholinergic effects.

Prolongation of the QRS complex.

Ventricular dysrhythmias.

276
Q

Organophosphate / carbamate toxicity: Laboratory tests.

A

Each of the following should be decreased:

Red-cell cholinesterase (more specific).

Plasma pseudocholinesterase (more sensitive).

277
Q

Acute mercury intoxication: Clinical manifestations.

A

Respiratory distress.

Renal failure.

278
Q

Chronic mercury intoxication: Clinical syndromes.

A

Acrodynia: Autonomic dysfunction, painful desquamating rash of palms and soles.

Erethism: Personality changes, irritability, loss of fine-motor coordination.

279
Q

Mercury toxicity: Laboratory tests.

A

Elemental mercury: 24-hour urinary mercury excretion.

Organic mercury: Analysis of whole blood or hair.

280
Q

Digoxin: Half-life.

A

36 hours.

281
Q

Digoxin: When to take the sample for measurement of the drug level.

A

8-12 hours after the last dose.

282
Q

Digoxin: Factors that can increase toxicity.

A 
Hypercalcemia.
Hypomagnesemia.
Hypokalemia.
Hypoxia.
Hypothyroidism.
Quinidine.
Calcium-channel blockers.
283
Q

Conditions that predispose to the production of digoxin-like immunoreactive substances (4).

A

Pregnancy.

Neonatal state.

Liver failure.

Renal failure.

284
Q

Procainamide: Metabolite.

A

N-acetylprocainamide: Synthesized in the liver but cleared by the kidneys; has pharmacological activity of its own.

285
Q

Aminoglycosides: Monitoring.

A

Peak: Efficacy.

Trough: Toxicity.

286
Q

Lithium: Therapeutic range.

A

0.4 to 1.2 mmol/L.

287
Q

Lithium: Range of possible toxicity.

A

> 1.5 mmol/L.

288
Q

Lithium: Schedule of routine monitoring.

A

Every 1-3 months, 12 hours after the last dose.

289
Q

Lithium: Half-life.

A

8-40 hours.

290
Q

Lithium: Monitoring after initiation of therapy or a change in dose.

A

After about 5 half-lives or about 2-8 days.

291
Q

Lipoproteins: Lipids.

A

Chylomicrons, VLDL: Triglycerides.

IDL, LDL, HDL: Cholesterol.

292
Q

Lipoproteins: Associated apolipoproteins.

A 
Chylomicrons: B48, A-1, C-II, E.
VLDL: B100, C, E.
IDL: B100, E.
LDL: B100.
HDL: A-1, C, E.
293
Q

Chylomicrons: Fate in the bloodstream.

A

Lipoprotein lipase removes the monoglycerides and the free fatty acids.

The remnants are taken up by the liver or the LDL receptor.

294
Q

VLDL: Origin.

A

Hepatic metabolism and repackaging of triglycerides and cholesterol.

295
Q

VLDL: Fate.

A

Lipoprotein lipase metabolizes it to IDL or eventually to LDL.

296
Q

LDL: Purpose and fate.

A

Main carrier of cholesterol to cells.

Taken up by means of its apo-B100 and the LDL receptor.

297
Q

HDL: Origin.

A

Synthesized in the liver.

298
Q

Measured lipoproteins.

A

Total cholesterol, HDL, triglycerides.

299
Q

Calculated estimate of VLDL:

A. Formula.
B. Invalidating factors.

A

A. VLDL ≈ Triglycerides ÷ 5.

B. Chylomicrons are present, TG >400 mg/dL, or there is type 3 dyslipidemia.

300
Q

Method of direct measurement of lipoproteins.

A

Ultracentrifugation.

301
Q

Effect of excess of lipoproteins on refrigerated plasma.

A

Chylomicrons: Cream layer.

VLDL: Turbidity or opacity.

Others: No visible change.

302
Q

Lipid excess associated with eruptive xanthomas.

A

Triglycerides.

303
Q

Lipoprotein excess associated with periorbital xanthelasma.

A

LDL.

304
Q

Dyslipidemias associated with increased triglycerides and normal cholesterol.

A

Type I: Chylomicrons.

Type IV: VLDL.

Type V: Chylomicrons and VLDL.

305
Q

Dyslipidemias associated with increased LDL and normal triglycerides.

A

Type IIa.

306
Q

Dyslipidemias associated with increase in both triglycerides and LDL.

A

Type IIb: VLDL and LDL.

Type III: IDL and remnant lipoproteins.

307
Q

Dyslipidemias associated with tendinous xanthomas.

A

Types IIa, IIb, and III.

