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Platelet function testing

7 DOH Abu Dhabi (HAAD) lab licensing practice questions on Platelet function testing, part of Coagulation and Hemostasis. The first 7 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

  1. Question 1 · Medium

    PFA-100 closure times are prolonged with both the collagen/epinephrine and collagen/ADP cartridges. Hemoglobin is 78 g/L (7.8 g/dL), hematocrit 0.24 L/L and platelets 85 x 10^9/L. What is the best interpretation?

    1. AThe pattern confirms an aspirin effect
    2. BThe pattern confirms von Willebrand disease
    3. CThe pattern confirms Glanzmann thrombasthenia
    4. DThe low hematocrit and platelets may explain the result
    Show answer

    Answer: D · The low hematocrit and platelets may explain the result

    The PFA-100 draws whole blood at high shear through an aperture coated with collagen and epinephrine or ADP, and records the time for a platelet plug to close it. Red cells push platelets toward the wall and help plug formation, so a low hematocrit, like a low platelet count, prolongs closure times with both cartridges. The result cannot be interpreted until these are corrected, or another method should be used. Aspirin typically prolongs only the collagen/epinephrine closure time.

    • A: Aspirin typically prolongs the collagen/epinephrine time and leaves collagen/ADP normal.
    • B: VWD can prolong both closure times, but anemia and thrombocytopenia can do the same, so nothing is confirmed.
    • C: Glanzmann thrombasthenia prolongs both, but low counts alone can explain this result, and diagnosis needs aggregometry.

  2. Question 2 · Easy

    Platelet-rich plasma for light transmission aggregometry is prepared from citrated blood by:

    1. ALow-speed centrifugation at room temperature
    2. BHigh-speed centrifugation at 2-8 °C
    3. CHigh-speed centrifugation at room temperature
    4. DLow-speed centrifugation at 2-8 °C
    Show answer

    Answer: A · Low-speed centrifugation at room temperature

    Gentle centrifugation (about 150-200 g for 10-15 minutes) settles the red and white cells but leaves most platelets suspended in the plasma. It is done at room temperature because cooling activates platelets and distorts their responses. The rest of the sample is then spun at high speed to make platelet-poor plasma for the 100% setting. Testing should be completed within about 4 hours of collection.

    • B: High-speed spinning in the cold removes the platelets and also chills them.
    • C: High-speed centrifugation spins the platelets down and gives platelet-poor plasma.
    • D: Cold activates platelets and makes aggregation results unreliable.

  3. Question 3 · Hard

    A 9-year-old girl with oculocutaneous albinism has nosebleeds and easy bruising. Platelet count and size are normal. Aggregometry: ADP and epinephrine, primary wave only; collagen, reduced; arachidonic acid, normal; ristocetin, normal. Lumi-aggregometry shows almost no ATP release. Which defect is most likely?

    1. ADense granule (delta) storage pool deficiency
    2. BCyclooxygenase defect, as with aspirin
    3. CGlanzmann thrombasthenia
    4. DBernard-Soulier syndrome
    Show answer

    Answer: A · Dense granule (delta) storage pool deficiency

    Dense granules store ADP, ATP, serotonin and calcium, and their release drives the secondary wave of aggregation. When they are missing, weak agonists such as ADP and epinephrine give only a primary wave, collagen responses are reduced, and lumi-aggregometry shows little ATP secretion. Arachidonic acid can still produce thromboxane, and ristocetin agglutination needs only VWF and GPIb, so both are normal here. Albinism with a dense granule deficiency is typical of Hermansky-Pudlak syndrome, which can be confirmed by electron microscopy showing absent dense bodies.

    • B: A cyclooxygenase defect abolishes the arachidonic acid response, which is normal here.
    • C: Glanzmann thrombasthenia abolishes aggregation with every agonist except ristocetin.
    • D: Bernard-Soulier syndrome gives giant platelets and an absent ristocetin response.

  4. Question 4 · Medium

    In a person with no bleeding history, light transmission aggregometry shows absent aggregation with epinephrine but normal responses to ADP, collagen, arachidonic acid and ristocetin. This is best interpreted as:

    1. AA defect of the GPIIb/IIIa receptor
    2. BA defect of the GPIb-IX-V receptor
    3. CA variant seen in healthy people, not a disorder
    4. DAn aspirin effect on cyclooxygenase
    Show answer

    Answer: C · A variant seen in healthy people, not a disorder

    A reduced or absent response to epinephrine is found in a small proportion of healthy people, probably because of variation in the platelet alpha-2 adrenergic receptor. When every other agonist gives a normal response and there is no bleeding history, an isolated epinephrine defect is not diagnostic of a platelet disorder. Aspirin would also abolish the response to arachidonic acid. A GPIIb/IIIa defect affects all aggregating agonists, and a GPIb-IX-V defect affects ristocetin.

    • A: A GPIIb/IIIa defect (Glanzmann thrombasthenia) abolishes aggregation with every agonist except ristocetin.
    • B: A GPIb-IX-V defect (Bernard-Soulier syndrome) abolishes the ristocetin response, which is normal here.
    • D: Aspirin also abolishes arachidonic acid aggregation, which is normal here.

  5. Question 5 · Easy

    In light transmission aggregometry, platelet aggregation is recorded as:

    1. AA fall in light passing through the plasma
    2. BA rise in light passing through the plasma
    3. CA rise in luminescence from released ATP
    4. DA rise in electrical impedance at electrodes
    Show answer

    Answer: B · A rise in light passing through the plasma

    Platelet-rich plasma is turbid because single platelets scatter light. When an agonist makes the platelets clump, the plasma clears and more light reaches the detector. The trace is scaled between the patient's platelet-rich plasma (0%) and platelet-poor plasma (100%). Impedance and luminescence are the signals of other methods: whole-blood impedance aggregometry and lumi-aggregometry.

    • A: Light transmission rises, not falls, as platelets clump.
    • C: Luminescence measures ATP secretion in lumi-aggregometry, not aggregation itself.
    • D: Impedance is the signal in whole-blood impedance aggregometry.

  6. Question 6 · Easy

    A patient in the coronary care unit is receiving one antiplatelet drug. The aggregation tracings of the patient's platelet-rich plasma are shown. Which drug best explains them?

    Figure: MedExams
    Four aggregation tracings over 6 minutes: ADP 5 µmol/L, collagen 2 µg/mL and arachidonic acid 0.5 mg/mL each stay below 3%; ristocetin 1.2 mg/mL rises to about 80%.
    1. AEptifibatide
    2. BClopidogrel
    3. CAspirin
    4. DRivaroxaban

    Answer and explanation in LearnFree account

  7. Question 7 · Medium

    A 66-year-old man who was prescribed aspirin 75 mg daily after a stroke has had a second stroke. His aggregation tracings are shown. They are best explained by:

    Figure: MedExams
    Four aggregation tracings over 6 minutes: ADP 5 µmol/L rises in two steps to about 78%; collagen 2 µg/mL rises after a short delay to about 80%; arachidonic acid 0.5 mg/mL rises to about 78%; ristocetin 1.2 mg/mL rises to about 82%.
    1. ANo aspirin effect, often non-adherence
    2. BThe expected effect of low-dose aspirin
    3. CA P2Y12 receptor defect
    4. DA dense granule secretion defect

    Answer and explanation in LearnFree account

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