Chapter 37 R E V I E W Q U E S T I O N S Flashcards

1
Q
  1. The clinical presentation of platelet-related bleeding may include all of the following except:

a. Bruising
b. Nosebleeds
c. Gastrointestinal bleeding
d. Bleeding into the joints (hemarthroses)

A

d. Bleeding into the joints (hemarthroses)

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2
Q
  1. A defect in GP IIb/IIIa causes:

a. Glanzmann thrombasthenia
b. Bernard-Soulier syndrome
c. Gray platelet syndrome
d. Storage pool disease

A

a. Glanzmann thrombasthenia

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3
Q
  1. Patients with Bernard-Soulier syndrome have which of the following laboratory test findings?

a. Abnormal platelet response to arachidonic acid
b. Abnormal platelet response to ristocetin
c. Abnormal platelet response to collagen
d. Thrombocytosis

A

b. Abnormal platelet response to ristocetin

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4
Q
  1. Which of the following is the most common of the hereditary platelet function defects?

a. Glanzmann thrombasthenia
b. Bernard-Soulier syndrome
c. Storage pool defects
d. Multiple myeloma

A

c. Storage pool defects

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5
Q
  1. A reduction in thrombin generation in patients with Scott syndrome results from:

a. Defective granule secretion
b. Altered platelet aggregation
c. Altered expression of phospholipids on the platelet membrane
d. Deficiency of vitamin K-dependent clotting factors

A

c. Altered expression of phospholipids on the platelet membrane

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6
Q
  1. The impaired platelet function in myeloproliferative neoplasms results from:

a. Abnormally shaped platelets
b. Extended platelet life span
c. Increased procoagulant activity
d. Decreased numbers of # granules and dense granules

A

d. Decreased numbers of # granules and dense granules

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7
Q
  1. The platelet defect associated with increased paraproteins is:

a. Impaired membrane activation, owing to protein coating
b. Hypercoagulability, owing to antibody binding and membrane activation
c. Impaired aggregation, because the hyperviscous plasma prevents platelet-endothelium interaction
d. Hypercoagulability, because the increased proteins bring platelets closer together, which leads to inappropriate aggregation

A

a. Impaired membrane activation, owing to protein coating

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8
Q
  1. In uremia, platelet function is impaired by higher than normal levels of:

a. Urea
b. Uric acid
c. Creatinine
d. NO

A

d. NO

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9
Q
  1. Thrombocytopenia associated with the use of cardiopulmonary bypass is not caused by:

a. Anti-GP IIb/IIIa antibodies
b. Hemodilution
c. Platelet binding to bypass circuitry
d. Platelet consumption associated with normal postsurgical hemostatic activity

A

a. Anti-GP IIb/IIIa antibodies

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10
Q
  1. Aspirin ingestion blocks the synthesis of:

a. Thromboxane A2
b. Ionized calcium
c. Collagen
d. ADP

A

a. Thromboxane A2

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11
Q
  1. A mechanism of antiplatelet drugs targeting GP IIb/IIIa function is:

a. Interference with platelet adhesion to the subendothelium by blocking of the collagen binding site
b. Inhibition of transcription of the GP IIb/IIIa gene
c. Direct binding to GP IIb/IIIa
d. Interference with platelet secretion

A

c. Direct binding to GP IIb/IIIa

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12
Q
  1. Which is a congenital qualitative platelet disorder?

a. Senile purpura
b. Ehlers-Danlos syndrome
c. Henoch-Schönlein purpura
d. Waldenström macroglobulinemia

A

b. Ehlers-Danlos syndrome

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