-
Thrombin
This lecture explains about the thrombin formation time and also about thrombin inhibitors. http://www.shomusbiology.com/
Get Shomu's Biology DVD set here-
http://www.shomusbiology.com/dvd-store/
Download the study materials here-
http://shomusbiology.com/bio-materials.html
Remember Shomu’s Biology is created to spread the knowledge of life science and biology by sharing all this free biology lectures video and animation presented by Suman Bhattacharjee in YouTube. All these tutorials are brought to you for free. Please subscribe to our channel so that we can grow together. You can check for any of the following services from Shomu’s Biology-
Buy Shomu’s Biology lecture DVD set- www.shomusbiology.com/dvd-store
Shomu’s Biology assignment services – www.shomusbiology.com/assignment -help
Joi...
published: 03 Apr 2015
-
Thrombin
Submitted by: Samuel DeSantis
published: 06 May 2016
-
Direct Thrombin Inhibitors and Factor Xa Inhibitors (DOACs) - Pharmacology - Hematology
Direct Thrombin Inhibitors and Factor Xa Inhibitors | Pharmacology | Hematology. Direct-Acting Oral Anticoagulants (DOACs).
Warfarin (anticoaulant) | Hematology & Pharmacology. Warfarin is an anticoagulant that inhibits the epoxide reductase enzyme which prevents the activation of vitamin K. Therefore, Warfarin inhibits the gamma carboxylation (gamma-glutamyl carboxylase) of the coagulation factors II, VII, IX, IX (2,7,9,10) as well as Protein C, Protein S, and Protein Z.
Heparin is an anticoagulant that stimulates antithrombin III (ATIII) which then inhibits coagulation factors VII, IX, X, XI, XII, as well as thrombin. This leads to prevention of thrombus formation (anticoagulation)...Heparin is used for ICU anticoagulation...Adverse effects of heparin includes bleeding, Heparin-induc...
published: 14 Aug 2020
-
Blood Coagulation Cascade: Intrinsic, Extrinsic & Common Pathway
● Hemostasis Physiology:
• Platelet Plug Formation: https://youtu.be/zfut06No5xE
• Blood Coagulation Cascade: (Current video)
• Clot Retraction & Fibrinolysis: https://youtu.be/zOvq1x9rbt4
• Anticoagulant Factors: https://youtu.be/ja_XiXsYfbw
• Vitamin K: Biochemistry/Pharmacology: https://youtu.be/r90ptZSF6q0
● Drugs affecting Hemostasis:
• Heparin, LMWH & Fondaparinux: https://youtu.be/TacjRFCNDeI
• Warfarin (Vitamin K Antagonists): https://youtu.be/CG8FrfSxomo
• Fibrinolytics & Antifibrinolytics: https://youtu.be/IIQyw-Rkdf4
• Antiplatelet Drugs: https://youtu.be/TJp7DTMWCx0
Coagulation usually occurs parallel to the platelet plug formation. It lay lays down fibrin mesh for clot formation. It starts by two pathway. Intrinsic and extrinsic. Intrinsic pathway starts when blood comes in ...
published: 21 Nov 2019
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What is THROMBIN TIME? What does THROMBIN TIME mean? THROMBIN TIME meaning & explanation
✪✪✪✪✪ http://www.theaudiopedia.com ✪✪✪✪✪
What is THROMBIN TIME? What does THROMBIN TIME mean? THROMBIN TIME meaning - THROMBIN TIME definition - THROMBIN TIME explanation.
SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6UuCPh7GrXznZi0Hz2YQnQ
Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/by-sa/3.0/ license.
The thrombin time (TT), also known as the thrombin clotting time (TCT) is a blood test that measures the time it takes for a clot to form in the plasma of a blood sample containing anticoagulant, after an excess of thrombin has been added. It is used to diagnose blood coagulation disorders and to assess the effectiveness of fibrinolytic therapy. This test is repeated with pooled plasma from normal patients. The di...
published: 15 Jul 2018
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Blood Clot Formation - Coagulation Factors & Platelets
About blood clot formation. Clot formation is the process by which blood forms clots, it's an important part of haemostasis.
Coagulation (thrombogenesis) is the process by which blood forms clots.
It is an important part of hemostasis, the cessation of blood loss from
a damaged vessel, wherein a damaged blood vessel wall is covered by a
platelet and fibrin-containing clot to stop bleeding and begin repair
of the damaged vessel. Disorders of coagulation can lead to an increased
risk of bleeding (hemorrhage) or obstructive clotting (thrombosis).
Approval Number: G.COM.GM.XA.10.2017.1884
published: 19 Dec 2013
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Pharmacology of anticoagulants [Heparin, Warfarin, Direct thrombin inhibitors, Coagulation cascade]
This video talks about the pharmacology of common anticoagulants, including Warfarin, Heparin, Hirudins, Dabigatran and Rivaroxaban. We discuss a little about the need for anticoagulation therapy, as well as the effects of each drug in the Coagulation Cascade. If you enjoy, please leave a like and subscribe! Comment below if you have any questions :)
published: 26 Sep 2020
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How do Direct Thrombin Inhibitors Work? (Dabigatran)
How do Direct Thrombin inhibitors (Dabigatran) Work? These direct thrombin inhibitors are anticoagulants that block clotting factor 2 which prevent the production of fibirin. This causes a decrease in blood clots and ultimately "thins" the blood.