308
Q

Familial hypercholesterolemia:

A. Underlying defect.
B. Inheritance.
C. Lethal state.

A

A. Lack of LDL receptors.

B. Autosomal dominant.

C. Homozygosity.

309
Q

Familial hypercholesterolemia:

A. Apolipoproteins normally taken up by the receptor.
B. Resulting lipoprotein excesses in disease.

A

A. Apo-B100, apo-E.

B. VLDL, IDL, LDL.

310
Q

Hyper-apo-B-lipoproteinemia:

A. Associated dyslipidemia.
B. Excess lipoprotein.
C. Mechanism of disease.

A

A. Type IIa.

B. LDL.

C. The mutant apo-B100 does not bind normally to the LDL receptor.

311
Q

IDL: Origin and fate.

A

Arises from the action of endothelial lipoprotein lipase on VLDL.

IDL gets taken up by the LDL receptor or converted by hepatic lipoprotein lipase to LDL.

312
Q

Lp(a).

A

LDL with an added apolipoprotein A.

Increase in Lp(a) is associated with atherosclerosis.

313
Q

Familial LPL deficiency: Associated type of dyslipidemia.

A

Type I.

314
Q

Apolipoprotein C-II deficiency:

A. Associated type of dyslipidemia.
B. Mechanism of disease.

A

A. Type I.

B. Apolipoprotein C-II is needed for lipoprotein lipase to be able to act on chylomicrons.

315
Q

Familial hypertriglyceridemia: Associated type of dyslipidemia.

A

Type IV.

316
Q

Familial dysbetalipoproteinemia: Associated type of dyslipidemia.

A

Type III.

317
Q

Familial combined hyperlipidemia:

A. Associated types of dyslipidemia.
B. Inheritance.
C. Underlying defect.

A

A. Types IIa, IIb, and IV.

B. Autosomal dominant.

C. Overproduction of apolipoprotein B100.

318
Q

Hypercholesterolemia: Major primary cause.

A

Familial hypercholesterolemia.

319
Q

Hypercholesterolemia: Secondary causes (7).

A 
Diabetes.
Hypothyroidism.
Cholestasis.
Cyclosporine.
Loop diuretics.
Thiazide diuretics.
Nephrotic syndrome.
320
Q

Hypertriglyceridemia: Primary causes.

A

LPL deficiency.

Apo-C-II deficiency.

Familial hypertriglyceridemia.

Familial combined hyperlipidemia.

321
Q

Hypertriglyceridemia: Secondary causes (10).

A 
Diabetes.
Pregnancy.
Obesity.
Renal insufficiency.
Hepatitis.
Nephrotic syndrome.
β-blockers.
Isotretinoin.
Corticosteroids.
Ethanol.
322
Q

Mixed hypertriglyceridemia and hypercholesterolemia: Primary causes.

A

Familial combined hyperlipidemia.

Dysbetalipoproteinemia.

323
Q

Tangier disease: Laboratory abnormalities.

A

Low total cholesterol.

Absence of HDL and apolipoprotein A-1.

324
Q

Tangier disease: Clinical manifestations.

A

Deposition of cholesterol esters in tonsils, spleen, lymph nodes, corneas, and blood vessels.

325
Q

Low HDL: Secondary causes.

A

Obesity.

Inactivity.

Smoking.

Anabolic steroids.

326
Q

Risk factors for coronary heart disease.

A

Smoking.

Hypertension.

Low HDL.

Family history of early CHD.

Age.

327
Q

Total cholesterol: Stratification (in mg/dL).

A

Desirable: <200.

Borderline: 200-239.

High: 240 or higher.

328
Q

LDL cholesterol: Stratification (in mg/dL).

A

Optimal: Less than 100.

Near-optimal: 100-129.

Borderline: 130-159.

High: 160-189.

Very high: 190 or higher.

329
Q

LDL target: Patient with 0 or 1 major risk factors.

A

<160 mg/dL.

330
Q

LDL target: Patient with 2 or more major risk factors.

A

<130 mg/dL.

331
Q

Coronary-heart-disease equivalents.

A

Diabetes.

Non-cardiac atherosclerosis.

Framingham risk for MI of 20% within 10 years.

332
Q

Normal ratio of C peptide to insulin.

A

5-15 to 1.

333
Q

Glycolysis in an unseparated tube of blood:

A. Rate.
B. Prevention.

A

A. About 5-10 mg/dL/hour.

B. NaF; takes 1-2 hours to act.

334
Q

Correlation of glucose level in whole blood with that in plasma.

A

Whole-blood glucose tends to run about 10-15% lower.

335
Q

How to use the HbA1c to estimate the average blood glucose.

