Hemostasis and Platelets
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1
What is hemostasis?
The physiologic process by which bleeding is stopped
2
Which three components mediate hemostasis?
Blood vessels (endothelium), platelets, and plasma factors (mainly coagulation factors)
3
What does disruption of hemostasis cause? 2
Bleeding disorders (hemorrhage) or thrombotic disorders (aberrant clotting)
4
What are the three phases of hemostasis?
Primary, secondary, and tertiary
5
What is primary hemostasis?
Vascular damage leading to formation of a platelet plug
6
What is secondary hemostasis?
Platelet plug leading to formation of a fibrin clot, involves coagulation factors
“Reinforce it with strong tape (the fibrin clot)”
“Reinforce it with strong tape (the fibrin clot)”
7
What is tertiary hemostasis?
Clot remodeling, dissolution of the fibrin clot, and vascular repair
“Remove the tape once the pipe heals and repair the pipe”
“Remove the tape once the pipe heals and repair the pipe”
8
Are mammalian platelets nucleated?
No, they are anucleate (birds and reptiles have nucleated thrombocytes)
9
What is the main function of platelets?
Principal facilitators of primary hemostasis, setting the stage for coagulation (secondary hemostasis)
“Slap a quick patch on the leak (the platelet plug)”
“Slap a quick patch on the leak (the platelet plug)”
10
Where does thrombopoiesis mainly occur?
Bone marrow
11
What is the platelet precursor cell?
Megakaryocyte
12
What is the megakaryocyte maturation sequence?
Megakaryoblast → promegakaryocyte → megakaryocyte
13
What process makes megakaryocytes multinucleated (up to 16 nuclei)?
Endomitosis
14
How many platelets can one megakaryocyte produce?
Up to 1,000
15
How do platelets form from megakaryocytes?
Proplatelet extensions bud off "beads" into the vascular lumen
16
What is the primary regulatory hormone of thrombopoiesis?
Where is ____ primarily produced?
Where is ____ primarily produced?
1. Thrombopoietin (TPO)
2. Liver (hepatocytes)
2. Liver (hepatocytes)
17
What regulates TPO activity?
Total platelet mass, since platelets “hold TPO” on their surfaces and destroy TPO which then limits the amount of “free TPO” in plasma
18
What happens to free TPO when platelet count is low?
Free TPO increases, stimulating megakaryocytes
19
What does TPO do to megakaryocytes?
Speeds maturation and increases size, number, and multinucleation
20
Which cytokines are secondary stimulators of thrombopoiesis?
IL-3, IL-6, IL-11, GM-CSF
21
What is the platelet lifespan if not used?
About 4-6 days
22
What percentage of platelet mass is stored in the spleen?
About 30%
23
What surface change triggers removal of aging platelets? senscence
Loss of sialic acid (desialylation)
“Old platelets lose a sugar coating (sialic acid). That is the "I'm old" tag“
“Old platelets lose a sugar coating (sialic acid). That is the "I'm old" tag“
24
Which cells remove most aging platelets?
Hepatocytes
25
What phospholipids face outward on a resting platelet?
Neutral phospholipids, giving a hemostatic-quiet surface
26
Which phospholipid flips outward on activation and is strongly procoagulant?
Phosphatidylserine (PS)
- negatively charged phospholipids flip to the surface
- negatively charged phospholipids flip to the surface
27
What does GPIb bind?
von Willebrand factor (vWF), tethering platelets
28
What does GPVI bind?
Collagen, tethering platelets
29
What does GPIIb/IIIa bind?
Fibrinogen, crosslinking platelets
30
What allows platelet shape change?
Circumferential microtubules and microfilaments
31
How does platelet shape change with activation?
Smooth discoid → spherical and spiny
32
What is the open canalicular system?
Internal channels that release granule products to the external surface
- “tunnels that let the platelet dump stuff out to the surface”
- “tunnels that let the platelet dump stuff out to the surface”
33
What is the dense tubular system?
Modified smooth ER that sequesters calcium and facilitates TXA2 synthesis (thromboxane A2)
- “a calcium storage tank that releases calcium when activated. It also helps make thromboxane A2”
- “a calcium storage tank that releases calcium when activated. It also helps make thromboxane A2”
34
Both alpha and dense granules contain
GPlb and GPllbllla
35
What 3 things keeps circulating platelets in a resting state?
PGI2 (suppresses multiple platelet activities), endothelial ADPase (degrades ADP, a platelet activator), and nitric oxide (suppressed platelet adhesion, activation, and aggregation)
36
What happens first when a vessel is damaged?
Reflex vasoconstriction; slows platelets down to interact with subendothelial connective tissue
- exposed ^ tethers down and activates platelets
- exposed ^ tethers down and activates platelets
37
How do platelets adhere to damaged vessels?
GPIb binds vWF in exposed subendothelium
38
What are the soluble mediators of platelet activation?
Thromboxane A2, ADP, thrombin
39
Which enzyme synthesizes thromboxane A2 precursors from arachidonic acid?
Cyclooxygenase-1 (COX-1)
40
Which drug irreversibly inhibits COX-1?
Aspirin
41
What is TXA2's role in platelets?
Potent recruiter and activator of platelets
42
What happens to GPIIb/IIIa when platelets activate?
It shifts to a high-affinity state that binds fibrinogen GPllbllla
43
What does platelet aggregation form?
The platelet plug, via fibrinogen crosslinking 
44
What helps dock coagulation factors to the platelet plug surface?
Phosphatidylserine and locally released calcium
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