Primary Hemostasis Flashcards
• 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)
• Inhibits platelet adhesion
13-HODE
PLATELET ADHESION
- PLATELET RESPONSE
EXPOSURE OF PLATELETS:
- Collagen
- Fibronectin
- Basement Membrane
COLLAGEN TYPE I AND II
Type I is the most common.
✓ Synthesized by: smooth muscle
✓ Location: Deep regions of BV wall
✓ Promotes platelet adhesion, aggregation, and release reaction
• Platelets ___________ with the __________________ due to the contraction of microtubules.
• Platelet granules move to the center of the platelet and fuse to the open canalicular system connected to the outer portion of the platelets. In this way, the contents of the _______ (______________________) are released outside.
• OCS/Open Canalicular System = Parts of the Membranous system and DTS
o In which the content of the platelet granules will pass through.
• Release of Platelet Granules:
o __________
○ __________
o __________ – Type 1 and 2
o __________ – Activation of Fibrinogen and Factor XII
o __________ – platelet aggregation
o __________ – platelet aggregation
- PLATELET SECRETION/RELEASE MECHANISM
- undergo shape changes
- intrusion of numerous pseudopods
- granules
- ADP, serotonin, β-thromboglobulin, PF4, vWF, PDGF
- Alpha granules
- Dense granules
- Collagen
- Thrombin
- Epinephrine
- Thromboxane A2
• _________
o Release of _________ in response to
______________________.
o Mediates ADP induced aggregation: Gp IIb/IIIa with calcium and fibrinogen
➢ _______ = IMPORTANT COFACTOR
➢ _______ = F1 INTO FACTOR IA WHICH IS THE FIBRIN
o Deficiency results to ___________
➢ Problem with __________
• Platelet stimulating agents (________________) binds to platelets, causing them to adhere to
one another.
- PLATELET AGGREGATION
- Release of ADP
- dense granules
- collagen, epinephrine, thrombin and TXA2
- CALCIUM
- FIBRINOGEN
- Glanzmann’s Thrombasthenia
- Platelet Aggregation
- collagen, ADP, epinephrine, thrombin
• ____________ – will be activated by collagen and epinephrine to release arachidonic acid.
• ____________ – Metabolized arachidonic acid to form PGD and endoperoxidases.
• _________________ will be exposed again when stimulated by calcium and magnesium to form mesh work
- Phospholipases
- Cyclooxygenase
- Fibrinogen binding sites
