Podcast
Questions and Answers
Which of the following drugs is known to enhance the effect of warfarin?
Which of the following drugs is known to enhance the effect of warfarin?
- Cimetidine (correct)
- Aluminum hydroxide
- Phenobarbital
- Rifampin
What effect do oral antibiotics have on warfarin levels?
What effect do oral antibiotics have on warfarin levels?
- Enhance the effect of clotting factors
- Inhibit warfarin metabolism
- Decrease vitamin K synthesis (correct)
- Increase warfarin absorption
Which of the following substances would likely decrease the absorption of vitamin K?
Which of the following substances would likely decrease the absorption of vitamin K?
- Oral contraceptives
- Liquid paraffin (correct)
- NSAIDs
- Aluminum hydroxide
Which of the following would NOT increase the effectiveness of warfarin?
Which of the following would NOT increase the effectiveness of warfarin?
How do fibrinolytic drugs like t-PAs work in the body?
How do fibrinolytic drugs like t-PAs work in the body?
Which of the following is a potential consequence of taking NSAIDs while on warfarin?
Which of the following is a potential consequence of taking NSAIDs while on warfarin?
What is the mechanism by which chloramphenicol affects warfarin levels?
What is the mechanism by which chloramphenicol affects warfarin levels?
Which of the following conditions must microsomal enzyme inducers like phenobarbital create for warfarin?
Which of the following conditions must microsomal enzyme inducers like phenobarbital create for warfarin?
What is the primary function of recombinant tissue plasminogen activators (t-PAs)?
What is the primary function of recombinant tissue plasminogen activators (t-PAs)?
Which of the following t-PAs allows for administration as a single intravenous injection?
Which of the following t-PAs allows for administration as a single intravenous injection?
What is a significant advantage of using reteplase and tenecteplase over alteplase?
What is a significant advantage of using reteplase and tenecteplase over alteplase?
In which scenario should thrombolytic drugs be administered within 12 hours?
In which scenario should thrombolytic drugs be administered within 12 hours?
How are thrombolytic drugs typically administered?
How are thrombolytic drugs typically administered?
What effect does local activation of plasminogen by t-PAs have on bleeding risk?
What effect does local activation of plasminogen by t-PAs have on bleeding risk?
Which of the following statements is true regarding the thrombolytic action of t-PAs?
Which of the following statements is true regarding the thrombolytic action of t-PAs?
Which condition is NOT a typical therapeutic use for thrombolytic drugs?
Which condition is NOT a typical therapeutic use for thrombolytic drugs?
What is the primary function of plasmin in the body?
What is the primary function of plasmin in the body?
What is a significant drawback of fibrinolytic drugs?
What is a significant drawback of fibrinolytic drugs?
Streptokinase and urokinase both activate plasminogen. How do they differ in their source?
Streptokinase and urokinase both activate plasminogen. How do they differ in their source?
Which statement about urokinase is true?
Which statement about urokinase is true?
What potential risk is associated with the use of fibrinolytic drugs?
What potential risk is associated with the use of fibrinolytic drugs?
What characteristic of streptokinase may pose a concern for some patients?
What characteristic of streptokinase may pose a concern for some patients?
How does plasminogen activation occur during fibrinolysis?
How does plasminogen activation occur during fibrinolysis?
What is a key advantage of endogenous activators over fibrinolytic drugs?
What is a key advantage of endogenous activators over fibrinolytic drugs?
What is the optimal time frame for administering treatment to obtain maximum benefit?
What is the optimal time frame for administering treatment to obtain maximum benefit?
What is the primary adverse effect associated with thrombolytic drugs?
What is the primary adverse effect associated with thrombolytic drugs?
Which thrombolytic agent is associated with a higher risk of allergic reactions?
Which thrombolytic agent is associated with a higher risk of allergic reactions?
How does aspirin inhibit platelet aggregation?
How does aspirin inhibit platelet aggregation?
What can be a critical site for assessing bleeding risk before thrombolysis?
What can be a critical site for assessing bleeding risk before thrombolysis?
What mechanism does aspirin use to cause irreversible inhibition in platelets?
What mechanism does aspirin use to cause irreversible inhibition in platelets?
Which thrombolytic agent has a lower associated risk of systemic bleeding?
Which thrombolytic agent has a lower associated risk of systemic bleeding?
