Hemostasis Flashcards
1
Q
Define hemostasis
A
Steps taken by the body to limit blood loss
2
Q
What are the four steps of hemostasis
A
1) Vascular spasm 2) Formation of platelet plug 3) Formation of blood clot 4) Damage repair
3
Q
Where is TPO synthesized? What triggers its release?
A
Liver It is constantly being released into the blood
4
Q
How are TPO levels controlled in the blood?
A
Internalization and destruction by circulating platelets
5
Q
What is the receptor for TPO?
A
MPL
6
Q
What is the overall effect of thrombopoeisis?
A
Increased division and maturation of ALL BLOOD CELL LINEAGES
7
Q
What pathway does TPO act on?
A
JAK2/STAT25
8
Q
- What are some of the components of platelets?
A
- Actin and myosin
- Mitochondria
- Remnants of ER (for Ca2+ storage)
- COX 1 (formation of thromboxane, arachidonic acid and prostaglandins)
- Fibrin stabilizing factor (clot stability)
- Platelet derived growth factor (repair)
- Serotonin 5HT-
9
Q
- The cell membranes of platelets have what 3 features?
- What is the function of each?
A
- Glycoproteins (when activated), phospholipids, collagen receptors
- Glycoproteins help make membrane sticky
- Phospholipids contain platelet factor 3 and help activate clotting cascade
- Receptors for collagen enable platelet binding
10
Q
- What type of response is a vascular spasm?
- What is the function of a vascular spasm?
A
- myogenic response (meaning that the smooth muscle surrounding the vasculature will contract on its own)
- Goal is to stop blood flow out of the hemorrhaged area
11
Q
- What else occurs during step 1 (vascular spasm)?
A
- Release of vasoconstricting agents from platelets (serotonin and thromboxane a2)
12
Q
- How is the platelet plug formed?
A
- Collagen is exposed on damaged membrane and enables platelets to bind
- For platelet to bind, 2 steps occur (1) Von Willebrand Facrtor and (2) binding of platelet receptor (integrin) to collagen
- Activation of platelet
- Platelet swelling and contraction
- Release of granules from the platelets
- More platelets are recruited and stick to one another via thromboxane A2 and ADP
13
Q
- What are the three key steps in coagulation?
A
- Activation of thrombin regulator
- Activation of thrombin
- Creation of fibrin from fibrinogen
14
Q
- What is the role of platelet derived growth factor in tissue healing
A
- Stimulates fibroblasts to grow into clotted area
- These fibroblasts differentiate into smooth muscle to close the hole
15
Q
- What enzymes and proteins are important in the removal of clots?
A
- tPA
- tPA inhibitor
- Plasminogen
- Protein C
16
Q
- What is the function of plasminogen when it is activated into plasmin?
- Where is plasminogen synthesized/stored?
A
- Lyses fibrin to destroy clot
- Synthesized in liver
- “Stored” in plasma
17
Q
- How is plasminogen converted into its active form?
A
- tPA inhibitor is inhibited by protein C
- tPA can activate plasminogen
NOTE: tPA is released in response to damaged tissye and is normally inhibited by tPA inhibitor (why we need protein c)
18
Q
- What are some of the ezymes/molecules that prevent clots from forming in the first place?
A
- FIbrin
- Prostacyclin
- Antithrombin
- Protein C
19
Q
- What are some physiological factors that inhibit clot formation?
A
- Smooth endothelial lining of vessels (interrrupted in diseases like atherosclerosis)
- Continuous flow of non-turbulent blood
- Platelet repelling action of glycolax
- Endogenous anticoagulants
- PKC
20
Q
- What are some examples of endogenous anticoagulants?
A
- Heparin
- Prostacyclin
- Anti-Thrombin II
21
Q
- In addition to inhibiting tPA inhibitor, what else does PKC do?
A
- Inactivates Factors 5 and 8
- This inactivation PROMOTES DESTRUCTION OF FIBRIN