A

Average glucose = (28.7 × HbA1c) − 46.7.

336
Q

Hypoglycemia: Classification based on symptoms.

A

Fasting (neuroglycopenic): Gradual onset; altered mental status.

Reactive: Faster onset, more profound hypoglycemia; adrenergic symptoms.

337
Q

Fasting hypoglycemia: Causes (other than fasting).

A 
Insulinoma.
Nesidioblastosis.
Sarcomas, large.
Errors of metabolism.
Liver disease, end-stage.
338
Q

Reactive hypoglycemia: Causes.

A

Dumping syndrome.
Early diabetes mellitus, type 2.
Fructose intolerance, hereditary.
Galactosemia.

339
Q

Diabetes mellitus, type I: Targets of autoantibodies.

A

Insulin.

Islet cells.

Glutamic acid decarboxylase.

Insulinoma antigens IA2 and ICA512.

340
Q

Diabetes mellitus, type I: Associated HLA loci.

A

DR3, DR4.

341
Q

Diagnosis of nongestational diabetes mellitus: Methods (4).

A

HbA1c >= 6.5.

Fasting plasma glucose >=126 mg/dL.

Random plasma glucose >=200 mg/dL, plus supporting clinical evidence.

Plasma glucose >=200 mg/dL at 2 hr in a 75-g OGTT.

342
Q

When are pregnant women tested for ___?

A. diabetes mellitus, type 2
B. gestational diabetes

A

A. At the first prenatal visit.

B. At 24-28 weeks of gestation.

343
Q

75-gram OGTT: Values at which gestational diabetes is diagnosed.

A

Fasting: >= 92 mg/dL.

At 1 hr: >= 180 mg/dL.

At 2 hr: >= 153 mg/dL.

344
Q

Monitoring of HbA1c: Frequency and goal.

A

At least twice a year; <7%.

345
Q

Additional tests used in the monitoring of diabetes.

A

Annual tests:

  • Estimated GFR based on creatinine.
  • Microalbuminuria screen.
  • Lipid panel.
346
Q

Serum potassium in diabetic ketoacidosis.

A

Initially high due to metabolic acidosis, but drops due to transcellular shifts.

Total-body potassium is severely depleted.

347
Q

Major serum ketones and their detection.

A

Acetone, acetoacetic acid, β-hydroxybutyrate.

The last is not detected by the nitroprusside method.

348
Q

How hyperglycemic hyperosmotic non-ketotic coma (HHNC) differs from DKA.

A

HHNC:

Associated with diabetes mellitus, type 2.
Glucose often >1000.
Osmolality often >330.
Normal ketones.
Normal bicarbonate.

In HHNC and DKA, total K+ is severely depleted.

349
Q

Tumor markers: Sources of error in their measurement.

A

Hook’s effect can cause a falsely low values.

Heterophile antibodies can cause falsely low or falsely high values.

350
Q

PSA: Percentage of men with an elevated value who have prostate cancer.

A

30-40%.

351
Q

Guaiac test: How it works.

A

Hemoglobin has intrinsic peroxidase activity and can oxidize guaiac in the presence of hydrogen peroxide.

352
Q

Guaiac test: Sources of error.

A

False positives: NSAIDs, exogenous heme, exogenous peroxidase.

False negative: Excessive intake of vitamin C.

353
Q

CEA: Uses in colon cancer.

A

Preoperative prediction of outcome.

Postoperative monitoring.

354
Q

CEA: Correlation of value with stage of colon cancer.

A

CEA is elevated in

25% of patients with disease confined to the colon,

50% of patients with nodal metastasis,

75% of patients with distant metastasis.

355
Q

Non-colonic cancers in which CEA can be elevated.

A 
Pancreatic.
Medullary thyroid.
Cervical.
Lung.
Urothelial.
Breast.
Stomach.
356
Q

Benign causes of elevated CEA (7).

A

Peptic-ulcer disease.
Inflammatory bowel disease.

Pancreatitis.
Biliary obstruction.
Cirrhosis.

Smoking.
Hypothyroidism.

357
Q

Thyroglobulin: Source of error.

A

Antithyroglobulin antibodies.

358
Q

CA 125: Malignant causes of elevation.

A

Carcinomas of

  • Ovary (nonmucinous).
  • Fallopian tube.
  • Endometrium.
  • Pancreas.
  • Breast.
  • Colon.
359
Q

CA 125: Benign causes of elevation.

A 
Pregnancy.
Pelvic inflammatory disease.
Benign ovarian cyst.
Leiomyoma.
Endometriosis.
Ascites.
360
Q

MUC1 protein: Epitopes of interest as tumor markers.