What effect does aspirin have on thromboxane A2 (TXA2) levels in platelets?
What effect does aspirin have on thromboxane A2 (TXA2) levels in platelets?
Microsomal enzyme inducers increase the metabolism of warfarin.
Microsomal enzyme inducers increase the metabolism of warfarin.
Chloramphenicol is a drug that decreases the effect of warfarin.
Chloramphenicol is a drug that decreases the effect of warfarin.
Liquid paraffin enhances the absorption of vitamin K.
Liquid paraffin enhances the absorption of vitamin K.
Oral antibiotics can lead to increased synthesis of vitamin K.
Oral antibiotics can lead to increased synthesis of vitamin K.
NSAIDs may displace warfarin from plasma proteins, enhancing its anticoagulant activity.
NSAIDs may displace warfarin from plasma proteins, enhancing its anticoagulant activity.
Thrombolytic drugs activate plasminogen into plasmin in the presence of fibrin clots.
Thrombolytic drugs activate plasminogen into plasmin in the presence of fibrin clots.
Aluminum hydroxide is known to increase the absorption of warfarin.
Aluminum hydroxide is known to increase the absorption of warfarin.
Vitamin K is critical for the activation of clotting factors.
Vitamin K is critical for the activation of clotting factors.
Recombinant tissue plasminogen activators (t-PAs) have a short half-life that requires continuous infusion for administration.
Recombinant tissue plasminogen activators (t-PAs) have a short half-life that requires continuous infusion for administration.
T-PAs are primarily used for the treatment of acute myocardial infarction within 24 hours of onset.
T-PAs are primarily used for the treatment of acute myocardial infarction within 24 hours of onset.
The local activation of plasminogen by t-PAs increases the risk of systemic bleeding.
The local activation of plasminogen by t-PAs increases the risk of systemic bleeding.
All therapeutic uses of thrombolytic drugs are limited to conditions involving ischemic strokes.
All therapeutic uses of thrombolytic drugs are limited to conditions involving ischemic strokes.
Reteplase can be administered through two intravenous injections that are separated by a full hour.
Reteplase can be administered through two intravenous injections that are separated by a full hour.
Tissue plasminogen activators are produced from cultured bacterial cells.
Tissue plasminogen activators are produced from cultured bacterial cells.
Tenecteplase is administered as a single intravenous injection for the treatment of acute conditions.
Tenecteplase is administered as a single intravenous injection for the treatment of acute conditions.
Plasmin is activated only at the systemic level during thrombolytic therapy.
Plasmin is activated only at the systemic level during thrombolytic therapy.
Treatment is most beneficial if given within 60 minutes of the onset of pain.
Treatment is most beneficial if given within 60 minutes of the onset of pain.
Streptokinase has a higher risk of causing allergic reactions compared to other thrombolytic agents.
Streptokinase has a higher risk of causing allergic reactions compared to other thrombolytic agents.
Systemic bleeding is considered a minor adverse effect of thrombolytic drugs.
Systemic bleeding is considered a minor adverse effect of thrombolytic drugs.
Aspirin inhibits platelet aggregation by enhancing the production of TXA2.
Aspirin inhibits platelet aggregation by enhancing the production of TXA2.
Thrombolytic drugs should be administered without concern for bleeding risks in critical sites.
Thrombolytic drugs should be administered without concern for bleeding risks in critical sites.
Aspirin causes reversible acetylation of platelet cell membranes, leading to decreased platelet adhesion.
Aspirin causes reversible acetylation of platelet cell membranes, leading to decreased platelet adhesion.
The risk of bleeding is low with streptokinase compared to recent recombinant tissue plasminogen activators.
The risk of bleeding is low with streptokinase compared to recent recombinant tissue plasminogen activators.
Thrombolytic drugs are always contraindicated in patients with a previous history of bleeding complications.
Thrombolytic drugs are always contraindicated in patients with a previous history of bleeding complications.
Plasmin is responsible for lysis of the clot.
Plasmin is responsible for lysis of the clot.
Streptokinase is an enzyme that activates plasminogen enzymatically.
Streptokinase is an enzyme that activates plasminogen enzymatically.
Urokinase has a higher antigenic potential than streptokinase.
Urokinase has a higher antigenic potential than streptokinase.
Fibrinolytic drugs preferentially activate plasminogen bound to circulating proteins.
Fibrinolytic drugs preferentially activate plasminogen bound to circulating proteins.