There are 5 main drugs in this class: Dabigatran (Pradaxa), Argatroban, Lepirudin, Desirudin & Bivalirudin. They are all anticoagulants These medications are used to treat and prevent blood clots from forming which may lead to heart attack and stroke patients. Anticoagulant therapy seeks to prevent the development of deep vein thrombosis and pulmonary embolisms.
Time Stamps:
- Intro 00:00
- Breakdown 00:19
- Direct Thrombin Inhibitor Overview 00:28
- Mechanism of Action 02:20
- When to use 04:20
- Dosing & Adjustments 06:49
- Clinical pearls...
published: 07 Jul 2020
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Coagulation Cascade SIMPLEST EXPLANATION !! The Extrinsic and Intrinsic Pathway of HEMOSTASIS
GET LECTURE HANDOUTS and other DOWNLOADABLE CONTENT FROM THIS VIDEO
SUPPORT US ON PATREON OR JOIN HERE ON YOUTUBE.
https://www.patreon.com/medsimplified
Coagulation (also known as clotting) is the process by which blood changes from a liquid to a gel, forming a clot. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion, and aggregation of platelets along with deposition and maturation of fibrin. Disorders of coagulation are disease states which can result in bleeding (hemorrhage or bruising) or obstructive clotting (thrombosis).[1]
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The coagulation factors are generally serine proteases (enzymes), which act by cleaving downstream proteins. There are som...
published: 22 Oct 2015
6:45
Thrombin
This lecture explains about the thrombin formation time and also about thrombin inhibitors. http://www.shomusbiology.com/
Get Shomu's Biology DVD set here-
http...
This lecture explains about the thrombin formation time and also about thrombin inhibitors. http://www.shomusbiology.com/
Get Shomu's Biology DVD set here-
http://www.shomusbiology.com/dvd-store/
Download the study materials here-
http://shomusbiology.com/bio-materials.html
Remember Shomu’s Biology is created to spread the knowledge of life science and biology by sharing all this free biology lectures video and animation presented by Suman Bhattacharjee in YouTube. All these tutorials are brought to you for free. Please subscribe to our channel so that we can grow together. You can check for any of the following services from Shomu’s Biology-
Buy Shomu’s Biology lecture DVD set- www.shomusbiology.com/dvd-store
Shomu’s Biology assignment services – www.shomusbiology.com/assignment -help
Join Online coaching for CSIR NET exam – www.shomusbiology.com/net-coaching
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Thank you for watching
https://wn.com/Thrombin
This lecture explains about the thrombin formation time and also about thrombin inhibitors. http://www.shomusbiology.com/
Get Shomu's Biology DVD set here-
http://www.shomusbiology.com/dvd-store/
Download the study materials here-
http://shomusbiology.com/bio-materials.html
Remember Shomu’s Biology is created to spread the knowledge of life science and biology by sharing all this free biology lectures video and animation presented by Suman Bhattacharjee in YouTube. All these tutorials are brought to you for free. Please subscribe to our channel so that we can grow together. You can check for any of the following services from Shomu’s Biology-
Buy Shomu’s Biology lecture DVD set- www.shomusbiology.com/dvd-store
Shomu’s Biology assignment services – www.shomusbiology.com/assignment -help
Join Online coaching for CSIR NET exam – www.shomusbiology.com/net-coaching
We are social. Find us on different sites here-
Our Website – www.shomusbiology.com
Facebook page- https://www.facebook.com/ShomusBiology/
Twitter - https://twitter.com/shomusbiology
SlideShare- www.slideshare.net/shomusbiology
Google plus- https://plus.google.com/113648584982732129198
LinkedIn - https://www.linkedin.com/in/suman-bhattacharjee-2a051661
Youtube- https://www.youtube.com/user/TheFunsuman
Thank you for watching
- published: 03 Apr 2015
- views: 29610
5:48
Thrombin
Submitted by: Samuel DeSantis
Submitted by: Samuel DeSantis
https://wn.com/Thrombin
Submitted by: Samuel DeSantis
- published: 06 May 2016
- views: 10503
7:21
Direct Thrombin Inhibitors and Factor Xa Inhibitors (DOACs) - Pharmacology - Hematology
Direct Thrombin Inhibitors and Factor Xa Inhibitors | Pharmacology | Hematology. Direct-Acting Oral Anticoagulants (DOACs).
Warfarin (anticoaulant) | Hematolog...
Direct Thrombin Inhibitors and Factor Xa Inhibitors | Pharmacology | Hematology. Direct-Acting Oral Anticoagulants (DOACs).