A

CA 27.29.

CA 15-3.

361
Q

MUC1 protein: Relation of epitopes to stage of cancer.

A

Both epitopes are elevated in 60-70% of women with breast cancer of advanced stage.

362
Q

CA 19-9: Relationship to cancer.

A

Elevated in 80% of patients with pancreatic adenocarcinoma at presentation.

363
Q

CA 19-9: Source of error.

A

Absence of Lewis antigens.

364
Q

α-fetoprotein: Benign causes of elevation.

A

Pregnancy.

Cirrhosis.

Hepatitis.

365
Q

β₂-microglobulin: General cause of elevation.

A

Cell death.

366
Q

β₂-microglobulin: Use as a tumor marker.

A

Independent prognostic factor in multiple myeloma.

367
Q

Serotonin: Chemical name, major metabolite.

A

5-hydroxytryptamine.

5-hydroxyindoleacetic acid.

368
Q

Products of foregut carcinoids.

A

5-hydroxytryptophan.

Histamine.

Catecholamines.

369
Q

Products of midgut carcinoids.

A

Usually serotonin only.

370
Q

Products of hindgut carcinoids.

A

Usually none.

371
Q

Metabolism of catecholamines.

A

Epinephrine -> metanephrine -> vanillylmandelic acid.

Norepinephrine -> normetanephrine -> vanillylmandelic acid.

372
Q

Metabolism of DOPA and dopamine.

A

Both are metabolized to homovanillic acid.

373
Q

Neuroblastoma: Relatively specific tumor markers.

A

Vanillylmandelic acid and homovanillic acid.

374
Q

Neuroblastoma: Nonspecific tumor markers.

A

Neuron-specific enolase.

Ferritin.

LDH.

375
Q

NMP 22 test: Analyte; use.

A

The nuclear mitotic apparatus (NuMA) released by the dying cells of urothelial carcinoma.

376
Q

BTA (bladder tumor antigen) test: Analytes.

A

Complement factor H.

Complement factor H−related protein.

377
Q

Cause of hyperthyroidism other than elevated T4.

A

Elevated T3.

378
Q

Proteins that bind thyroxine.

A

Thyroxine-binding globulin.

Prealbumin.

379
Q

Causes of increase in thyroxine-binding globulin.

A

Estrogens.
Pregnancy.
Oral contraceptives.

Active hepatitis.
Hypothyroidism.

380
Q

Causes of decreased thyroxine-binding globulin.

A

Hypoproteinemia.

Androgens.

Cortisol.

381
Q

Correlation of T3 resin uptake with thyroid function.

A

High uptake: Hyperthyroidism.

Low uptake: Hypothyroidism.

382
Q

Reverse T3: Definition; clinical significance.

A

Alternate metabolite of T4.

Elevated in the euthyroid sick syndrome.

383
Q

Use of TRH in the work-up of hypothyroidism.

A

Increased secretion of TSH: Thyroidal problem.

Weak or no response: Pituitary problem.

384
Q

Situations in which measuring the TSH alone may miss hypothyroidism.

A

Neonatal state.

Pituitary dysfunction.

Hypothalamic dysfunction.

385
Q

What should be done when a low TSH is accompanied by a normal free T4?

A

Measure the free T3 to exclude T3 toxicosis.

386
Q

Graves’ disease: Autoantibodies.

A

Thyroid-stimulating antibodies.

Anti-thyroid peroxidase (antimicrosomal).

Anti-thyroglobulin.

387
Q

Drugs that can cause hypothyroidism.

A

Iodine.

Lithium.

Interleukin-2.

IFN-α.

388
Q

Hashimoto’s thyroiditis: Antibodies.

A

Anti-thyroid peroxidase.

Anti-thyroglobulin.

389
Q

Neonatal hypothyroidism: Leading cause.

A

Thyroidal dysgenesis.

390
Q

Neonatal hypothyroidism: Other causes (5).

A

Dyshormonogenetic goiter.
Refetoff’s syndrome.
Hypopituitarism.

Maternal autoantibodies.
Maternal drugs.

391
Q

Euthyroid sick syndrome: Results of tests of thyroid function.

A

Elevated reverse T3.

Decreased T3.

Normal T4 and TSH.

392
Q

Amiodarone: Effects on the thyroid function.

A

Often causes hyperthyroidism in iodine-poor areas and hypothyroidism in iodine-rich areas.

393
Q

Lithium: Effect on thyroid function.

A

Prevents release of thyroxine.

394
Q

Serum cortisol: Diurnal variation and relevance to testing.