The use of fibrinolytic drugs does not pose a risk of systemic bleeding.
The use of fibrinolytic drugs does not pose a risk of systemic bleeding.
Plasminogen activation is solely dependent on endogenous activators in the body.
Plasminogen activation is solely dependent on endogenous activators in the body.
Fibrinolysis is a process that aims to avoid systemic activation of plasminogen.
Fibrinolysis is a process that aims to avoid systemic activation of plasminogen.
Recombinant urokinase is derived from cultured kidney cells.
Recombinant urokinase is derived from cultured kidney cells.
What specific condition allows t-PAs to reduce the incidence of systemic bleeding during thrombolysis?
What specific condition allows t-PAs to reduce the incidence of systemic bleeding during thrombolysis?
Why are reteplase and tenecteplase favored over alteplase in some clinical scenarios?
Why are reteplase and tenecteplase favored over alteplase in some clinical scenarios?
In what time frame should thrombolytic therapy be initiated for acute myocardial infarction for optimal effectiveness?
In what time frame should thrombolytic therapy be initiated for acute myocardial infarction for optimal effectiveness?
Describe the administration approach for reteplase in emergency situations.
Describe the administration approach for reteplase in emergency situations.
What is the primary administration route for thrombolytic drugs when treating conditions like pulmonary embolism?
What is the primary administration route for thrombolytic drugs when treating conditions like pulmonary embolism?
Explain the mechanism by which t-PAs achieve their therapeutic effect?
Explain the mechanism by which t-PAs achieve their therapeutic effect?
What are the therapeutic indications for administering thrombolytic drugs?
What are the therapeutic indications for administering thrombolytic drugs?
What is a significant drawback of using alteplase compared to reteplase or tenecteplase?
What is a significant drawback of using alteplase compared to reteplase or tenecteplase?
What is the primary role of plasmin in the clotting process?
What is the primary role of plasmin in the clotting process?
How does streptokinase non-enzymatically activate plasminogen?
How does streptokinase non-enzymatically activate plasminogen?
In what way does urokinase differ from streptokinase in terms of immunogenicity?
In what way does urokinase differ from streptokinase in terms of immunogenicity?
Why is the systemic activation of plasminogen by fibrinolytic drugs concerning?
Why is the systemic activation of plasminogen by fibrinolytic drugs concerning?
What is the mechanism by which endogenous activators limit fibrinolysis to formed thrombi?
What is the mechanism by which endogenous activators limit fibrinolysis to formed thrombi?
What are the implications of using fibrinolytic drugs in patients with existing thrombi?
What are the implications of using fibrinolytic drugs in patients with existing thrombi?
Discuss the source and preparation method of urokinase.
Discuss the source and preparation method of urokinase.
Why might some patients experience allergic reactions to streptokinase?
Why might some patients experience allergic reactions to streptokinase?
What role do oral antibiotics play in the metabolism of warfarin?
What role do oral antibiotics play in the metabolism of warfarin?
How does liquid paraffin affect the absorption of vitamin K?
How does liquid paraffin affect the absorption of vitamin K?
What is the effect of NSAIDs on warfarin levels in the bloodstream?
What is the effect of NSAIDs on warfarin levels in the bloodstream?
What is the mechanism by which microsomal enzyme inducers affect warfarin?
What is the mechanism by which microsomal enzyme inducers affect warfarin?
How do fibrinolytic drugs like t-PAs activate plasminogen?
How do fibrinolytic drugs like t-PAs activate plasminogen?
What common effect do microsomal enzyme inhibitors have on warfarin levels?
What common effect do microsomal enzyme inhibitors have on warfarin levels?
Which substance can increase the synthesis of clotting factors while on warfarin?
Which substance can increase the synthesis of clotting factors while on warfarin?
What is a potential consequence of the use of aluminum hydroxide with warfarin?
What is a potential consequence of the use of aluminum hydroxide with warfarin?
What is the ideal time frame for administering thrombolytic treatment to achieve maximum benefit?
What is the ideal time frame for administering thrombolytic treatment to achieve maximum benefit?
What is the major adverse effect associated with systemic use of thrombolytic drugs?
What is the major adverse effect associated with systemic use of thrombolytic drugs?
Which thrombolytic agent has a higher likelihood of inducing allergic reactions?
Which thrombolytic agent has a higher likelihood of inducing allergic reactions?
