Primary Hemostasis Flashcards
(31 cards)
• There is no vessel injury in this blood vessel, so there is no bleeding present yet. Blood flow is also normal.
• There are 3 processes wherein we can prevent clot formation in a normal blood vessel without
vessel injury. ________________________:
o Endothelial cellssecrete ________ and _____
➢ PGI2 + NO – ____________. Therefore, there is no capacity for platelets to adhere to ECs.
o ECs secretes Heparan sulphate – ___________
➢ This inactivates/inhibits the __________
o ECs secretes Thrombomodulin – _________
➢ Then it will become __________ →then this ________ ______ and __ (both are labile factors)
➢ Protein C is __________
- NORMAL BLOOD FLOW OF INTACT BLOOD VESSELS
- The following are the process on how we maintain the liquidity of the blood
- Prostacyclin/PGI2
- Nitric Oxide
- inactivates/inhibits platelets
- enhances antithrombin.
- Coagulation Factor II, IX, and IX.
- binds to Protein C
- Activated protein C
- degrades/inactivates
- Factor V and VIII
- Vitamin K dependent
PLATELET FUNCTION
• Adhesion
• Secretion
• Activation
• Aggregation
• Physiological process that involves the stoppage of bleeding
HEMOSTASIS
_________ – involves smooth muscle and
platelets
_________ – involves coagulation factors and
platelets
- Phases of Hemostasis
- Primary Hemostasis
- Secondary Hemostasis
• Mechanism of Primary Hemostasis involves platelets to form _____________.
• If there is a vessel injury, there would be a release of the ______ (Tissue Factor) that would then activate the ________.
• Secondary hemostasis involved the _________
- platelet plug formation
- Factor III
- Factor VII
- Coagulation Factors
_________ and _______ to blood vessels
• Take note whether it is big or small injuries we
need to stop the leaking out of the blood.
Involves ________ and ______
______, short-lived response
Damaged or activated endothelial cells
- Primary Hemostasis
- Desquamation
- small injuries
- Vascular intima
- Platelets
- Rapid
Large injuries to blood vessels and surrounding tissues
Involves ______ and ________
_______, long-term response
Tissue factor is exposed on cell membranes
• IF THERE IS A VESSEL INJURY, there will be a
release of tissue factor or the ____ that will then
activate the ____.
- Secondary Hemostasis
- Platelets
- Coagulation system
- Delayed
- FIII
- FVII
• Role of ________ and ______ in response to vascular injury.
• Formation of _______
- Primary Hemostasis
- blood vessels
- platelets
- platelet plug
• Step 1-3 is for ________
• Step 4-5 is for _________
- Primary Hemostasis
- Secondary Hemostasis
• Controlled by _________; enhanced by chemicals secreted by platelets.
o Blood flow is _______
o Vessel injury = _________
o WBC and RBC will also help in stopping the bleeding temporarily. However, it is platelets that goes first in the site of bleeding.
o There are chemicals that are secreted by the
platelets involved in its constriction/spasm.
o Involves _______ and _______
- STEP 1: VASOCONSTRICTION
- vessel smooth muscle
- decreased
- Vasoconstriction
- smooth muscles
- platelets
• _______ – is released by the endothelium that will ___________________. Once it binds, it will have a cellular mechanism with ______. This will then lead to contraction.
• ___________ – direct contact or damage in the vessel wall or smooth muscles, it will lead to myogenic action.
• ___________________ – releases ______________ such as ________ that stimulates the neurons, which then leads to vasoconstriction.
- 3 NATURAL WAYS OF VASCULAR SPASM
- Endothelin
- bind to the receptor of smooth muscle
- calcium
- Myogenic action
- Pain receptors/nociceptors
- antiinflammatory chemicals
- histamine
• Adhesion to exposed ____________
o Binding of __________
o Releases _____ and _____
- STEP 2: PLATELET ADHESION
- subendothelial connective tissue
- platelets to non-platelets
- GP-Ib and vWF
• vWF are secreted by the ECs and meets up with its receptor which is the GP-Ib. After this, the platelet will now adhere to the endothelial cells.
• _____________ or _____________ =
________________ = PROBLEM WITH PLATELET ADHESION
- Problem with GP-Ib
- Deficiency of GP-Ib
- BERNARD-SOULIER SYNDROME
• Interaction and adhesion of platelets to one another to form ________________.
o Primary goal: Formation of the ________
o Involves GP-IIb/IIIa and Fibrinogen
o __________________
o Product of Primary hemostasis: _________
- STEP 3: PLATELET AGGREGATION
- initial plug at injury site
- initial plug
- Platelet to Platelet aggregation
- Hemostatic plug
• Before aggregation, the contents of the platelet must be released first.
• ________ = secretes granules to call more platelets for aggregation such as:
o a-granules
o delta-granules
o ADP
o TXA2 (Thromboxane A2)
o Serotonin = for contraction
• ___ and ____ will work together to ___________________ in the site of injury.
• ____ and _______ will _________ to _________ that will lead to vasoconstriction.
• Once the platelets are activated, they develop
pseudopods or thorns because the contents are released.
• End product for Primary Hemostasis is _______________
- Platelets
- ADP
- TXA2
- stimulate the platelets to call more platelets
- TXA2
- Serotonin
- stimulate smooth muscle
- activate contraction
- Initial Platelet Plug Formation
• Coagulation factors interact on platelet surface to produce fibrin; __________ then forms at site of vessel injury
o This step as well as Step 5 are now part
of the ____________.
o Fibrin won’t be fibrin without Thrombin.
Fibrin without Fibrinogen won’t be Fibrin.
o ______ is protein mesh-like that will support the platelet plug.
o _________ will be the one to activate the Factor XIII to become XIIIa (activated). This stabilizes the hemostatic plug.
- STEP 4: FIBRIN-PLATELET PLUG FORMATION
- fibrin-platelet plug
- Secondary Hemostasis
- Fibrin
- Thrombin
• Role of _______ and ______ in response to vascular injury.
• Formation of ________
- PRIMARY HEMOSTASIS
- blood vessels
- platelets
- platelet plug
- __________
• Occurs the ______________
• Chemicals are secreted by the platelets.
- VASCULAR RESPONSE
- vasoconstriction/vessel spasm
• Inhibits platelet aggregation
• Induces vasodilation
Prostacyclin
• Induces vasodilation
Adenosine
• Inactivates thrombin
• Enhances anticoagulant activity of Protein C
o Inactivates Factor V and VIII (both labile factor)
o Dependent that works with Protein C
Thrombomodulin
• Enhances activity of antithrombin III
o Inactivates thrombin
o Balances bleeding and clotting
Heparan sulphate
• Converts plasminogen to plasmin
o Plasmin is responsible for the dissolution of the Fibrin or the Fibrinolysis
Tissue Plasminogen Activator
• Required for platelet adhesion
• A carrier of Factor VIII
o High VIII = High vWF
o Won’t attach without the GP-Ib
vWF (von Willebrand Factor)
