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Questions and Answers
What is the primary mechanism of action of tranexamic acid?
What is the primary mechanism of action of tranexamic acid?
- Stimulates thrombus formation
- Inhibits vitamin K synthesis
- Prevents activation of plasminogen (correct)
- Increases fibrinolysis
In which scenario is tranexamic acid NOT typically used?
In which scenario is tranexamic acid NOT typically used?
- Life-threatening bleeding after thrombolytic therapy
- Hypoprothrombinemic hemorrhage (correct)
- Menorrhagia
- Hereditary angioedema
Which factors are synthesized in the liver under the influence of vitamin K?
Which factors are synthesized in the liver under the influence of vitamin K?
- II, VI, IX, X
- I, III, VIII, X
- II, VII, IX, X (correct)
- I, II, V, VII
What most significantly affects the absorption of vitamin K?
What most significantly affects the absorption of vitamin K?
What is a potential risk associated with the administration of antifibrinolytics like tranexamic acid?
What is a potential risk associated with the administration of antifibrinolytics like tranexamic acid?
What is the primary mechanism of action of acenocoumarol and warfarin?
What is the primary mechanism of action of acenocoumarol and warfarin?
Which of the following factors decreases the effectiveness of warfarin?
Which of the following factors decreases the effectiveness of warfarin?
What significant monitoring is required during therapy with oral anticoagulants like warfarin?
What significant monitoring is required during therapy with oral anticoagulants like warfarin?
What is the peak pharmacological effect timing after administration of warfarin?
What is the peak pharmacological effect timing after administration of warfarin?
Which patient condition requires careful dose adjustment of warfarin to avoid excessive effects?
Which patient condition requires careful dose adjustment of warfarin to avoid excessive effects?
What is a primary reason that LMWH has a lower incidence of HIT compared to standard heparin?
What is a primary reason that LMWH has a lower incidence of HIT compared to standard heparin?
Which condition is a contraindication for the use of heparin?
Which condition is a contraindication for the use of heparin?
What is the mechanism of action of warfarin?
What is the mechanism of action of warfarin?
Which factor is NOT dependent on vitamin K for its synthesis?
Which factor is NOT dependent on vitamin K for its synthesis?
What must be monitored when administering hirudin?
What must be monitored when administering hirudin?
Which anticoagulant is specifically indicated for patients with type II HIT?
Which anticoagulant is specifically indicated for patients with type II HIT?
For which procedure is bivalirudin commonly used?
For which procedure is bivalirudin commonly used?
What is the potential complication associated with over-anticoagulation of direct thrombin inhibitors?
What is the potential complication associated with over-anticoagulation of direct thrombin inhibitors?
Which condition can lead to an increased effect of warfarin due to increased plasma concentration?
Which condition can lead to an increased effect of warfarin due to increased plasma concentration?
Which of the following antibiotics is known to inhibit platelet function?
Which of the following antibiotics is known to inhibit platelet function?
What is a critical adverse effect of warfarin that requires immediate intervention?
What is a critical adverse effect of warfarin that requires immediate intervention?
Which type of oral anticoagulant directly inhibits thrombin?
Which type of oral anticoagulant directly inhibits thrombin?
What effect do broad-spectrum antibiotics have on vitamin K levels?
What effect do broad-spectrum antibiotics have on vitamin K levels?
Which of the following is NOT a known adverse reaction (ADR) of direct oral anticoagulants (DOACs)?
Which of the following is NOT a known adverse reaction (ADR) of direct oral anticoagulants (DOACs)?
What is the appropriate response for minor hemorrhagic events associated with warfarin therapy?
What is the appropriate response for minor hemorrhagic events associated with warfarin therapy?
Which of these drugs displaces warfarin from plasma albumin binding sites, potentially increasing its effect?
Which of these drugs displaces warfarin from plasma albumin binding sites, potentially increasing its effect?
What is the primary mechanism of action of streptokinase?
What is the primary mechanism of action of streptokinase?
Which of the following drugs is considered 'clot selective'?
Which of the following drugs is considered 'clot selective'?
What is a common adverse drug reaction of fibrinolytic therapy?
What is a common adverse drug reaction of fibrinolytic therapy?
In which condition should the use of fibrinolytic drugs be avoided?
In which condition should the use of fibrinolytic drugs be avoided?
What is the recommended time frame for administering fibrinolytic therapy in acute thrombotic stroke?
What is the recommended time frame for administering fibrinolytic therapy in acute thrombotic stroke?
What is the main drug class that includes alteplase and reteplase?
What is the main drug class that includes alteplase and reteplase?
What is the clinical significance of waiting a minimum of 6 months before repeating streptokinase therapy?
What is the clinical significance of waiting a minimum of 6 months before repeating streptokinase therapy?
What additional treatment is suggested for managing bleeding due to fibrinolytic therapy?