How does aspirin affect platelet aggregation?
How does aspirin affect platelet aggregation?
What precautions should be taken concerning critical sites before administering thrombolysis?
What precautions should be taken concerning critical sites before administering thrombolysis?
What effect does the irreversible acetylation by aspirin have on platelets?
What effect does the irreversible acetylation by aspirin have on platelets?
What are the two mechanisms by which aspirin inhibits platelet aggregation?
What are the two mechanisms by which aspirin inhibits platelet aggregation?
What conditions are advised to be assessed for bleeding liability before thrombolytic therapy?
What conditions are advised to be assessed for bleeding liability before thrombolytic therapy?
Drugs that potentiate warfarin include microsomal enzyme ______
Drugs that potentiate warfarin include microsomal enzyme ______
Oral antibiotics decrease vitamin K synthesis by killing the gut ______
Oral antibiotics decrease vitamin K synthesis by killing the gut ______
Liquid paraffin results in decreased absorption of vitamin ______
Liquid paraffin results in decreased absorption of vitamin ______
NSAIDs may ______ warfarin from plasma proteins, enhancing its anticoagulant activity.
NSAIDs may ______ warfarin from plasma proteins, enhancing its anticoagulant activity.
Fibrinolytic drugs activate plasminogen into plasmin in the presence of ______ clots.
Fibrinolytic drugs activate plasminogen into plasmin in the presence of ______ clots.
Aluminum hydroxide is known to decrease the absorption of ______.
Aluminum hydroxide is known to decrease the absorption of ______.
Vitamin K is critical for the activation of clotting ______.
Vitamin K is critical for the activation of clotting ______.
Tissue plasminogen activators (t-PAs) are produced from cultured ______ cells.
Tissue plasminogen activators (t-PAs) are produced from cultured ______ cells.
Recombinant tissue plasminogen activators (t-PAs) are produced in cultured ______.
Recombinant tissue plasminogen activators (t-PAs) are produced in cultured ______.
Reteplase and tenecteplase have a long half-life which allows for ______ administration as a bolus.
Reteplase and tenecteplase have a long half-life which allows for ______ administration as a bolus.
Thrombolytic drugs are given by the ______ route in cases of acute myocardial infarction.
Thrombolytic drugs are given by the ______ route in cases of acute myocardial infarction.
The local activation of plasminogen at the thrombus site reduces the incidence of ______ bleeding.
The local activation of plasminogen at the thrombus site reduces the incidence of ______ bleeding.
Therapeutic uses of thrombolytic drugs include treatment for pulmonary ______ and arterial thrombosis.
Therapeutic uses of thrombolytic drugs include treatment for pulmonary ______ and arterial thrombosis.
In acute myocardial infarction, thrombolytic drugs should be administered within ______ hours of onset.
In acute myocardial infarction, thrombolytic drugs should be administered within ______ hours of onset.
Alteplase, reteplase, and tenecteplase are examples of ______ tissue plasminogen activators.
Alteplase, reteplase, and tenecteplase are examples of ______ tissue plasminogen activators.
Reteplase requires two intravenous injections separated by ______ minutes.
Reteplase requires two intravenous injections separated by ______ minutes.
Plasmin causes lysis of the ______.
Plasmin causes lysis of the ______.
Fibronolytic drugs cause rapid activation of plasminogen to form ______.
Fibronolytic drugs cause rapid activation of plasminogen to form ______.
Streptokinase is a protein isolated from ______.
Streptokinase is a protein isolated from ______.
Urokinase is a protease originally isolated from ______.
Urokinase is a protease originally isolated from ______.
Streptokinase activates plasminogen into plasmin ______.
Streptokinase activates plasminogen into plasmin ______.
Urokinase is less ______ than streptokinase.
Urokinase is less ______ than streptokinase.
The activation of plasminogen is preferentially confined to the ______ thrombus.
The activation of plasminogen is preferentially confined to the ______ thrombus.
Fibrinolytic drugs may break down protective hemostatic thrombi and pathogenic ______.
Fibrinolytic drugs may break down protective hemostatic thrombi and pathogenic ______.
The maximum benefit is obtained if treatment is given within ______ minutes of the onset of pain.
The maximum benefit is obtained if treatment is given within ______ minutes of the onset of pain.
Systemic bleeding is the major adverse effect, with the risk being high with ______ and low with recombinant tissue plasminogen activators.