A

Serum cortisol is highest around 8 a.m. and lowest around midnight.

A low morning cortisol suggests adrenal insufficiency. A high midnight cortisol suggests Cushing’s syndrome.

395
Q

Urine free cortisol: Advantage, disadvantage.

A

Not affected by diurnal variation.

Requires collection of urine for 24 hours.

396
Q

Dexamethasone: Normal effect.

A

Suppresses secretion of cortisol and ACTH.

397
Q

Low-dose dexamethasone suppression test: Purpose.

A

To determine whether a patient has Cushing’s syndrome (hypercortisolism).

398
Q

Low-dose dexamethasone suppression test: Types.

A

Standard: Two days.

Rapid: Overnight.

399
Q

Low-dose dexamethasone suppression test: Causes of failure of suppression.

A

Hypercortisolism.
Severe stress.

Depression.
Alcoholism.

400
Q

High-dose dexamethasone suppression test: Purpose.

A

To determine whether a patient has Cushing’s disease (ACTH-producing pituitary adenoma).

401
Q

High-dose dexamethasone suppression test: Interpretation.

A

Suppression: Pituitary adenoma.

No suppression: Measure plasma ACTH.

  • High: Ectopic ACTH.
  • Low: Primary hypercortisolism.
402
Q

CRH stimulation test: Interpretation.

A

Exaggerated secretion of ACTH: Pituitary adenoma.

No response: Ectopic ACTH or primary hypercortisolism.

403
Q

Cushing’s syndrome: Recommended screening tests.

A

Low-dexamethasone suppression test.

24-hour urinary cortisol, or one-time serum or salivary cortisol collected at midnight.

404
Q

ACTH-dependent Cushing’s syndrome: Additional confirmatory test.

A

Sampling of bilateral inferior petrosal sinuses.

405
Q

Hypercortisolism: Leading cause.

A

Exogenous corticosteroids.

406
Q

Hormones secreted by the basophilic cells of the anterior pituitary.

A

FSH, LH, ACTH, TSH.

407
Q

Adrenal insufficiency: Screening tests.

A

Cosyntropin stimulation test.

Morning cortisol.

408
Q

Adrenal insufficiency: Additional test and its interpretation.

A

Plasma ACTH . . .

  • High: Primary adrenal insufficiency.
  • Low or normal: Pituitary disease or cessation of exogenous corticosteroids.
409
Q

Adrenal insufficiency: Leading cause.

A

Autoimmune disease.

410
Q

Adrenal insufficiency: Congenital causes.

A

Congenital adrenal hyperplasia.

Adrenoleukodystrophy.

411
Q

Adrenal insufficiency: Pharmacological causes.

A

Ketoconazole.

Etomidate.

Mitotane.

412
Q

Addisonian crisis: Acid-base disorder.

A

Metabolic acidosis.

413
Q

Secondary adrenal insufficiency: Clinical differences from primary adrenal insufficiency.

A

Secondary adrenal sufficiency:

  • Not as severe.
  • Preserved mineralocorticoid function.
  • No hyperpigmentation.
414
Q

Hyperaldosteronism: Primary causes.

A

Adrenal hyperplasia.

Adrenal adenoma.

415
Q

Hyperaldosteronism: Secondary causes.

A

Renal-artery stenosis.

Renin-secreting tumor.

416
Q

Hyperaldosteronism: Acid-base and electrolyte abnormality.

A

Metabolic alkalosis.

Hypokalemia.

417
Q

Hyperaldosteronism: Screening and confirmatory tests.

A

Screening: Ratio of plasma aldosterone concentration to plasma renin activity.

Confirmatory: 24-hour urinary aldosterone.

418
Q

Congenital adrenal hyperplasia: Most common types.

A

21-hydroxylase deficiency.

11-hydroxylase deficiency.

419
Q

21-hydroxylase: Location of gene.

A

6p21.3.

420
Q

21-hydroxylase deficiency: Clinical manifestations.

A

Adrenal hyperplasia.

Virilization.

Salt-wasting in about one third of patients.

421
Q

21-hydroxylase deficiency: Laboratory findings.

A

Increased ACTH.

Decreased cortisol and aldosterone.

Increased 17-ketosteroids and 17-α-hydroxyprogesterone.

422
Q

11-hydroxylase deficiency: Laboratory findings.

A

Increased ACTH.

Decreased cortisol.

Increased 17-ketosteroids, deoxycorticosterone, and 11-deoxycortisol.

423
Q

The stalk effect.

A

Disruption of the pituitary stalk leads to a decrease in all hormones except prolactin, whose secretion is normally inhibited by dopamine secreted by the hypothalamus.