Warfarin (anticoaulant) | Hematology & Pharmacology. Warfarin is an anticoagulant that inhibits the epoxide reductase enzyme which prevents the activation of vitamin K. Therefore, Warfarin inhibits the gamma carboxylation (gamma-glutamyl carboxylase) of the coagulation factors II, VII, IX, IX (2,7,9,10) as well as Protein C, Protein S, and Protein Z.
Heparin is an anticoagulant that stimulates antithrombin III (ATIII) which then inhibits coagulation factors VII, IX, X, XI, XII, as well as thrombin. This leads to prevention of thrombus formation (anticoagulation)...Heparin is used for ICU anticoagulation...Adverse effects of heparin includes bleeding, Heparin-induced thrombocytopenia (HIT), and osteoporosis.
Anticoaulants are chemicals that inhibit blood coagulation (secondary hemostasis).
Complete the Survey: https://airtable.com/shrYWjvabooT7DrcG
📊 Support the channel by signing up for Airtable: https://airtable.com/invite/r/2zH40fus/
Vitamin K Deficiency | Hemorrhagic Disease of the Newborn or Vitamin K dependent bleeding (VKDB) is a bleeding disorder that occurs due to deficiency of vitamin K.
► 💊 My Antibioitcs course is on sale...Use the discount code: ANTIBIOTICS25 at checkout to get a 25% discount: https://www.medicosisperfectionalis.com/products/courses/antibiotics/
Coagulation Tests (PT, aPTT, TT, Fibrinogen, Mixing Studies,..etc).
The coagulation factors are divided into 3 coagulation groups | Fibrinogen group, Prothrombin group, and Contact Group..
😍🖼Animated Mnemonics (Picmonic): https://www.picmonic.com/viphookup/medicosis/
- With Picmonic, get your life back by studying less and remembering more. Medical and Nursing students say that Picmonic is the most comprehensive and effective way to bridge learning and test prep...
Picmonic has hundreds of animated medical mnemonics...These are very interactive Picmonics that help you memorize and retain tons of medical topics.
They also have a mobile app so that you can learn and have fun on the run.
Disclaimer: I use affiliate links...
Platelet count is one of the lab tests used by a doctor or a hematologist to assess whether your platelet number is normal, low (thrombocytopenia) or high (thrombocytosis).
Bleeding 🩸 time (BT) is another test for platelet function.
💊 Cardiac Pharmacology Lectures:
https://www.medicosisperfectionalis.com/products/cardiac-pharmacology-course ...
— 💊Antibiotics Lectures: https://www.medicosisperfectionalis.com/
► Get my Leukemia Notebook:
https://www.medicosisperfectionalis.com/products/leukemia-notebook/
💊 Cardiac Pharmacology Lectures:
https://www.medicosisperfectionalis.com/products/cardiac-pharmacology-course ...
— 💊Antibiotics Lectures: https://www.medicosisperfectionalis.com/
► Watch my hematology videos: https://www.youtube.com/playlist?list=PLYcLrRDaR8_eoNz6dxXolh1XMEietcniU
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► Watch my Cardiac Pharmacology Playlist on YouTube: https://www.youtube.com/playlist?list=PLYcLrRDaR8_e3pM6ifeZDfNPlE3K4KF3J
► Watch my Rheumatology Playlist: https://www.youtube.com/playlist?list=PLYcLrRDaR8_ckdsow-7buX1rIzIEKfxZQ
► If you have any questions, please email me at:
[email protected]
► Watch the entire playlist of Rheumatology https://www.youtube.com/playlist?list=PLYcLrRDaR8_ckdsow-7buX1rIzIEKfxZQ
--If you have joined my channel on youtube (the join button that's next to the subscribe button), then go to the "community tab" and you will find some member-only posts.
Thank you so much for supporting my channel! Love ❤️
Happy studying!!
😍🖼Animated Mnemonics (Picmonic): https://www.picmonic.com/viphookup/medicosis/ My Favorite Productivity App: https://airtable.com/invite/r/2zH40fus/
📊 My favorite Productivity Apps: https://airtable.com/invite/r/2zH40fus/ 📱Save on your mobile phone bill: http://fbuy.me/q6bMj 🏦 Qbank (TrueLearn): https://truelearn.referralrock.com/l/MEDICOSIS/
https://wn.com/Direct_Thrombin_Inhibitors_And_Factor_Xa_Inhibitors_(Doacs)_Pharmacology_Hematology
Direct Thrombin Inhibitors and Factor Xa Inhibitors | Pharmacology | Hematology. Direct-Acting Oral Anticoagulants (DOACs).
Warfarin (anticoaulant) | Hematology & Pharmacology. Warfarin is an anticoagulant that inhibits the epoxide reductase enzyme which prevents the activation of vitamin K. Therefore, Warfarin inhibits the gamma carboxylation (gamma-glutamyl carboxylase) of the coagulation factors II, VII, IX, IX (2,7,9,10) as well as Protein C, Protein S, and Protein Z.
