In the light transmission aggregometry tracing shown, what does the segment labelled 3 represent?

Secondary wave from granule secretion

Primary wave from fibrinogen binding

Lab: platelet function, aggregation and thromboelastography

8 ASCP MLS practice questions on Lab: platelet function, aggregation and thromboelastography, part of Hematology. The first 8 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

Question 1 · Medium
Light transmission aggregometry on a patient's platelet-rich plasma gives the curves shown. The pattern is most consistent with:
Figure: MedExams
1. AGlanzmann thrombasthenia
2. BAspirin effect
3. CVon Willebrand disease
4. DBernard-Soulier syndrome
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Answer: B · Aspirin effect
Arachidonic acid gives no aggregation, collagen gives a small, delayed response, ADP gives only a primary wave that reverses, and ristocetin is normal. Aspirin irreversibly acetylates cyclooxygenase-1, so platelets cannot make thromboxane A2 from arachidonic acid and the release-dependent responses are lost. Glanzmann thrombasthenia abolishes aggregation with every agonist except ristocetin, while Bernard-Soulier syndrome and von Willebrand disease reduce the ristocetin response. Ask about aspirin before testing, since its effect lasts the 7-10-day platelet lifespan.
- A: Glanzmann thrombasthenia gives not even a primary wave with ADP.
- C: Von Willebrand disease gives a reduced ristocetin response.
- D: Bernard-Soulier syndrome gives an absent ristocetin response.
Question 2 · Easy
In the light transmission aggregometry tracing shown, what does the segment labelled 3 represent?
Figure: MedExams
1. ASecondary wave from granule secretion
2. BPlatelet shape change
3. CPlatelet disaggregation
4. DPrimary wave from fibrinogen binding
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Answer: A · Secondary wave from granule secretion
After ADP is added, platelets first change shape, which briefly lowers light transmission (1). The primary wave (2) is reversible aggregation as activated GPIIb/IIIa binds fibrinogen. The secondary wave (3) follows when platelets release their dense-granule ADP and make thromboxane A2, giving irreversible aggregation. Aspirin and storage pool disease abolish the secondary wave with epinephrine and low-dose ADP.
- B: Shape change is the small dip at segment 1.
- C: Disaggregation would be a falling curve, which this tracing does not show.
- D: The primary wave is segment 2.
Question 3 · Medium
A patient is bleeding during liver transplant surgery. Refer to the kaolin TEG tracing shown (reference intervals: R 5-10 min, MA 50-70 mm, LY30 0-8%). Which treatment do the results support?
Figure: MedExams
1. AProtamine sulfate
2. BTranexamic acid
3. CPlasma transfusion
4. DPlatelet transfusion
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Answer: B · Tranexamic acid
The R time (6 min) and maximum amplitude (58 mm) are within their reference intervals, so clotting factors, fibrinogen and platelets are forming a clot of normal strength. After MA the amplitude falls steadily, and LY30 is 32% against a reference of 0-8%: the clot is being broken down by excess fibrinolysis. An antifibrinolytic such as tranexamic acid is indicated. Hyperfibrinolysis is common during liver transplant, when the liver cannot clear tissue plasminogen activator.
- A: Protamine reverses heparin, which would prolong R; R is normal.
- C: Plasma replaces clotting factors, whose lack would prolong R; R is normal.
- D: Platelets are adequate, because MA is normal.
Question 4 · Easy
In light transmission aggregometry, the instrument's 100% aggregation setting is made with:
1. APlatelet-rich plasma
2. BWashed platelets in buffer
3. CPlatelet-poor plasma
4. DCitrated whole blood
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Answer: C · Platelet-poor plasma
Platelet-rich plasma is turbid and lets little light through, so it sets 0% aggregation. Platelet-poor plasma from the same patient is clear and sets 100%, the transmission expected if every platelet clumped. As an agonist makes the platelets aggregate, the platelet-rich plasma clears and transmission rises toward the platelet-poor value. Samples are kept at room temperature and tested within about 4 hours, because cold activates platelets.
- A: Platelet-rich plasma sets the 0% baseline.
- B: Washed platelets are not the blank used in routine light transmission testing.
- D: Whole blood is used in impedance aggregometry, not light transmission.
Question 5 · Medium
Light transmission aggregometry shows no aggregation with ADP, collagen, epinephrine or arachidonic acid, but a normal response to ristocetin. Platelet count and size are normal. These results are most consistent with:
1. AAspirin effect
2. BGlanzmann thrombasthenia
3. CBernard-Soulier syndrome
4. Dvon Willebrand disease
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Answer: B · Glanzmann thrombasthenia
ADP, collagen, epinephrine and arachidonic acid all cause aggregation through fibrinogen binding to the GPIIb/IIIa (integrin αIIbβ3) complex, which is absent or defective in Glanzmann thrombasthenia. Ristocetin causes agglutination instead, by binding von Willebrand factor to GPIb, so that response is preserved. Normal platelet count and size separate it from Bernard-Soulier syndrome. Flow cytometry showing reduced or absent CD41 and CD61 supports the diagnosis.
- A: Aspirin abolishes arachidonic acid aggregation but not the primary response to ADP.
- C: Bernard-Soulier syndrome shows an absent ristocetin response with giant platelets.
- D: von Willebrand disease reduces the ristocetin response while other agonists are normal.
Question 6 · Easy
The PFA-100 closure time is the time it takes for:
1. ALight transmission to rise as platelets clump
2. BBleeding to stop from a standard skin incision
3. CFibrin to form after thrombin is added to the plasma
4. DPlatelets to seal a coated aperture at high shear
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Question 7 · Medium
PFA-100 results: collagen/epinephrine closure time 248 s (reference 85-165 s), collagen/ADP closure time 96 s (reference 70-120 s). Platelet count and hematocrit are normal. Which cause best fits?
1. AAspirin use
2. BHemophilia A
3. CGlanzmann thrombasthenia
4. Dvon Willebrand disease
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Question 8 · Hard
A 66-year-old man is bleeding after cardiac bypass surgery and protamine. Kaolin TEG: R time 15 min in the plain cup and 6 min in the heparinase cup (reference 4-8 min), MA 61 mm (reference 54-72 mm), LY30 1% (reference 0-8%). Which treatment is most appropriate?
1. AA further dose of protamine
2. BPlasma transfusion
3. CTranexamic acid
4. DPlatelet transfusion
Answer and explanation in LearnFree account

Lab: platelet function, aggregation and thromboelastography

Light transmission aggregometry on a patient's platelet-rich plasma gives the curves shown. The pattern is most consistent with:

In the light transmission aggregometry tracing shown, what does the segment labelled 3 represent?

A patient is bleeding during liver transplant surgery. Refer to the kaolin TEG tracing shown (reference intervals: R 5-10 min, MA 50-70 mm, LY30 0-8%). Which treatment do the results support?

In light transmission aggregometry, the instrument's 100% aggregation setting is made with:

Light transmission aggregometry shows no aggregation with ADP, collagen, epinephrine or arachidonic acid, but a normal response to ristocetin. Platelet count and size are normal. These results are most consistent with:

The PFA-100 closure time is the time it takes for:

PFA-100 results: collagen/epinephrine closure time 248 s (reference 85-165 s), collagen/ADP closure time 96 s (reference 70-120 s). Platelet count and hematocrit are normal. Which cause best fits?

A 66-year-old man is bleeding after cardiac bypass surgery and protamine. Kaolin TEG: R time 15 min in the plain cup and 6 min in the heparinase cup (reference 4-8 min), MA 61 mm (reference 54-72 mm), LY30 1% (reference 0-8%). Which treatment is most appropriate?