424
Q

Growth hormone: Stimulants of secretion.

A

Exercise.
Fasting.
Sleep.

Insulin.
Arginine.

425
Q

Growth hormone: Tests for hypersecretion.

A

Markedly high random level of GH.

IGF-1: If low or normal, then there is no excess of GH.

Failure of glucose infusion to suppress GH.

426
Q

Use of FSH level to diagnose early menopause.

A

A persistently high FSH suggests ovarian failure.

427
Q

Hyperprolactinemia: Clinical manifestations in each sex.

A

Women: Galactorrhea, amenorrhea.

Men: Gynecomastia, testicular atrophy, impotence.

428
Q

Hyperprolactinemia: Pharmacological cause.

A

Phenothiazines.

429
Q

Nephrogenic diabetes insipidus: Physiologic cause.

A

Normal aging.

430
Q

Diabetes insipidus: Diagnosis.

A

Overnight water-deprivation test.

If urine osmolality increases progressively, then DI is excluded.

Otherwise, urine osmolality will increase in response to exogenous ADH in central DI but not in nephrogenic DI.

431
Q

What happens to postmortem glucose (2), and why?

A

Blood: Increases due to glycogenolysis.

Vitreous fluid: Decreases due to glycolysis.

432
Q

What abnormality of glucose concentration can be diagnosed postmortem?

A

Diabetic ketaacidosis – in vitreous fluid.

433
Q

What happens to BUN and creatinine after death?

A

They remain stable.

434
Q

What happens to sodium and chloride after death (2)?

A

Blood: They decrease immediately after death.

Vitreous fluid: They remain stable.

435
Q

What happens to potassium after death (2)?

A

Blood, CSF: It increases abruptly.

Vitreous fluid: It increases linearly.

436
Q

Postmortem chemical pattern of dehydration.

A

Increase in Na, Cl, BUN, creatinine.

Relatively normal K.

437
Q

Postmortem chemical pattern of uremia.

A

Elevated BUN, creatinine.

Relatively normal Na, Cl, K.

438
Q

Postmortem chemical pattern of decomposition.

A

Increased K.

Decreased Na, Cl.

Relatively normal BUN, creatinine.

439
Q

Value of measuring postmortem tryptase.

A

A low or normal value makes anaphylaxis unlikely, but a high value does not prove it.

440
Q

“Renal threshold” for glucose.

A

180 mg/dL.

441
Q

Cause of glycosuria other than hyperglycemia.

A

Tubular dysfunction.

442
Q

Sugars detected by the urine dipstick.

A

Mainly glucose; sensitivity for the other reducing substances is relatively low.

443
Q

A test for sugars in the urine other than the dipstick.

A

Benedict’s copper sulfate method detects glucose, fructose, galactose, lactose, maltose, and pentoses but not sucrose.

444
Q

Types of proteinuria that are not associated with disease.

A

Positional.

Intermittent.

Exercise-induced.

445
Q

Detection of ketones in the urine.

A

The dipstick detects acetoacetate better than acetone and does not detect β-hydroxybutyrate at all.

446
Q

How to recognize hemoglobinuria.

A

Dipstick is positive for blood.

Haptoglobin is low.

Microscopy reveals hemosiderin-laden macrophages.

447
Q

How to recognize myoglobinuria.

A

Dipstick is positive for blood.

Creatine kinase is elevated.

No evidence of hemoglobinuria.

448
Q

Causes of increased urinary urobilinogen.

A

Liver disease.

Hemolysis.

449
Q

Causes of false-positive leukocyte esterase.

A

Eosinophils.

Trichomonads.

450
Q

Tests on the urine dipstick that may be inhibited by ascorbic acid.

A

Blood.
Bilirubin.
Glucose.

Leukocyte esterase.
Nitrite.

451
Q

Urine pH:

A. In most cases of acidosis.
B. In renal tubular acidosis.

A

A. Around 6.

B. >=6.5.

452
Q

Crystal morphology: Calcium oxalate.

A

“Envelopes”.

453
Q

Crystal morphology: Uric acid.

A

Squares, diamonds, rods.

454
Q

Crystal morphology: Triple phosphate.

A

“Coffin lids”.

455
Q

Crystal morphology: Ammonium biurate.

A

“Thorn apples”.

456
Q

Crystal morphology: Cystine.

A

Hexagons.

457
Q

Crystal morphology: Tyrosine.

A

“Sheaves of wheat”.

458
Q

Crystal morphology: Cholesterol.

A

“Broken window panes”.

459
Q

Crystal morphology: Sulfa.

A

“Fans”.