Heparin is an anticoagulant that stimulates antithrombin III (ATIII) which then inhibits coagulation factors VII, IX, X, XI, XII, as well as thrombin. This leads to prevention of thrombus formation (anticoagulation)...Heparin is used for ICU anticoagulation...Adverse effects of heparin includes bleeding, Heparin-induced thrombocytopenia (HIT), and osteoporosis.
Anticoaulants are chemicals that inhibit blood coagulation (secondary hemostasis).
Complete the Survey: https://airtable.com/shrYWjvabooT7DrcG
📊 Support the channel by signing up for Airtable: https://airtable.com/invite/r/2zH40fus/
Vitamin K Deficiency | Hemorrhagic Disease of the Newborn or Vitamin K dependent bleeding (VKDB) is a bleeding disorder that occurs due to deficiency of vitamin K.
► 💊 My Antibioitcs course is on sale...Use the discount code: ANTIBIOTICS25 at checkout to get a 25% discount: https://www.medicosisperfectionalis.com/products/courses/antibiotics/
Coagulation Tests (PT, aPTT, TT, Fibrinogen, Mixing Studies,..etc).
The coagulation factors are divided into 3 coagulation groups | Fibrinogen group, Prothrombin group, and Contact Group..
😍🖼Animated Mnemonics (Picmonic): https://www.picmonic.com/viphookup/medicosis/
- With Picmonic, get your life back by studying less and remembering more. Medical and Nursing students say that Picmonic is the most comprehensive and effective way to bridge learning and test prep...
Picmonic has hundreds of animated medical mnemonics...These are very interactive Picmonics that help you memorize and retain tons of medical topics.
They also have a mobile app so that you can learn and have fun on the run.
Disclaimer: I use affiliate links...
Platelet count is one of the lab tests used by a doctor or a hematologist to assess whether your platelet number is normal, low (thrombocytopenia) or high (thrombocytosis).
Bleeding 🩸 time (BT) is another test for platelet function.
💊 Cardiac Pharmacology Lectures:
https://www.medicosisperfectionalis.com/products/cardiac-pharmacology-course ...
— 💊Antibiotics Lectures: https://www.medicosisperfectionalis.com/
► Get my Leukemia Notebook:
https://www.medicosisperfectionalis.com/products/leukemia-notebook/
💊 Cardiac Pharmacology Lectures:
https://www.medicosisperfectionalis.com/products/cardiac-pharmacology-course ...
— 💊Antibiotics Lectures: https://www.medicosisperfectionalis.com/
► Watch my hematology videos: https://www.youtube.com/playlist?list=PLYcLrRDaR8_eoNz6dxXolh1XMEietcniU
► Support me on Patreon: https://www.patreon.com/medicosis/
► Support me on PayPal: https://www.paypal.me/perfectionalis/
► Join my Channel on YouTube: https://www.youtube.com/channel/UCl-J-ovSJhA3or73Q2uVpow/join
► All of my premium courses are ON SALE: https://www.medicosisperfectionalis.com/
► Watch my Cardiac Pharmacology Playlist on YouTube: https://www.youtube.com/playlist?list=PLYcLrRDaR8_e3pM6ifeZDfNPlE3K4KF3J
► Watch my Rheumatology Playlist: https://www.youtube.com/playlist?list=PLYcLrRDaR8_ckdsow-7buX1rIzIEKfxZQ
► If you have any questions, please email me at:
[email protected]
► Watch the entire playlist of Rheumatology https://www.youtube.com/playlist?list=PLYcLrRDaR8_ckdsow-7buX1rIzIEKfxZQ
--If you have joined my channel on youtube (the join button that's next to the subscribe button), then go to the "community tab" and you will find some member-only posts.
Thank you so much for supporting my channel! Love ❤️
Happy studying!!
😍🖼Animated Mnemonics (Picmonic): https://www.picmonic.com/viphookup/medicosis/ My Favorite Productivity App: https://airtable.com/invite/r/2zH40fus/
📊 My favorite Productivity Apps: https://airtable.com/invite/r/2zH40fus/ 📱Save on your mobile phone bill: http://fbuy.me/q6bMj 🏦 Qbank (TrueLearn): https://truelearn.referralrock.com/l/MEDICOSIS/
- published: 14 Aug 2020
- views: 29900
5:44
Blood Coagulation Cascade: Intrinsic, Extrinsic & Common Pathway
● Hemostasis Physiology:
• Platelet Plug Formation: https://youtu.be/zfut06No5xE
• Blood Coagulation Cascade: (Current video)
• Clot Retraction & Fibrinolysis: ...
