1.3 Blood clotting & Blood types Flashcards
What is Hemostasis
- series of reactions to stop bleeding that has 3 phases that occur in rapid sequence
step 1: Vasucular spasm (smooth muscle constriction
step 2: platelet plug formation: injury to lining of essel exposes collagen fibers; platelets adhere -> platelet plug forms
step 3: coagulation, fibrin clot with trapped red blood cells
describe step 1 of hemostasis
vascular spasm
- there are 3 stimuli that cause vasospasm
1. direct injurt to vascular smooth muscle
2. chemicals released by endothelial cells & platelets
3. Reflexes initiated by local pain receptors
*Spasm becomes more efficient with increasing tissue damage -> more damage = inc vasospasm
*local response
describe step 2 of hemostasis
- platelet plug formation
- when clots not neeed, platelets don’t stick to intact endothelium because of PGI1 and NO
- CD39 on surface of endothelial cells conv ADP -> AMP to prevent abnormal platelet activation
0 damage to endothelium allows platelts to bind to exposed collagen
- von tillebrand factor inc bond by bindin to collagen and paltlets
- after binding to collagen, platelets release ADP, serotonin and thromboxane A2 (ecosinoid, activates paltelets)
*VWF anf collagen activate paltelets when endothelial cell is damaged ( bc are under it)
- Serotonin and TxA2 stimulate vasoconstriction reducing blood flow to wound (local vascular spasm)
- ADP and TxA2 cause oher paltlets to become sticky and attach
- platelet plug is limited to immedite area of injury bc of PGI2 and NO
describe step 3 of coagulation
- ser of reactions that transforms blood to gel
- coagulation follows intrinsic and extrinsic pathways
- 3 steps of this reactions are:
- > prothrombin activtor is formed
- > prothrombin conv to thrombin
- > thrombin catalyzes the joining of fibringogen into fibrin mesh
describe phase 1 of coagulation
- prothrombin activator
- triggered by tisue damaging events
- invovled series of procoagulatns
- each pathway cascades towards factor X
- can be initiated by intrinsic or extrinsic pathway
*Once factor X has been activated, it complexes with Ca2+, PF3 (phosphatidylserine) and factor V to form prothrombin activator
describe the intrinsic pathway
- vessel endothelium ruptrues -> exposes underling tissues (ex collagen)
- plateleys cling and theri surfaces provide sites for mobilization of factors
Factor XII -> XIIa -> XI -> XIa -> IX –(Ca)–> IXa
- PF3 released by aggregated platelets, IXa —(VIII -> VIIIa) –> IXa/VIIIa complex
- this activates X, then X, PF3 and Ca form prothombin activator
describe the extrinsic pathway
- tissue cell trauma exposes blood to tissue factor (protein in cell membrane)
- tissue factor uses Ca2+ to activate Facotr VII that then directly activates factor X
OR can go via intrinsic & activate factor 9 (bypasses factor 11 and 12)
- once X is activated, it then does same as intrinsic -> combiens with V, PR3 and Ca to fomr prothrombin factor
describe phase 2 of coagulation
pathway to trhombin
- Prothrombin activator catalyzes the transformation of prothrombin to the active enzyme thrombin
descirbe phase 3 of coagulation
- fibrin mesh
- Thrombin catalyzes the polymerization of fibrinogen into fibrin
- Insoluble fibrin strands form the structural basis of a clot
- Fibrin causes plasma to become a gel-like trap
- Thrombin in the presence of Ca2+ activates factor XIII that:
- Cross-links fibrin
- Strengthens and stabilizes the clot
hemostasis summary
what is clot retration
stabilization of the clot by squeezing serum from the fibrin strands
what is clot repair
Fibroblasts form a connective tissue patch
Platelet-derived growth factor (PDGF) stimulates rebuilding of blood vessel wall
Stimulated by vascular endothelial growth factor (VEGF), endothelial cells multiply and restore the endothelial lining
what limits clot growth and formation
- two mechanisms
- swift removal of clotting factors and inhibition of activated clotting factors
how is thrombin inhibited
- Fibrin acts as an anticoagulant by binding thrombin and preventing its:
- > positive fedback effects of coagulation
- > ability to speed up production of prothrombin activator via factor V
- > acceleration of the intrinsic pathway by activating plateelts
- thrombin not absorbed to fibric is inactivated by anti thombin III
- heparin another anticoagulant, also inhibits thrombin activity
how is plateelt adhesion prevented
* Unnecessary clotting is prevented by endothelial lining the blood vessels
- platelet adhesino prevented by
- > The smooth endothelial lining of blood vessels
- > Heparin, NO and PGI2 secreted by endothelial cells
- > Vitamin E quinone, a potent anticoagulant
can you go back and do the highlight factors i literally cant rn
describe the ABO blood groups
consists of:
- two antigens (A and B) on surface of RBCs and two antibodies in plasma (Anti-A and anti-B)
- Agglutinogens and their corresponding antibodies cannot be mixed without serious hemolytic reactions
* B has anti A, A has anti B, O has noth anti B and A
describe Hemolytic Disease of the Newborn
- Rh– mother becomes sensitized when exposure to Rh+ blood (ex if Rh+ baby, during brith process, would impact a second pregancy with Rh+ baby)
- Rh+ antibodies of a sensitized Rh– mother cross the placenta and attack and destroy the RBCs of a Rh+ baby
- RhoGAM can prevent Rh– mother from becoming sensitized (Blocks interaction)
- Treatment involves pre-birth and transfusions after birth
what are transfusion reactions
Donor’s cells are attacked by the recipient’s agglutinins causing:
- > Diminished oxygen-carrying capacity
- > Clumped cells that impede blood flow
- > Ruptured RBCs release Hb into the bloodstream
- Circulating Hb precipitates in the kidneys causing renal failure