460
Q

Crystal morphology: Bilirubin.

A

Yellow-brown needles.

461
Q

Top five urinary stones in order of decreasing frequency.

A

Calcium oxalate.

Calcium phosphate.

Triple phosphate.

Uric acid.

Cystine.

462
Q

Factor predisposing to the formation of all types of urinary stones.

A

Low urinary volume.

463
Q

Oxalate stones: Additional predisposing factors (3).

A

Hypercalciuria.

Oxaluria.

Low urinary citrate.

464
Q

Oxalate stones: Disease associations.

A

Crohn’s disease.

Resection or bypass of small bowel.

465
Q

Calcium phosphate stones: Predisposing factors (2).

A

Hypercalciuria.

Alkaline urinary pH.

466
Q

Triple-phosphate stones: Predisposing factor.

A

Infections by urea-splitting organisms.

467
Q

Urate stones: Predisposing factors.

A

Hyperuricosuria.

Acidic urinary pH.

468
Q

Cystine stones: Associated disease.

A

Cystinuria, an autosomal-recessive disorder of renal handling of cysteine, ornithine, lysine, and arginine.

469
Q

Red blood cells: Glomerular-type bleeding (3).

A

Dysmorphic red cells.

Red-cell casts.

Erythrophagocytosis.

470
Q

Red blood cells: Nonglomerular-type bleeding.

A

Normal morphology.

471
Q

Hyaline casts: Clinical associations.

A

Renal disease.

Dehydration.

Heat injury.

Vigorous exercise.

472
Q

Red-cell casts: Clinical association.

A

Glomerulonephritis.

473
Q

White-cell casts: Clinical association.

A

Tubulointerstitial nephritis, esp. pyelonephritis.

474
Q

Tubular casts: Clinical association.

A

Acute tubular necrosis.

475
Q

Granular casts: Clinical associations.

A

Renal disease.

Dehydration.

Heat injury.

Vigorous exercise.

476
Q

Waxy casts: Clinical associations.

A

Severe renal disease.

477
Q

Broad casts: Clinical association.

A

End-stage renal disease.

478
Q

Fatty casts:

A. Clinical association.
B. Unique morphology.

A

A. Nephrotic syndrome.

B. “Maltese cross” pattern with polarized light.

479
Q

Amorphous crystals: Clinical association.

A

Usually insignificant.

480
Q

Oxalate crystals: Toxicological association.

A

Ethylene glycol.

481
Q

Biurate crystals:

A. Predisposing factor.
B. Clinical association.

A

A. Alkaline urinary pH.

B. Usually insignificant.

482
Q

Tyrosine crystals: Clinical associations (3).

A

Tyrosinosis.

Liver disease.

Hyperbilirubinemia.

483
Q

Pink xanthochromia: Interpretation.

A

Free hemoglobin in the CSF, as in subarachnoid hemorrhage.

484
Q

Yellow xanthochromia: Interpretation.

A

Old (12 hours to 2 weeks) hemorrhage.

485
Q

Artifactual xanthochromia: Causes (6).

A

Melanin.
Increased CSF protein (>150 mg/dL).
Severe hyperbilirubinemia.

Carotenoids.
Rifampin.

Delay of examination >1 hour.

486
Q

Possible signs of a truly bloody tap.

A

Persistence of blood in all tubes.

Xanthochromia.

Hemosiderin-laden macrophages, erythrophagocytosis.

487
Q

CSF protein: Normal value.

A

15-45 mg/dL.

488
Q

CSF albumin: Normal ratio to serum albumin.

A

1 to 230.

489
Q

How to detect a CSF leak from the nose or ear.

A

CSF has

  • Less glucose.
  • A double transferrin peak and a prominent prealbumin peak.
  • Asialated transferrin.
490
Q

CSF glucose relative to serum glucose:

A. Normal.
B. In bacterial meningitis.

A

A. About 60%.

B. <30%.

491
Q

CSF IgG index:

A. Purpose.
B. Formula.

A

A. To assess for intrathecal production of immunoglobulin while controlling for a leak in the blood-brain barrier.

B. CSF IgG ÷ serum IgG / CSF albumin ÷ serum albumin.

492
Q

Oligoclonal bands: Sensitivity and specificity for multiple sclerosis.

A

Sensitivity: 50-75%.

Specificity: 95-97%.

493
Q

CSF: Normal cell count in adults and neonates.

A

Adults: 0-5/mL.

Neonates: 0-20/mL.

494
Q

CSF: Normal lymphocyte percentage in adults and in neonates.

A

Adults: 30-90%.

Neonates: 10-40%.

495
Q

CSF: Normal monocytes percentage in adults and in neonates.