● Hemostasis Physiology:
• Platelet Plug Formation: https://youtu.be/zfut06No5xE
• Blood Coagulation Cascade: (Current video)
• Clot Retraction & Fibrinolysis: https://youtu.be/zOvq1x9rbt4
• Anticoagulant Factors: https://youtu.be/ja_XiXsYfbw
• Vitamin K: Biochemistry/Pharmacology: https://youtu.be/r90ptZSF6q0
● Drugs affecting Hemostasis:
• Heparin, LMWH & Fondaparinux: https://youtu.be/TacjRFCNDeI
• Warfarin (Vitamin K Antagonists): https://youtu.be/CG8FrfSxomo
• Fibrinolytics & Antifibrinolytics: https://youtu.be/IIQyw-Rkdf4
• Antiplatelet Drugs: https://youtu.be/TJp7DTMWCx0
Coagulation usually occurs parallel to the platelet plug formation. It lay lays down fibrin mesh for clot formation. It starts by two pathway. Intrinsic and extrinsic. Intrinsic pathway starts when blood comes in contact with negatively charged surface. Extrinsic pathway starts when tissue factor is exposed to the blood. Both the pathways merge at common pathway i.e. synthesis of factor Xa. It activates prothrombin into thrombin which converts fibrinogen into fibrin monomers. Fibrin monomers polymerize spontaneously and form fibrin strands. Factor XIIIa cause crosslinking between fibrin polymers and forms mesh. Thus we have a stable clot. During the process other blood cells like red blood cell and white blood cells are also trapped in the clot. Arterial clots are rich in platelets and venous clots are rich in fibrin.
#NonstopHemostasis
DISCLAIMER: This video is for education purpose only. Although every effort is made to ensure accuracy of material, viewer should refer to the appropriate regulatory body/authorised websites, guidelines and other suitable sources of information as deemed relevant and applicable. In view of possibility of human error or changes in medical science, any person or organization involved in preparation of this work accepts no responsibility for any errors or omissions or results obtained from use of information in this video.
https://wn.com/Blood_Coagulation_Cascade_Intrinsic,_Extrinsic_Common_Pathway
● Hemostasis Physiology:
• Platelet Plug Formation: https://youtu.be/zfut06No5xE
• Blood Coagulation Cascade: (Current video)
• Clot Retraction & Fibrinolysis: https://youtu.be/zOvq1x9rbt4
• Anticoagulant Factors: https://youtu.be/ja_XiXsYfbw
• Vitamin K: Biochemistry/Pharmacology: https://youtu.be/r90ptZSF6q0
● Drugs affecting Hemostasis:
• Heparin, LMWH & Fondaparinux: https://youtu.be/TacjRFCNDeI
• Warfarin (Vitamin K Antagonists): https://youtu.be/CG8FrfSxomo
• Fibrinolytics & Antifibrinolytics: https://youtu.be/IIQyw-Rkdf4
• Antiplatelet Drugs: https://youtu.be/TJp7DTMWCx0
Coagulation usually occurs parallel to the platelet plug formation. It lay lays down fibrin mesh for clot formation. It starts by two pathway. Intrinsic and extrinsic. Intrinsic pathway starts when blood comes in contact with negatively charged surface. Extrinsic pathway starts when tissue factor is exposed to the blood. Both the pathways merge at common pathway i.e. synthesis of factor Xa. It activates prothrombin into thrombin which converts fibrinogen into fibrin monomers. Fibrin monomers polymerize spontaneously and form fibrin strands. Factor XIIIa cause crosslinking between fibrin polymers and forms mesh. Thus we have a stable clot. During the process other blood cells like red blood cell and white blood cells are also trapped in the clot. Arterial clots are rich in platelets and venous clots are rich in fibrin.
#NonstopHemostasis
DISCLAIMER: This video is for education purpose only. Although every effort is made to ensure accuracy of material, viewer should refer to the appropriate regulatory body/authorised websites, guidelines and other suitable sources of information as deemed relevant and applicable. In view of possibility of human error or changes in medical science, any person or organization involved in preparation of this work accepts no responsibility for any errors or omissions or results obtained from use of information in this video.
- published: 21 Nov 2019
- views: 3216
3:18
What is THROMBIN TIME? What does THROMBIN TIME mean? THROMBIN TIME meaning & explanation
✪✪✪✪✪ http://www.theaudiopedia.com ✪✪✪✪✪
What is THROMBIN TIME? What does THROMBIN TIME mean? THROMBIN TIME meaning - THROMBIN TIME definition - THROMBIN TIME ...
✪✪✪✪✪ http://www.theaudiopedia.com ✪✪✪✪✪
What is THROMBIN TIME? What does THROMBIN TIME mean? THROMBIN TIME meaning - THROMBIN TIME definition - THROMBIN TIME explanation.
SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6UuCPh7GrXznZi0Hz2YQnQ
Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/by-sa/3.0/ license.
The thrombin time (TT), also known as the thrombin clotting time (TCT) is a blood test that measures the time it takes for a clot to form in the plasma of a blood sample containing anticoagulant, after an excess of thrombin has been added. It is used to diagnose blood coagulation disorders and to assess the effectiveness of fibrinolytic therapy. This test is repeated with pooled plasma from normal patients. The difference in time between the test and the 'normal' indicates an abnormality in the conversion of fibrinogen (a soluble protein) to fibrin, an insoluble protein.