What additional treatment is suggested for managing bleeding due to fibrinolytic therapy?
What is the primary mechanism by which heparin acts as an anticoagulant?
What is the primary mechanism by which heparin acts as an anticoagulant?
Which type of heparin is primarily preferred for long-term treatment due to its longer acting properties?
Which type of heparin is primarily preferred for long-term treatment due to its longer acting properties?
In which scenario is Unfractionated Heparin (UFH) typically used?
In which scenario is Unfractionated Heparin (UFH) typically used?
What characterizes the administration and action of Heparin when given intravenously?
What characterizes the administration and action of Heparin when given intravenously?
Which of the following correctly orders the anticoagulant effect of Heparin types from strongest to weakest for general anticoagulation?
Which of the following correctly orders the anticoagulant effect of Heparin types from strongest to weakest for general anticoagulation?
What action do direct thrombin inhibitors primarily target in the coagulation cascade?
What action do direct thrombin inhibitors primarily target in the coagulation cascade?
What is the key advantage of Low Molecular Weight Heparins (LMWH) over Unfractionated Heparin (UFH)?
What is the key advantage of Low Molecular Weight Heparins (LMWH) over Unfractionated Heparin (UFH)?
What treatment is indicated for a deficit leading to vascular thrombosis?
What treatment is indicated for a deficit leading to vascular thrombosis?
Flashcards
How do oral anticoagulants work?
How do oral anticoagulants work?
Oral anticoagulants, like warfarin and acenocoumarol, work by blocking the regeneration of Vitamin K, which is needed for the production of clotting factors. They reduce the ability of the blood to clot.
What is special about warfarin?
What is special about warfarin?
The most important oral anticoagulant, warfarin needs close monitoring with blood tests to adjust the dose. It has a narrow safety margin, meaning it needs to be carefully balanced to be effective but avoid too much bleeding.
How is the effect of warfarin monitored?
How is the effect of warfarin monitored?
The effect of warfarin and acenocoumarol is measured by the prothrombin time (PT). The International Normalized Ratio (INR) standardizes PT across labs for better monitoring.
Why is it important to understand interactions with warfarin?
Why is it important to understand interactions with warfarin?
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What can weaken the effect of warfarin?
What can weaken the effect of warfarin?
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What is Heparin?
What is Heparin?
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What are LMWHs?
What are LMWHs?
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What is Fondaparinux?
What is Fondaparinux?
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What is Unfractionated Heparin (UFH)?
What is Unfractionated Heparin (UFH)?
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How does Heparin work?
How does Heparin work?
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How is Heparin administered and how long does it last?
How is Heparin administered and how long does it last?
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What are the benefits of LMWHs compared to UFH?
What are the benefits of LMWHs compared to UFH?
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How is Heparin dosing managed?
How is Heparin dosing managed?
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Heparin
Heparin
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APTT (Activated Partial Thromboplastin Time)
APTT (Activated Partial Thromboplastin Time)
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Anticoagulants
Anticoagulants
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Heparin-Induced Thrombocytopenia (HIT)
Heparin-Induced Thrombocytopenia (HIT)
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Direct Thrombin Inhibitors
Direct Thrombin Inhibitors
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Anti-vitamin K Agents
Anti-vitamin K Agents
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Warfarin
Warfarin
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Acenocoumarol
Acenocoumarol
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What is plasmin?
What is plasmin?
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What are fibrinolytic drugs?
What are fibrinolytic drugs?
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What is streptokinase?
What is streptokinase?
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What is alteplase?
What is alteplase?
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What is reteplase?
What is reteplase?
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What's a major risk associated with fibrinolytic drugs?
What's a major risk associated with fibrinolytic drugs?
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What's the main clinical use for fibrinolytic drugs?
What's the main clinical use for fibrinolytic drugs?
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What are some contraindications for fibrinolytic drugs?
What are some contraindications for fibrinolytic drugs?
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What drugs can increase Warfarin's effect?
What drugs can increase Warfarin's effect?
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How do broad-spectrum antibiotics impact Warfarin?
How do broad-spectrum antibiotics impact Warfarin?
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What is the mechanism of action of Dabigatran?
What is the mechanism of action of Dabigatran?
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What are the main uses of Dabigatran?
What are the main uses of Dabigatran?
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How can other drugs affect Warfarin's effect?
How can other drugs affect Warfarin's effect?
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What are some of the adverse effects of Warfarin?
What are some of the adverse effects of Warfarin?
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What are some of the side effects of Dabigatran?
What are some of the side effects of Dabigatran?
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Antifibrinolytic Drug
Antifibrinolytic Drug
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Tranexamic Acid
Tranexamic Acid
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Hypoprothrombinemic Hemorrhage
Hypoprothrombinemic Hemorrhage
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Vitamin K
Vitamin K
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Lack of Bile, Obstructive Jaundice
Lack of Bile, Obstructive Jaundice
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Study Notes
Coagulation and Aggregation
- Lesson 23 covered in 3rd-year Medicine.