Systemic bleeding is the major adverse effect, with the risk being high with ______ and low with recombinant tissue plasminogen activators.
Aspirin inhibits platelet aggregation by irreversible inhibition of the ______ enzyme.
Aspirin inhibits platelet aggregation by irreversible inhibition of the ______ enzyme.
Irreversible acetylation of platelet cell membranes leads to decreased platelet ______.
Irreversible acetylation of platelet cell membranes leads to decreased platelet ______.
Streptokinase can cause allergy, fever, and ______ during i.v. infusion.
Streptokinase can cause allergy, fever, and ______ during i.v. infusion.
The major adverse effect of thrombolytic drugs is ______ in critical sites.
The major adverse effect of thrombolytic drugs is ______ in critical sites.
The risk of bleeding increases if thrombolytic therapy is not monitored for critical ______ sites.
The risk of bleeding increases if thrombolytic therapy is not monitored for critical ______ sites.
Aspirin leads to decreased levels of ______ in platelets.
Aspirin leads to decreased levels of ______ in platelets.
Match the following drugs with their effects on warfarin:
Match the following drugs with their effects on warfarin:
Match the following drug classes with their interactions with warfarin:
Match the following drug classes with their interactions with warfarin:
Match the following conditions with the appropriate effects on warfarin:
Match the following conditions with the appropriate effects on warfarin:
Match the following agents with their effects on vitamin K:
Match the following agents with their effects on vitamin K:
Match the following thrombolytic agents with their characteristics:
Match the following thrombolytic agents with their characteristics:
Match the following statements with their context regarding plasminogen activation:
Match the following statements with their context regarding plasminogen activation:
Match the following statements regarding vitamin K interactions:
Match the following statements regarding vitamin K interactions:
Match the drugs with their respective effects on anticoagulant agents:
Match the drugs with their respective effects on anticoagulant agents:
Match the thrombolytic drugs with their associated risks or characteristics:
Match the thrombolytic drugs with their associated risks or characteristics:
Match the components of aspirin's mechanism to its effects on platelet aggregation:
Match the components of aspirin's mechanism to its effects on platelet aggregation:
Match the adverse effects with the respective thrombolytic drugs:
Match the adverse effects with the respective thrombolytic drugs:
Match the following terms with their descriptions:
Match the following terms with their descriptions:
Match the adverse effects of thrombolytic therapy with their potential implications:
Match the adverse effects of thrombolytic therapy with their potential implications:
Match the thrombolytic drug with its primary mechanism of action:
Match the thrombolytic drug with its primary mechanism of action:
Match the concept of maximal benefit timing with the respective time frame:
Match the concept of maximal benefit timing with the respective time frame:
Match the type of bleeding risk with its critical site:
Match the type of bleeding risk with its critical site:
Match the following recombinant tissue plasminogen activators (t-PAs) with their characteristics:
Match the following recombinant tissue plasminogen activators (t-PAs) with their characteristics:
Match the following thrombolytic conditions with their appropriate administration timing:
Match the following thrombolytic conditions with their appropriate administration timing:
Match the following activating processes of t-PAs with their description:
Match the following activating processes of t-PAs with their description:
Match the following therapeutic uses of thrombolytic drugs with their corresponding conditions:
Match the following therapeutic uses of thrombolytic drugs with their corresponding conditions:
Match the following intravenous administration features of t-PAs with their effects:
Match the following intravenous administration features of t-PAs with their effects:
Match the following characteristics of recombinant human proteins with their details:
Match the following characteristics of recombinant human proteins with their details:
Match the following aspects of thrombolytic therapy with their outcomes:
Match the following aspects of thrombolytic therapy with their outcomes:
Match the following t-PAs with their production sources:
Match the following t-PAs with their production sources:
Match the following thrombolytic agents with their source:
Match the following thrombolytic agents with their source:
Match the following properties with the corresponding thrombolytic agent:
Match the following properties with the corresponding thrombolytic agent:
Match the following statements with their corresponding effects:
Match the following statements with their corresponding effects:
Match the following drugs with their activation mechanisms:
Match the following drugs with their activation mechanisms:
Match the following definitions to their terms:
Match the following definitions to their terms:
Match the following properties of drugs with their comparison:
Match the following properties of drugs with their comparison:
Match the following risk factors to their descriptions:
Match the following risk factors to their descriptions:
Match the following conditions with their effects on thrombolysis:
Match the following conditions with their effects on thrombolysis:
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Study Notes
Drug Interactions with Oral Anticoagulants (Warfarin)
-
Potentiating Drugs: Medications that increase warfarin's effects.