The thrombin time compares the rate of clot formation to that of a sample of normal pooled plasma. Thrombin is added to the samples of plasma. If the time it takes for the plasma to clot is prolonged, a quantitative (fibrinogen deficiency) or qualitative (dysfunctional fibrinogen) defect is present. In blood samples containing heparin, a substance derived from snake venom called batroxobin (formerly reptilase) is used instead of thrombin. Batroxobin has a similar action to thrombin but unlike thrombin it is not inhibited by heparin.
Normal values for thrombin time are 12 to 14 seconds. If batroxobin is used, the time should be between 15 and 20 seconds. Thrombin time can be prolonged by heparin, fibrin degradation products, and fibrinogen deficiency or abnormality.
After separating the plasma from the whole blood by centrifugation, bovine thrombin is added to the sample of plasma. Clot formation is detected optically or mechanically by a coagulation instrument. The time between the addition of the thrombin and the clot formation is recorded as the thrombin clotting time.
Whole blood is taken with either citrate or oxalate additive (if using the vacutainer system, this is a light blue top tube). As with other coagulation assays, the tube must not be over- or under-filled in order to ensure the correct anticoagulant-to-blood ratio: one part anticoagulant per nine parts blood.
The reference ranges of the thrombin clotting time is generally 22 seconds, and from 14 to 16 seconds. Laboratories usually calculate their own ranges, based on the method used and the results obtained from healthy individuals from the local population. Separate ranges are used for infants.
Blood samples that are more than eight hours old can give inaccurate results when tested.
https://wn.com/What_Is_Thrombin_Time_What_Does_Thrombin_Time_Mean_Thrombin_Time_Meaning_Explanation
✪✪✪✪✪ http://www.theaudiopedia.com ✪✪✪✪✪
What is THROMBIN TIME? What does THROMBIN TIME mean? THROMBIN TIME meaning - THROMBIN TIME definition - THROMBIN TIME explanation.
SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6UuCPh7GrXznZi0Hz2YQnQ
Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/by-sa/3.0/ license.
The thrombin time (TT), also known as the thrombin clotting time (TCT) is a blood test that measures the time it takes for a clot to form in the plasma of a blood sample containing anticoagulant, after an excess of thrombin has been added. It is used to diagnose blood coagulation disorders and to assess the effectiveness of fibrinolytic therapy. This test is repeated with pooled plasma from normal patients. The difference in time between the test and the 'normal' indicates an abnormality in the conversion of fibrinogen (a soluble protein) to fibrin, an insoluble protein.
The thrombin time compares the rate of clot formation to that of a sample of normal pooled plasma. Thrombin is added to the samples of plasma. If the time it takes for the plasma to clot is prolonged, a quantitative (fibrinogen deficiency) or qualitative (dysfunctional fibrinogen) defect is present. In blood samples containing heparin, a substance derived from snake venom called batroxobin (formerly reptilase) is used instead of thrombin. Batroxobin has a similar action to thrombin but unlike thrombin it is not inhibited by heparin.
Normal values for thrombin time are 12 to 14 seconds. If batroxobin is used, the time should be between 15 and 20 seconds. Thrombin time can be prolonged by heparin, fibrin degradation products, and fibrinogen deficiency or abnormality.
After separating the plasma from the whole blood by centrifugation, bovine thrombin is added to the sample of plasma. Clot formation is detected optically or mechanically by a coagulation instrument. The time between the addition of the thrombin and the clot formation is recorded as the thrombin clotting time.
Whole blood is taken with either citrate or oxalate additive (if using the vacutainer system, this is a light blue top tube). As with other coagulation assays, the tube must not be over- or under-filled in order to ensure the correct anticoagulant-to-blood ratio: one part anticoagulant per nine parts blood.
The reference ranges of the thrombin clotting time is generally 22 seconds, and from 14 to 16 seconds. Laboratories usually calculate their own ranges, based on the method used and the results obtained from healthy individuals from the local population. Separate ranges are used for infants.
Blood samples that are more than eight hours old can give inaccurate results when tested.
- published: 15 Jul 2018
- views: 3255
1:54
Blood Clot Formation - Coagulation Factors & Platelets
About blood clot formation. Clot formation is the process by which blood forms clots, it's an important part of haemostasis.
Coagulation (thrombogenesis) is th...
About blood clot formation. Clot formation is the process by which blood forms clots, it's an important part of haemostasis.
Coagulation (thrombogenesis) is the process by which blood forms clots.
It is an important part of hemostasis, the cessation of blood loss from
a damaged vessel, wherein a damaged blood vessel wall is covered by a
platelet and fibrin-containing clot to stop bleeding and begin repair
of the damaged vessel. Disorders of coagulation can lead to an increased
risk of bleeding (hemorrhage) or obstructive clotting (thrombosis).
