Blood clotting + Drugs Flashcards
Primary Hemostatsis
- Collagen exposed
- calls in uncoild VWF”
- bind to collagen domain A3 and A1 (on VWF) to prep for platelets
- Chef VWF lasagna - col, VWF,Plat, VWF, Plat
“TTP cant break down VWF
Secondary Hemostatsis
- sauce added - clotting factors 7, 9, 11, 10 and spicy - 8, 5
- creates sticky cross link of everything
Intrinsic clotting pathway
the side bars are the tests to see what is deficent
DRVVT- test for ani-phosplipid syndrom or lupus anti-coag
Platelet Bleeding problems
VWF or Platelets
1. mucosal
2. skin - bruising
Clotting bleeding problems
- joints
- muscles
- spotaneous
Virchow Triad
Reason: Thrombotic disorder
Symptoms:
1. trubulant and abnormal blood flow
2. think or inflammed vessel walls
3. abnormal coag, fibrinolytic, platelet
Findings:
Labs:
Which clotting is more abundant in which for Arterial vs. Venous
Arterial - Platelet rich bc high flow to so cure = antiplatelet
Venous - lower flow and so fibrin-rich so use antifibrinolytics
Platelet functions
- hemeostasis
- Inflammation
- immunity and immune system building
- atherosclerosis
- cancer
Platelet maturation
- Thrombopoietin (Liver 90% 10% kidney)
- megakaryoblast
- Megakaryocte
- then becomes platelets and dont have a nucleous
- first action to a bleed
Platelet stats
- 7-10 lifespan
- 150-450 normal
- STIM BY TPO
- 1/3 held in spleen and all destryoed in the spleen
Thrombocytopenia
Reason: Low Platelets < 150
Symptoms: Petechiae/purpura (blood dotted skin), Spontaneous mucosal bleeding, prolonged bleeding, easy brusing
Findings: Decrease productions, increased destruction, splenic sequestration (blood staying in spleen)
Labs:
Thrombocytosis
Reason: increased platelets > 450
Symptoms: increased arterial and venous thrombosis
Findings: Inflammation, infection, splenectomy, neoplasm
Labs:
Von WilleBrand Factor Characteristics
VWF
- made by endo cell
- floats with VIII to protect inactivation
- helps platelets adhere (GP- Ib)
- largest and most effective multimers
Platelets adherence to Endo
4 receptors 2 top and 2 bottom
1. bottom binds to VWF (GP-Ib) and collagen
2. top binds to collagen and fibrinogen
once intial contact TXA and ADP strengthen the adhesion and stim growth for 2nd layer
Glanzmann Thrombasthenia
lack of GP2b/3a and cant bind to fibrogen
Bernard-Soulier Syndrome
lack of G1b no platelet to VWF
Von Willebrand disease
unable to do Platelet to endo
Thrombin Burst/ feedback loop
aThrobin goes and actives factor 5a, 8a, 11a
What are the prothrombic Co-Factors
- 7a binds with TF
- Tenase complex - 9a + 8a
- Protrombinase complex 10a + 5a
Fibrogen
dimeric head to head and has 3 chains alpah, beta and gamma
made in the liver 200-400
bind to gp2b/3a
Factor 13 and 13a position and role
13a convalently links the fibirn polymers Alpha to gamm
activated by thrombin
made in liver and stored in platelets
HL - 19 days
Fibrinoolysis and inhibition of it
- TPA gets relased by endo and bind to PLG -> Plasmin
- Plasmin cleaves fibrin and the Lysine accelerates tpa PLG binding
- INHIBITORS
TAFI - binds the lysine
Alpha2-antiplasmin - binds plasmin
PAI-1- bind TPA (both come from endo cells)
IIa coag function
it is Thrombin and starts the postitve feedback loop
IIa anti coag function
- IIa binds to Endo protien C - R = APC
- APC inactivates F8a and F5a (s is a confactor)
synthesised in liver