- Microsomal Enzyme Inhibitors: Includes cimetidine and chloramphenicol, which decrease warfarin metabolism.
- Oral Antibiotics: Reduce Vitamin K synthesis by killing gut flora, impacting clotting factor production.
- Liquid Paraffin: Decreases Vitamin K absorption in the body.
- NSAIDs: Displace warfarin from plasma protein binding, leading to increased anticoagulant effects.
-
Inhibiting Drugs: Medications that decrease warfarin's effects.
- Microsomal Enzyme Inducers: Such as phenobarbital and rifampicin, which increase warfarin metabolism.
- Oral Contraceptives and Vitamin K: Increase synthesis of clotting factors, counteracting warfarin.
Fibrinolytic (Thrombolytic) Drugs
- Mechanism of Action: Plasminogen is activated to plasmin, which lyses fibrin clots, predominantly in areas where thrombi are present to minimize systemic effects.
- Risks: Fibrinolytic agents can activate circulating plasminogen as well, resulting in bleeding risks from both protective and pathologic thrombi.
Key Fibrinolytic Agents
-
Streptokinase:
- Protein isolated from streptococci, activates plasminogen non-enzymatically.
- Can be antigenic, posing a risk for allergic reactions.
-
Urokinase:
- Protease derived from urine, now primarily available in recombinant form.
- Less antigenic compared to streptokinase.
-
Recombinant Tissue Plasminogen Activators (t-PAs):
- Includes alteplase, reteplase, and tenecteplase, designed to act specifically on fibrin-bound plasminogen, reducing systemic bleeding risks.
- Reteplase and tenecteplase have longer half-lives, allowing for less frequent dosing.
Therapeutic Uses of Thrombolytic Drugs
- Administered intravenously for acute myocardial infarction (MI), ischemic stroke, pulmonary embolism, and arterial thrombosis.
- Optimal efficacy if given within 90 minutes of the onset of symptoms, particularly for acute MI.
- Precautions necessary to avoid bleeding risks, especially in critical areas like the CNS or retina.
Adverse Effects of Thrombolytic Drugs
- High risk of systemic bleeding, particularly with streptokinase.
- Possible allergic reactions and transient side effects (fever, hypotension) during streptokinase administration.
Antiplatelet Drugs
- Aspirin:
- Inhibits platelet aggregation through irreversible COX enzyme inhibition, reducing thromboxane A2 (TXA2) levels and subsequent platelet aggregation and adhesion.
Drug Interactions with Oral Anticoagulants (Warfarin)
-
Potentiating Drugs: Medications that increase warfarin's effects.
- Microsomal Enzyme Inhibitors: Includes cimetidine and chloramphenicol, which decrease warfarin metabolism.
- Oral Antibiotics: Reduce Vitamin K synthesis by killing gut flora, impacting clotting factor production.
- Liquid Paraffin: Decreases Vitamin K absorption in the body.
- NSAIDs: Displace warfarin from plasma protein binding, leading to increased anticoagulant effects.
-
Inhibiting Drugs: Medications that decrease warfarin's effects.
- Microsomal Enzyme Inducers: Such as phenobarbital and rifampicin, which increase warfarin metabolism.
- Oral Contraceptives and Vitamin K: Increase synthesis of clotting factors, counteracting warfarin.
Fibrinolytic (Thrombolytic) Drugs
- Mechanism of Action: Plasminogen is activated to plasmin, which lyses fibrin clots, predominantly in areas where thrombi are present to minimize systemic effects.
- Risks: Fibrinolytic agents can activate circulating plasminogen as well, resulting in bleeding risks from both protective and pathologic thrombi.
Key Fibrinolytic Agents
-
Streptokinase:
- Protein isolated from streptococci, activates plasminogen non-enzymatically.
- Can be antigenic, posing a risk for allergic reactions.
-
Urokinase:
- Protease derived from urine, now primarily available in recombinant form.
- Less antigenic compared to streptokinase.
-
Recombinant Tissue Plasminogen Activators (t-PAs):
- Includes alteplase, reteplase, and tenecteplase, designed to act specifically on fibrin-bound plasminogen, reducing systemic bleeding risks.