Approval Number: G.COM.GM.XA.10.2017.1884
https://wn.com/Blood_Clot_Formation_Coagulation_Factors_Platelets
About blood clot formation. Clot formation is the process by which blood forms clots, it's an important part of haemostasis.
Coagulation (thrombogenesis) is the process by which blood forms clots.
It is an important part of hemostasis, the cessation of blood loss from
a damaged vessel, wherein a damaged blood vessel wall is covered by a
platelet and fibrin-containing clot to stop bleeding and begin repair
of the damaged vessel. Disorders of coagulation can lead to an increased
risk of bleeding (hemorrhage) or obstructive clotting (thrombosis).
Approval Number: G.COM.GM.XA.10.2017.1884
- published: 19 Dec 2013
- views: 737935
7:04
Pharmacology of anticoagulants [Heparin, Warfarin, Direct thrombin inhibitors, Coagulation cascade]
This video talks about the pharmacology of common anticoagulants, including Warfarin, Heparin, Hirudins, Dabigatran and Rivaroxaban. We discuss a little about t...
This video talks about the pharmacology of common anticoagulants, including Warfarin, Heparin, Hirudins, Dabigatran and Rivaroxaban. We discuss a little about the need for anticoagulation therapy, as well as the effects of each drug in the Coagulation Cascade. If you enjoy, please leave a like and subscribe! Comment below if you have any questions :)
https://wn.com/Pharmacology_Of_Anticoagulants_Heparin,_Warfarin,_Direct_Thrombin_Inhibitors,_Coagulation_Cascade
This video talks about the pharmacology of common anticoagulants, including Warfarin, Heparin, Hirudins, Dabigatran and Rivaroxaban. We discuss a little about the need for anticoagulation therapy, as well as the effects of each drug in the Coagulation Cascade. If you enjoy, please leave a like and subscribe! Comment below if you have any questions :)
- published: 26 Sep 2020
- views: 2297
14:42
How do Direct Thrombin Inhibitors Work? (Dabigatran)
How do Direct Thrombin inhibitors (Dabigatran) Work? These direct thrombin inhibitors are anticoagulants that block clotting factor 2 which prevent the product...
How do Direct Thrombin inhibitors (Dabigatran) Work? These direct thrombin inhibitors are anticoagulants that block clotting factor 2 which prevent the production of fibirin. This causes a decrease in blood clots and ultimately "thins" the blood.
There are 5 main drugs in this class: Dabigatran (Pradaxa), Argatroban, Lepirudin, Desirudin & Bivalirudin. They are all anticoagulants These medications are used to treat and prevent blood clots from forming which may lead to heart attack and stroke patients. Anticoagulant therapy seeks to prevent the development of deep vein thrombosis and pulmonary embolisms.
Time Stamps:
- Intro 00:00
- Breakdown 00:19
- Direct Thrombin Inhibitor Overview 00:28
- Mechanism of Action 02:20
- When to use 04:20
- Dosing & Adjustments 06:49
- Clinical pearls & Side effects 08:49
- Quick Summary 11:29
- Short Quiz 13:30
=======================================================
👉 Support us & Grab some awesome Merch! 👈
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Answers:
1.)D
2.)A
3.)B
4.)B
=======================================================
This pharmacology lecture covers topics such as Anticoagulant drugs. We talk about Dabigatran, Argatroban, Lepirudin Desirudin & Bivalirudin. We discuss how these drugs help block the clotting factor 2 which leads to less fibrin being formed. This causes the lowering of blood clots. Also, we talk about the pathophysiology of the clotting cascade, heart attack and stroke and how anti-coagulation therapy is beneficial. We discuss the mechanism of action of these DOAC's and their side effects. Brand name of these medications include: Pradaxa.
=======================================================
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=======================================================
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=======================================================
Images used & Licensed through:
http://clipartmag.com/
https://wn.com/How_Do_Direct_Thrombin_Inhibitors_Work_(Dabigatran)
How do Direct Thrombin inhibitors (Dabigatran) Work? These direct thrombin inhibitors are anticoagulants that block clotting factor 2 which prevent the production of fibirin. This causes a decrease in blood clots and ultimately "thins" the blood.
There are 5 main drugs in this class: Dabigatran (Pradaxa), Argatroban, Lepirudin, Desirudin & Bivalirudin. They are all anticoagulants These medications are used to treat and prevent blood clots from forming which may lead to heart attack and stroke patients. Anticoagulant therapy seeks to prevent the development of deep vein thrombosis and pulmonary embolisms.
