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Questions and Answers
What occurs as a result of healthy endothelial cells secreting prostacyclin?
What occurs as a result of healthy endothelial cells secreting prostacyclin?
Which component is primarily responsible for stopping bleeding by forming a platelet-fibrin plug at the site of physical trauma?
Which component is primarily responsible for stopping bleeding by forming a platelet-fibrin plug at the site of physical trauma?
What is the main structural difference between heparin and warfarin?
What is the main structural difference between heparin and warfarin?
What initiates the activation and aggregation of platelets in response to vascular injury?
What initiates the activation and aggregation of platelets in response to vascular injury?
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Why do resting platelets not activate in healthy blood vessels?
Why do resting platelets not activate in healthy blood vessels?
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What is the primary mechanism of action for warfarin?
What is the primary mechanism of action for warfarin?
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Which of the following correctly describes the onset and duration of heparin compared to warfarin?
Which of the following correctly describes the onset and duration of heparin compared to warfarin?
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What is a common side effect associated with heparin therapy?
What is a common side effect associated with heparin therapy?
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Which method is used for monitoring therapy for warfarin?
Which method is used for monitoring therapy for warfarin?
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What is the difference between low-molecular-weight heparins (LMWH) and standard heparin?
What is the difference between low-molecular-weight heparins (LMWH) and standard heparin?
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Study Notes
Physiology of Coagulation
- Physical trauma to blood vessels starts the coagulation process.
- Interactions between platelets, endothelial cells, and coagulation factors lead to clot formation.
- A platelet-fibrin plug forms at the site of injury to stop bleeding.
- Thrombus formation involves the same steps as normal clotting but is triggered by a pathological condition.
- A clot is composed of a platelet plug reinforced by fibrin.
Resting Platelets
- Healthy endothelial cells release prostacyclin (PGI2) to inhibit platelet activation.
- Prostacyclin binds to platelet receptors, increasing cyclic AMP (cAMP) and lowering calcium (Ca2+).
- This process prevents the release of platelet aggregation agents.
- In healthy vessels, thrombin and thromboxane levels are low, and an intact endothelium covers collagen.
- These factors prevent spontaneous platelet activation and aggregation.
Platelet Plug Formation
- Damage to endothelial cells leads to decreased prostacyclin production.
- Platelets adhere to exposed collagen, increasing calcium levels and activating platelets.
- Activated platelets release ADP, thromboxane A2, serotonin, platelet activation factor, and thrombin.
- These substances activate nearby platelets, amplifying the process.
- Activated platelets express GP IIb/IIIa receptors, which bind fibrinogen, linking platelets together.
- The platelet plug is unstable and requires reinforcement with fibrin.
Fibrin Formation (Coagulation)
- This process solidifies the platelet plug.
Anticoagulants
- Medications that prevent blood clotting.
Heparin
- A natural sulfated polysaccharide found in mast cells.
- Carries a negative charge.
- Not absorbed orally due to precipitation in gastric acid.
- 100% bioavailability when administered intravenously or subcutaneously.
- Does not cross the blood-brain barrier or placenta.
- Mechanism: Activates antithrombin III, inhibiting several clotting factors, especially factor X and thrombin (factor II).
- Immediate onset and short duration (2-4 hours).
- Used to prevent thrombosis.
- Monitored by activated partial thromboplastin time (aPTT) which should be 2-3 times the normal value.
- Side effects include hematomas, thrombocytopenia, alopecia, dermatitis, and bleeding.
Warfarin
- A synthetic coumarin compound.
- Well absorbed orally.
- Can cross the blood-brain barrier and placenta.
- Mechanism: Inhibits vitamin K epoxide reductase in the liver, reducing the synthesis of vitamin K-dependent clotting factors (II, VII, IX, and X).
- Delayed onset and long duration (3-7 days).
- Used to prevent thrombosis.
- Monitored by prothrombin time (PT) or International Normalized Ratio (INR) which should be 2-3 times the normal value.
- Side effects include hemorrhagic skin necrosis, teratogenicity, CNS hemorrhage in the fetus, osteoporosis with long use, and sudden withdrawal leading to thrombosis.
Low-Molecular-Weight Heparin (LMWH)
- Examples: enoxaparin, dalteparin.
- Have a lower molecular weight than standard heparin (less than 8000 Da).
- More specific for inhibition of factor X with minimal effects on platelets and other clotting factors.
- Reduced risk of thrombocytopenia.
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Description
Test your knowledge on the physiology of coagulation, including the processes involved in clot formation, the role of platelets, and the influence of endothelial cells. This quiz covers critical aspects from the initiation of coagulation to the prevention of spontaneous platelet activation. Perfect for students studying hematology or physiology!