- Reteplase and tenecteplase have longer half-lives, allowing for less frequent dosing.
Therapeutic Uses of Thrombolytic Drugs
- Administered intravenously for acute myocardial infarction (MI), ischemic stroke, pulmonary embolism, and arterial thrombosis.
- Optimal efficacy if given within 90 minutes of the onset of symptoms, particularly for acute MI.
- Precautions necessary to avoid bleeding risks, especially in critical areas like the CNS or retina.
Adverse Effects of Thrombolytic Drugs
- High risk of systemic bleeding, particularly with streptokinase.
- Possible allergic reactions and transient side effects (fever, hypotension) during streptokinase administration.
Antiplatelet Drugs
- Aspirin:
- Inhibits platelet aggregation through irreversible COX enzyme inhibition, reducing thromboxane A2 (TXA2) levels and subsequent platelet aggregation and adhesion.
Drug Interactions with Oral Anticoagulants (Warfarin)
-
Potentiating Drugs: Medications that increase warfarin's effects.
- Microsomal Enzyme Inhibitors: Includes cimetidine and chloramphenicol, which decrease warfarin metabolism.
- Oral Antibiotics: Reduce Vitamin K synthesis by killing gut flora, impacting clotting factor production.
- Liquid Paraffin: Decreases Vitamin K absorption in the body.
- NSAIDs: Displace warfarin from plasma protein binding, leading to increased anticoagulant effects.
-
Inhibiting Drugs: Medications that decrease warfarin's effects.
- Microsomal Enzyme Inducers: Such as phenobarbital and rifampicin, which increase warfarin metabolism.
- Oral Contraceptives and Vitamin K: Increase synthesis of clotting factors, counteracting warfarin.
Fibrinolytic (Thrombolytic) Drugs
- Mechanism of Action: Plasminogen is activated to plasmin, which lyses fibrin clots, predominantly in areas where thrombi are present to minimize systemic effects.
- Risks: Fibrinolytic agents can activate circulating plasminogen as well, resulting in bleeding risks from both protective and pathologic thrombi.
Key Fibrinolytic Agents
-
Streptokinase:
- Protein isolated from streptococci, activates plasminogen non-enzymatically.
- Can be antigenic, posing a risk for allergic reactions.
-
Urokinase:
- Protease derived from urine, now primarily available in recombinant form.
- Less antigenic compared to streptokinase.
-
Recombinant Tissue Plasminogen Activators (t-PAs):
- Includes alteplase, reteplase, and tenecteplase, designed to act specifically on fibrin-bound plasminogen, reducing systemic bleeding risks.
- Reteplase and tenecteplase have longer half-lives, allowing for less frequent dosing.
Therapeutic Uses of Thrombolytic Drugs
- Administered intravenously for acute myocardial infarction (MI), ischemic stroke, pulmonary embolism, and arterial thrombosis.
- Optimal efficacy if given within 90 minutes of the onset of symptoms, particularly for acute MI.
- Precautions necessary to avoid bleeding risks, especially in critical areas like the CNS or retina.
Adverse Effects of Thrombolytic Drugs
- High risk of systemic bleeding, particularly with streptokinase.
- Possible allergic reactions and transient side effects (fever, hypotension) during streptokinase administration.
Antiplatelet Drugs
- Aspirin:
- Inhibits platelet aggregation through irreversible COX enzyme inhibition, reducing thromboxane A2 (TXA2) levels and subsequent platelet aggregation and adhesion.
Drug Interactions with Oral Anticoagulants (Warfarin)
-
Potentiating Drugs: Medications that increase warfarin's effects.
- Microsomal Enzyme Inhibitors: Includes cimetidine and chloramphenicol, which decrease warfarin metabolism.
- Oral Antibiotics: Reduce Vitamin K synthesis by killing gut flora, impacting clotting factor production.
- Liquid Paraffin: Decreases Vitamin K absorption in the body.
- NSAIDs: Displace warfarin from plasma protein binding, leading to increased anticoagulant effects.
-
Inhibiting Drugs: Medications that decrease warfarin's effects.
- Microsomal Enzyme Inducers: Such as phenobarbital and rifampicin, which increase warfarin metabolism.
- Oral Contraceptives and Vitamin K: Increase synthesis of clotting factors, counteracting warfarin.