A

Adults: 10-50%.

Neonates: 50-90%.

496
Q

Bacterial meningitis: Typical CSF cell count.

A

1000 to 10,000/mL.

497
Q

Bacterial meningitis: Typical concentration of protein in the CSF.

A

> 100 mg/dL.

498
Q

Bacterial meningitis: Dominant leukocytes.

A

Neutrophils; lymphocytes may predominate in partially treated infections.

499
Q

Viral meningitis: Dominant leukocytes.

A

Neutrophils early, lymphocytes later.

500
Q

Viral meningitis: Typical glucose concentration in CSF.

A

Normal; may be decreased in herpes encephalitis.

501
Q

Light’s criteria.

A

Any of the following will make it an exudate:

Effusion protein >= 0.5 that of serum.
Effusion LDH >= 0.6 that of serum.
Effusion LDH >= ⅔ of the upper limit of normal for the serum.

502
Q

Transudates: Causes (3).

A

Cirrhosis.

Nephrosis.

CHF.

503
Q

Chylous vs. pseudochylous effusions: Origin.

A

Chylous: Obstruction or disruption of the thoracic duct.

Pseudochylous: Lipids from dead cells.

504
Q

Chylous vs. pseudochylous effusions: Chemical differences.

A

Chylous: Triglycerides often >110 mg/dL; chylomicrons on electrophoresis.

Pseudochylous: Triglycerides <50 mg/dL; no chylomicrons.

505
Q

Congestive heart failure:

A. Frequent location of effusion.
B. Possible effect of treatment.

A

A. Right hemithorax.

B. Conversion of transudate to exudate.

506
Q

Empyema: Criteria.

A

Neutrophils often >100,000/mL.

pH <7.2.

Bacteria on Gram stain.

507
Q

Tuberculous pleural effusion: Laboratory findings.

A

Predominantly lymphocytic.

Few mesothelial cells.

Elevated adenosine deaminase.

508
Q

Effusion associated with pulmonary embolism: Laboratory findings.

A

Usually bloody.

May show hyperplasia and/or atypia of mesothelial cells.

509
Q

Pleural effusion associated with collagen-vascular disease: Chemical findings.

A

Often

LDH >700.
pH less than 7.2.
Glucose less than 30.

510
Q

Pleural effusion associated with collagen-vascular disease: Cytological findings.

A

Much fibrin.

Few mesothelial cells.

Occasional histiocytes.

511
Q

Neutrophilic pleural effusion: Causes.

A

Pulmonary embolism (early).

Empyema.

512
Q

Lymphocytic pleural effusion: Causes.

A

Lymphoma.

Lymphatic obstruction.

Tuberculosis.

513
Q

Eosinophilic pleural effusion: Causes.

A

Previous instrumentation.

Introduction of air into the pleural space.

514
Q

Lack of mesothelial cells in a pleural effusion: Causes.

A

Rheumatoid pleural effusion.

Tuberculosis.

Pleurodesis.

515
Q

Serum-ascites albumin gradient: Interpretation.

A

A value of greater than 1.1 g/dL suggests portal hypertension.

516
Q

Peritoneal fluid: Significance of neutrophils.

A

A count of more than 250/mm³ suggests infection.

517
Q

Peritoneal fluid: Significance of Gram stain.

A

A negative stain does not exclude spontaneous bacterial peritonitis.

Florid positivity suggests secondary bacterial peritonitis.

518
Q

Synovial fluid: Effect of inflammation.

A

Reduces viscosity.

519
Q

Normal synovial fluid: WBC count, neutrophils (%), difference in glucose from serum.

A

0-150.

<25%.

0-10.

520
Q

Noninflammatory effusion: WBC count, neutrophils (%), difference in glucose from serum.

A

0-3000.

<25%.

0-10.

521
Q

Inflammatory effusion: WBC count, neutrophils (%), difference in glucose from serum.

A

3000-75,000.

30-75%.

0-40.

522
Q

Septic, gouty, or RA effusion: WBC count, neutrophils (%), difference in glucose from serum.

A

> 100,000.

> 90%.

0-100.

523
Q

Septic arthritis: Significance of Gram stain.

A

Positive in only about half of cases.

524
Q

Monosodium urate crystals: Length and birefringence.

A

2-20 μm, negatively birefringent needles.

525
Q

Calcium pyrophosphate crystals: Length, birefringence.

A

2-20 μm, weakly positively birefringent “rhomboids, rods, or rectangles”.

526
Q

ALT is mainly found in what tissues?

A

Liver.

Kidney.

CP Reviewer 2 (8 decks)

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