Chapter 12 Flashcards
When a blood vessel is sealed to prevent blood loss or hemorrhage.
Hemostasis (asis- stop bleeding)
when inappropriate blood clotting occurs or when clotting is insufficient to stop the flow of blood from the vascular compartment.
Abnormal hemostasis
Is needed to activate factors II, VII, IX, X
Vitamin K
what happens during normal hemostasis?
sealing of broken blood vessel
what happens during abnormal hemostasis?
inappropriate clotting- thrombosis insufficient clotting
platelets live up to:
8-9 days in circulation
platelets are also called
thrombocytes
platelets are large fragments of _____ that come from ___
megakaryocytes, bone marrow
What triggers platelet production
thrombopoietin (hormone) that triggers new megkaryocyte formation
platelets are made in the :
liver, kidney, smooth muscle, and bone marrow
platelets are stored in the:
spleen
healthy people have what # of platelets
150,000-400,000 circulating at any given time
platelet structure is:
* a hybrid between RBC and WBC * have glycoproteins that stick out from cell to help them connect to other platelets (clot formation) * inside: glycogen, enzymes, mitochondria *A granules, and B granules
a granules are made of what and do what?
fibrinogen, coagulation factors, plasminogen * they facilitate platelet aggregation, blood clotting, and vessel repair * Return things to normal
B granules are made of what and do what?
ADP, ATP, calcium, histamine, serotonin. * they vasoconstrict and perform platelet adhesion to injured site
Coagualtion Factors: (2)
Plasma Proteins & Calcium (Favor IV)
Plasma proteins:
circulate as inactive pro-coagulation factors synthesized by liver EX: vWF made my megakaryocytes and endothelium
Examples of anticoagulants:
Antithrombin III Protein C&S Plasmnogen __> Plasmin
Damaged Endothelial ___ clotting while healthy endothelium ___ clotting
encourages prevents
Clot Formation and Dissolution Steps (5)
- Vessel Spasm 2. Platelet plug formation 3. blood coagulation 4. clot retraction 5. clot dissolution and lysis
1.) Vessel spasm
1st thing in clot formation * TXA2- released by Nervous System to spasm vessel
2.) Platelet plug formation
2nd step in clot formation *vWF is needed to bind to collagen and create adhesion Adhesion–> granule release–>platelet aggregation
- Blood coagulation
3rd step in clot formation * coagulation cascade of factors
- Clot Retraction
4th step in clot formation- 1st in dissolution * actin and myosin pull damaged vessel closed *exudate is squeezed out of cells in the process
- Clot dissolution and lysis
5th step in clot formation- 2nd in dissolution *plasminogen–> plasmin: fiber breakdown
Plasminogen is activated by?
Tissue plasminogen factor (TPa)
1st thing to happen when tissue gets damaged * is the spark that starts the coagulation cascade*
Tissue Factor gets released from the extrinsic pathway
prothrombin turns into thrombin with what activator?
calcium Ca++
Factor XIII 13 helps do what?
turn fibrin strands into the platelet plug by creating the meshwork that holds the clot together
What converts fibrinogen into fibrin?
thrombin
Extrinsic meets the intrinsic pathway in the coagulation cascade where?
Factor X and Factor V
the important last 3 factors in the intrinsic pathway are?
Factor X and V: activates prothrombin–> Factor II: thrombin –> which activates –> Factor I: Fibrinogen –> Fibrin
Tissue plasminogen activator (tPA) does what?
fast acting clot breakdown (stroke patients)
examples of anticoagulants made by Endothelial cells:
prostacyclin and Nitric Oxide
Adenosine Diphosphate- breaks down ADP
Histamine
Thrombomodulin- breakdown clots/inhibit formation
TPa- breaks down clots already formed, fast acting.
hypercoagulability
increased ability of the body to clot (abnormal)
hypercoagulability can be grouped into two categories:
increased platelet function Accelerated coagulation system activity
Increased platelet formation in Hypercoagulability:
- increased platelet # - blood flow disturbances - endothelial damage - platelet aggregation
Accelerated coagulation system activity in Hypercoagulability:
- Increased procoagulation factors - decreased anticoagulation factors
with accelerated coagulation systems activity in hypercoagulability, what are pt’s most at risk for?
deep vein thrombosis
accelerated coagulation system activity can be a result of what?
mutation of Factor V (5) it mutates so that Protein C can’t recognize it and break it down.