Fibrinolytic (Thrombolytic) Drugs
- Mechanism of Action: Plasminogen is activated to plasmin, which lyses fibrin clots, predominantly in areas where thrombi are present to minimize systemic effects.
- Risks: Fibrinolytic agents can activate circulating plasminogen as well, resulting in bleeding risks from both protective and pathologic thrombi.
Key Fibrinolytic Agents
-
Streptokinase:
- Protein isolated from streptococci, activates plasminogen non-enzymatically.
- Can be antigenic, posing a risk for allergic reactions.
-
Urokinase:
- Protease derived from urine, now primarily available in recombinant form.
- Less antigenic compared to streptokinase.
-
Recombinant Tissue Plasminogen Activators (t-PAs):
- Includes alteplase, reteplase, and tenecteplase, designed to act specifically on fibrin-bound plasminogen, reducing systemic bleeding risks.
- Reteplase and tenecteplase have longer half-lives, allowing for less frequent dosing.
Therapeutic Uses of Thrombolytic Drugs
- Administered intravenously for acute myocardial infarction (MI), ischemic stroke, pulmonary embolism, and arterial thrombosis.
- Optimal efficacy if given within 90 minutes of the onset of symptoms, particularly for acute MI.
- Precautions necessary to avoid bleeding risks, especially in critical areas like the CNS or retina.
Adverse Effects of Thrombolytic Drugs
- High risk of systemic bleeding, particularly with streptokinase.
- Possible allergic reactions and transient side effects (fever, hypotension) during streptokinase administration.
Antiplatelet Drugs
- Aspirin:
- Inhibits platelet aggregation through irreversible COX enzyme inhibition, reducing thromboxane A2 (TXA2) levels and subsequent platelet aggregation and adhesion.
Drug Interactions with Oral Anticoagulants (Warfarin)
-
Potentiating Drugs: Medications that increase warfarin's effects.
- Microsomal Enzyme Inhibitors: Includes cimetidine and chloramphenicol, which decrease warfarin metabolism.
- Oral Antibiotics: Reduce Vitamin K synthesis by killing gut flora, impacting clotting factor production.
- Liquid Paraffin: Decreases Vitamin K absorption in the body.
- NSAIDs: Displace warfarin from plasma protein binding, leading to increased anticoagulant effects.
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Inhibiting Drugs: Medications that decrease warfarin's effects.
- Microsomal Enzyme Inducers: Such as phenobarbital and rifampicin, which increase warfarin metabolism.
- Oral Contraceptives and Vitamin K: Increase synthesis of clotting factors, counteracting warfarin.
Fibrinolytic (Thrombolytic) Drugs
- Mechanism of Action: Plasminogen is activated to plasmin, which lyses fibrin clots, predominantly in areas where thrombi are present to minimize systemic effects.
- Risks: Fibrinolytic agents can activate circulating plasminogen as well, resulting in bleeding risks from both protective and pathologic thrombi.
Key Fibrinolytic Agents
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Streptokinase:
- Protein isolated from streptococci, activates plasminogen non-enzymatically.
- Can be antigenic, posing a risk for allergic reactions.
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Urokinase:
- Protease derived from urine, now primarily available in recombinant form.
- Less antigenic compared to streptokinase.
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Recombinant Tissue Plasminogen Activators (t-PAs):
- Includes alteplase, reteplase, and tenecteplase, designed to act specifically on fibrin-bound plasminogen, reducing systemic bleeding risks.
- Reteplase and tenecteplase have longer half-lives, allowing for less frequent dosing.
Therapeutic Uses of Thrombolytic Drugs
- Administered intravenously for acute myocardial infarction (MI), ischemic stroke, pulmonary embolism, and arterial thrombosis.
- Optimal efficacy if given within 90 minutes of the onset of symptoms, particularly for acute MI.
- Precautions necessary to avoid bleeding risks, especially in critical areas like the CNS or retina.
Adverse Effects of Thrombolytic Drugs
- High risk of systemic bleeding, particularly with streptokinase.
- Possible allergic reactions and transient side effects (fever, hypotension) during streptokinase administration.
Antiplatelet Drugs
- Aspirin:
- Inhibits platelet aggregation through irreversible COX enzyme inhibition, reducing thromboxane A2 (TXA2) levels and subsequent platelet aggregation and adhesion.
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