At the high shear rates of arterioles, platelet adhesion to exposed collagen depends on von Willebrand factor, but at low venous shear it depends on VWF much less. Why?

Only GPIb-VWF bonds form fast enough at high flow

Platelets in veins have no GPIb receptors

Venous endothelium produces no VWF

Arteriole walls have little collagen beneath them

Resting platelets carry many GPIIb/IIIa receptors on their surface, yet they do not bind plasma fibrinogen. Why?

The receptor stays in a low-affinity shape until activation

Fibrinogen must first be converted to fibrin by thrombin

Plasma calcium is too low for the receptor to work

Prostacyclin occupies the receptor's binding site

Primary hemostasis: vessels and platelets

8 DOH Abu Dhabi (HAAD) lab licensing practice questions on Primary hemostasis: vessels and platelets, part of Coagulation and Hemostasis. 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 · Easy
Which platelet receptor binds directly to collagen and sends the main activation signal after adhesion?
1. AGlycoprotein VI
2. BP2Y12 receptor
3. CGlycoprotein IIb/IIIa
4. DGlycoprotein Ib-IX-V
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Answer: A · Glycoprotein VI
GPVI binds exposed collagen fibres and signals through its associated FcR gamma chain, which triggers granule release, thromboxane A2 synthesis and activation of GPIIb/IIIa. Integrin alpha2beta1 (GPIa/IIa) also binds collagen and firms up the attachment. GPIb-IX-V reaches collagen only indirectly, through von Willebrand factor.
- B: P2Y12 responds to released ADP, not to collagen.
- C: GPIIb/IIIa binds fibrinogen and VWF during aggregation, after activation.
- D: GPIb-IX-V binds VWF, which in turn binds collagen; it does not bind collagen itself.
Question 2 · Medium
At the high shear rates of arterioles, platelet adhesion to exposed collagen depends on von Willebrand factor, but at low venous shear it depends on VWF much less. Why?
1. APlatelets in veins have no GPIb receptors
2. BVenous endothelium produces no VWF
3. COnly GPIb-VWF bonds form fast enough at high flow
4. DArteriole walls have little collagen beneath them
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Answer: C · Only GPIb-VWF bonds form fast enough at high flow
In fast-moving blood, platelets pass the injury too quickly for collagen receptors to catch them. VWF bound to collagen is stretched by shear, exposing its A1 domain, which binds GPIb-IX-V with very fast on-off kinetics and tethers the platelets so they roll and slow down. GPVI, alpha2beta1 and GPIIb/IIIa then make the attachment firm. Loss of this VWF-GPIb step explains the mucosal bleeding of VWD and Bernard-Soulier syndrome.
- A: Platelets carry GPIb wherever they circulate.
- B: Venous endothelium also makes VWF.
- D: Arterioles have subendothelial collagen; that is what VWF binds.
Question 3 · Medium
Resting platelets carry many GPIIb/IIIa receptors on their surface, yet they do not bind plasma fibrinogen. Why?
1. AFibrinogen must first be converted to fibrin by thrombin
2. BPlasma calcium is too low for the receptor to work
3. CProstacyclin occupies the receptor's binding site
4. DThe receptor stays in a low-affinity shape until activation
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Answer: D · The receptor stays in a low-affinity shape until activation
On resting platelets GPIIb/IIIa is held in a bent, low-affinity form. Agonists such as ADP, thrombin, collagen and thromboxane A2 send signals inside the platelet (inside-out signalling through talin and kindlin) that open the receptor so it binds fibrinogen tightly. This keeps platelets from clumping in the circulation even though plasma fibrinogen is high.
- A: Activated GPIIb/IIIa binds soluble fibrinogen; fibrin is not needed.
- B: Normal plasma ionized calcium is enough for integrin binding.
- C: Prostacyclin acts on its own receptor to raise cyclic AMP; it does not block GPIIb/IIIa.
Question 4 · Easy
The first response of a small blood vessel to injury, which slows blood loss before a platelet plug forms, is:
1. APlatelet aggregation
2. BFormation of a fibrin clot
3. CReflex vasoconstriction
4. DClot retraction
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Answer: C · Reflex vasoconstriction
Injury causes immediate reflex and neurogenic contraction of the smooth muscle in the vessel wall, which cuts flow through the damaged segment. Endothelin from injured endothelium, and later thromboxane A2 and serotonin from platelets, keep the vessel constricted. Platelet adhesion and aggregation follow within seconds to minutes, and fibrin then reinforces the plug.
- A: Aggregation follows adhesion; the vessel constricts first.
- B: Fibrin forms later, in secondary hemostasis, on and around the platelet plug.
- D: Clot retraction happens after a fibrin clot has formed.
Question 5 · Easy
During aggregation, activated platelets are linked to one another mainly by fibrinogen bound to:
1. AGlycoprotein Ib-IX-V
2. BGlycoprotein IIb/IIIa
3. CGlycoprotein VI
4. DP-selectin
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Answer: B · Glycoprotein IIb/IIIa
Activation converts GPIIb/IIIa (integrin alphaIIb beta3) into a high-affinity form. Fibrinogen is a symmetrical molecule, so it can bind GPIIb/IIIa on two platelets at once and bridge them; VWF does the same at high shear. Aggregation therefore needs both activated platelets and fibrinogen, and lack of GPIIb/IIIa causes Glanzmann thrombasthenia.
- A: GPIb-IX-V binds VWF during adhesion, not fibrinogen during aggregation.
- C: GPVI is a collagen receptor that triggers activation.
- D: P-selectin from alpha granules binds leukocytes, not fibrinogen.
Question 6 · Hard
A 64-year-old man took aspirin 75 mg daily and stopped it 2 days ago. His platelet count is 250 × 10^9/L, yet his platelets still make little thromboxane A2. Why has the effect not worn off?
1. AAspirin has also blocked his P2Y12 receptors
2. BAspirin stays in the plasma for about a week
3. CHis platelets cannot make new cyclooxygenase-1
4. DHis endothelium is still making less prostacyclin
Answer and explanation in LearnFree account
Question 7 · Medium
Activated platelets support the tenase and prothrombinase complexes mainly by:
1. AExposing phosphatidylserine on their outer membrane
2. BSecreting factor VII from their dense granules
3. CBinding fibrinogen to glycoprotein IIb/IIIa
4. DReleasing tissue factor from their alpha granules
Answer and explanation in LearnFree account
Question 8 · Easy
Which substance is stored in platelet alpha granules rather than dense granules?
1. AIonized calcium
2. BSerotonin
3. CAdenosine diphosphate
4. DPlatelet factor 4
Answer and explanation in LearnFree account

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Primary hemostasis: vessels and platelets

Which platelet receptor binds directly to collagen and sends the main activation signal after adhesion?

At the high shear rates of arterioles, platelet adhesion to exposed collagen depends on von Willebrand factor, but at low venous shear it depends on VWF much less. Why?

Resting platelets carry many GPIIb/IIIa receptors on their surface, yet they do not bind plasma fibrinogen. Why?

The first response of a small blood vessel to injury, which slows blood loss before a platelet plug forms, is:

During aggregation, activated platelets are linked to one another mainly by fibrinogen bound to:

A 64-year-old man took aspirin 75 mg daily and stopped it 2 days ago. His platelet count is 250 × 10^9/L, yet his platelets still make little thromboxane A2. Why has the effect not worn off?

Activated platelets support the tenase and prothrombinase complexes mainly by:

Which substance is stored in platelet alpha granules rather than dense granules?