- Professor: Vittoria Carrabs PhD
- Academic year: 2024/25
Pharmacology of Hemostasis
- Platelet aggregation:
- Deficit: Hemorrhage
- Excess: Vascular thrombosis -Drugs: Platelet Concentrate, Antiplatelet agents
- Coagulation:
- Deficit: Bleeding
- Excess: Vascular thrombosis
- Drugs: Procoagulants, anticoagulants
- Fibrinolysis:
- Deficit: Vascular thrombosis
- Excess: Bleeding
- Drugs: Fibrinolytics, antifibrinolytics
Drugs that Act on the Coagulation Cascade
- Anticoagulants:
- Heparin:
- A group of sulfated glycosaminoglycans
- Dosing in units of activity
- Types: LMWHs (enoxaparin, dalteparin), fondaparinux, UFH
- Mechanism: Interferes with blood clotting by binding to antithrombin III, enhancing its effects on factor Ila (thrombin) and factor Xa.
- Administration: IV (immediate) or subcutaneous (delayed 60 min)
- Half-life: approximately 40-90 minutes
- Dosage adjusted as needed
- Used for shorter-term needs.
- Alternative administration route (e.g. SC, IV infusion dose) often considered
- Direct Thrombin Inhibitors:
- Hirudin, lepirudin (recombinant)
- Bivalirudin -Used during percutaneous coronary artery surgeries. IV bolus followed by an infusion.
- Dabigatran -Used for thromboembolic disease, type II HIT patients. Adjusted dosages based on APTT -Causes bleeding or hypersensitivity reactions.
- Direct Xa Inhibitors:
- Rivaroxaban, apixaban, edoxaban -Mechanism of action: directly inhibit factor Xa. -Adverse Drug Reactions (ADR): Nausea, tachycardia, anemia, thrombocytopenia, increased transaminases, and hepatoxicity (rivaroxaban in particular).
- Heparin:
Oral Anticoagulants
- Acenocoumarol, Warfarin:
- Anti-Vitamin K agents
- Mechanism: prevent the physiological regeneration of the active form of vitamin K, necessary for the formation of coagulation factors II, VII, IX, and X, protein C, and S which inhibit VKOCR1 (Vitamin K epoxide reductase).
- Importance: The most important oral anticoagulant drug.
- Frequent blood tests to individualize the dose.
- Monitoring of INR (International Normalized Ratio), used for the detection of the effect of the drug.
- Peak pharmacological effect ~48 hours, lasts 4-5 days.
- Teratogenic.
- Appears in milk during lactation.
- Factors reducing effect: Physiological state/disease (pregnancy, hypothyroidism), several drugs (vitamin K, drugs which induce hepatic P450 enzymes, drugs that reduce absorption).
Fibrinolysis
- Mechanism: Fibrinolysis is the breakdown of fibrin clots.
- Key enzyme: Plasmin, a trypsin-like protease
- Purpose: Prevents persistence of clots, ensures prompt removal of thrombus
- Fibrinolytic drugs:
- Streptokinase: A plasminogen activating protein (non-specific), administered IV, reduces mortality in acute myocardial infarction.
- Alteplase/Duteplase: Tissue plasminogen activator ("clot selective"). Can be used in patients with antibodies to streptokinase.
- Reteplase: Administered as bolus, often used in cases of myocardial infarction.
- Adverse Drug Reactions (ADRs): Bleeding (treated with Tranexamic Acid, Fresh Plasma, Coagulation Factors)
- Contraindications: Includes internal bleeding, hemorrhagic cerebrovascular disease, bleeding diaseses, pregnancy, uncontrolled hypertension, invasive procedures (where hemostasis is important), recent trauma
- Clinical uses: treating acute myocardial infarction within 12 hrs of onset; clearing thrombosed shunts/cannulae; acute arterial thromboembolism; and life-threatening deep venous thrombosis and pulmonary embolism
- Antifibrinolytic drugs: Tranexamic acid
Vitamin K
- Importance: Vital for the production of clotting factors (II, VII, IX, X) - "the vitamin of coagulation"
- Administration: Oral or parenteral
- Absorption: Requires bile salts.
- Colelithiasis: Reduces its absorption.
- Clinical uses: Treating bleeding from excessive oral anticoagulation, preventing hemorrhagic disease in babies, or used to treat deficiencies
- Sprue, coeliac disease, steatorrhoea or lack of bile (e.g. in obstructive jaundice).
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Description
This quiz focuses on the pharmacology of hemostasis, including platelet aggregation and coagulation mechanisms as taught in Lesson 23 of the 3rd-year Medicine course. It covers various drugs that influence these processes and describes conditions associated with deficiencies or excesses. Test your understanding of these critical medical concepts.