Hemostasis Study Questions Flashcards
(36 cards)
It has been recommended that patients at risk for myocardial infarction (heart attack) take 1 aspirin a day to reduce the risk. In addition, it has been shown that one aspirin taken early in the course of an M.I. significantly reduces the risk of death. Given that the final event leading to a heart attack is usually the formation of a blood clot that occludes the lumen of a vessel already partially occluded by an atherosclerotic plaque, why is an aspirin effective?
Aspirin and other NSAIDS are non-selective blockers of the cyclooxygenase (COX) enzymes. Aspirin in fact, produces irreversible blockade of the COX1 found in the platelets. By blocking COX, we prevent the formation of thromboxane A2, which is responsible for much of the vascular spasm and platelet aggregation/clumping. This limits the degree of vascular spasm and limits the possibility that a blood clot will start in one of these partially occluded vessels.
Why does thrombocytopenia (decreased number of platelets) lead to spontaneous bleeding even though the other aspects of hemostasis (e.g. vascular spasm, clotting) are still functioning?
Remember that many of the small breaks in blood vessels that occur every day are actually sealed ONLY by the action of the platelet plug. Since we have deficient numbers of platelets, we not only don=t make an effective platelet plug, we also don=t initiate the clotting cascade very well (most of these small breaks don=t involve much tissue damage, so we can’t rely on the extrinsic cascade).
Bleeding time is the time it takes bleeding to stop after a deliberate (but small) cut is made in the skin. In the person with thromobcytopenia the bleeding time is quite prolonged. Why?
That small deliberate cut (made by a really sharp thing, by the way) does relatively little tissue damage and the bleeding is stopped by the development of a platelet plug. The bleeding time in someone with thrombocytopenia is prolonged because we don=t have enough platelets to stop the bleeding and the clotting cycle takes longer to stop the bleeding.
In many hemophiliacs (where clotting is impaired due to a genetic deficiency of one of the clotting factors), the bleeding time is normal. Explain this!
Hemophiliacs, although they don=t have a specific clotting factor, do have plenty of platelets, whose function is normal. Therefore the bleeding time is normal (since it is the platelets that close the hole initially).
what do platelets bind to?
thrombopoietin (mpl) receptor
what things are on the cell membrane of platelets?
glycoproteins, phospholipids (platelet factor 3), receptors for collagen
what are platelets derived from?
megakaryocytes
what do platelets contain?
mitochondria, actin, myosin, COX1, serotonin (in vesicles)
what makes TPO?
liver and kidney
what does TPO act on?
all blood cell lines
how is TPO controlled?
internalization and destruction of TPO by platelets
what cause vascular spasm?
myogenic (no reflexes, direct response), platelet factors: serotonin, thromboxane A2
what are the two steps of platelets binding to collagen?
1: Von Willebrand Factor: between collagen and platelet receptor
2: platelet receptor (integrin) binding to collagen
Formation of platelet plug steps
1: platelet swelling
2: contraction
3: granules leave platelet
4: platelets stick to vessel wall and each other (thromboxane A2 & ADP)
platelets do what when activated?
platelet swells, extends podocytes
what are the 3 essential steps of blood coagulation?
- formation of prothrombin activator
- activation of thrombin
- creation of fibrin from fibrinogen
what does clot retraction do?
gets rid of excess fluid within clot, solidifies clot
what is required for clot retraction?
platelets (bind fibrin polymer, actin and myosin in platelet: contraction), calcium
what does platelet derived growth factor do?
stimulates fibroblasts to grow into area (differentiate into smooth m., etc.) to close hole
what makes plasminogen?
liver
what activates plasminogen? where does it come from?
tissue plasminogen activator, released by damaged tissue
what inhibits plasminogen?
tPA inhibitor in blood
4 steps of hemostasis?
vascular spasm, platelet plug, blood clot, damage repair
where is TPO gene?
chromosome 3