Time Stamps:
- Intro 00:00
- Breakdown 00:19
- Direct Thrombin Inhibitor Overview 00:28
- Mechanism of Action 02:20
- When to use 04:20
- Dosing & Adjustments 06:49
- Clinical pearls & Side effects 08:49
- Quick Summary 11:29
- Short Quiz 13:30
=======================================================
👉 Support us & Grab some awesome Merch! 👈
https://teespring.com/stores/drug-chug
Answers:
1.)D
2.)A
3.)B
4.)B
=======================================================
This pharmacology lecture covers topics such as Anticoagulant drugs. We talk about Dabigatran, Argatroban, Lepirudin Desirudin & Bivalirudin. We discuss how these drugs help block the clotting factor 2 which leads to less fibrin being formed. This causes the lowering of blood clots. Also, we talk about the pathophysiology of the clotting cascade, heart attack and stroke and how anti-coagulation therapy is beneficial. We discuss the mechanism of action of these DOAC's and their side effects. Brand name of these medications include: Pradaxa.
=======================================================
Thanks for watching and don't forget to SUBSCRIBE, hit the LIKE button👍 and click the BELL button🔔 for future notifications!
=======================================================
Like what we do? Learn how to support us on Patreon! 💪
👉 https://www.patreon.com/DrugChug
Looking for more pharmacology knowledge? Follow us on Instagram Facebook & Twitter!💊
👉 https://www.instagram.com/DrugChug/
👉 https://www.facebook.com/DrugChug
👉 https://www.twitter.com/Drug_Chug
👉 https://www.DrugChug.com
=======================================================
Images used & Licensed through:
http://clipartmag.com/
- published: 07 Jul 2020
- views: 6133
5:23
Coagulation Cascade SIMPLEST EXPLANATION !! The Extrinsic and Intrinsic Pathway of HEMOSTASIS
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Coagu...
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Coagulation (also known as clotting) is the process by which blood changes from a liquid to a gel, forming a clot. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion, and aggregation of platelets along with deposition and maturation of fibrin. Disorders of coagulation are disease states which can result in bleeding (hemorrhage or bruising) or obstructive clotting (thrombosis).[1]
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The coagulation factors are generally serine proteases (enzymes), which act by cleaving downstream proteins. There are some exceptions. For example, FVIII and FV are glycoproteins, and Factor XIII is a transglutaminase.[7] The coagulation factors circulate as inactive zymogens. The coagulation cascade is therefore classically divided into three pathways. The tissue factor and contact activation pathways both activate the "final common pathway" of factor X, thrombin and fibrin
Tissue factor pathway (extrinsic)[edit]
The main role of the tissue factor pathway is to generate a "thrombin burst", a process by which thrombin, the most important constituent of the coagulation cascade in terms of its feedback activation roles, is released very rapidly. FVIIa circulates in a higher amount than any other activated coagulation factor. The process includes the following steps:[7]
Following damage to the blood vessel, FVII leaves the circulation and comes into contact with tissue factor (TF) expressed on tissue-factor-bearing cells (stromal fibroblasts and leukocytes), forming an activated complex (TF-FVIIa).
TF-FVIIa activates FIX and FX.
FVII is itself activated by thrombin, FXIa, FXII and FXa.
The activation of FX (to form FXa) by TF-FVIIa is almost immediately inhibited by tissue factor pathway inhibitor (TFPI).
FXa and its co-factor FVa form the prothrombinase complex, which activates prothrombin to thrombin.
Thrombin then activates other components of the coagulation cascade, including FV and FVIII (which activates FXI, which, in turn, activates FIX), and activates and releases FVIII from being bound to vWF.
FVIIIa is the co-factor of FIXa, and together they form the "tenase" complex, which activates FX; and so the cycle continues. ("Tenase" is a contraction of "ten" and the suffix "-ase" used for enzymes.)
Contact activation pathway (intrinsic)[edit]
The contact activation pathway begins with formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and FXII (Hageman factor). Prekallikrein is converted to kallikrein and FXII becomes FXIIa. FXIIa converts FXI into FXIa. Factor XIa activates FIX, which with its co-factor FVIIIa form the tenase complex, which activates FX to FXa. The minor role that the contact activation pathway has in initiating clot formation can be illustrated by the fact that patients with severe deficiencies of FXII, HMWK, and prekallikrein do not have a bleeding disorder. Instead, contact activation system seems to be more involved in inflammation.[7]
Final common pathway[edit]
The division of coagulation in two pathways is mainly artificial, it originates from laboratory tests in which clotting times were measured after the clotting was initiated by glass (intrinsic pathway) or by thromboplastin (a mix of tissue factor and phospholipids). In fact thrombin is present from the very beginning, already when platelets are making the plug. Thrombin has a large array of functions, not only the conversion of fibrinogen to fibrin, the building block of a hemostatic plug. In addition, it is the most important platelet activator and on top of that it activates Factors VIII and V and their inhibitor protein C (in the presence of thrombomodulin), and it activates Factor XIII, which forms covalent bonds that crosslink the fibrin polymers that form from activated monomers.[7]
Following activation by the contact factor or tissue factor pathways, the coagulation cascade is maintained in a prothrombotic state by the continued activation of FVIII and FIX to form the tenase complex, until it is down-regulated by the anticoagulant pathways
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https://wn.com/Coagulation_Cascade_Simplest_Explanation_The_Extrinsic_And_Intrinsic_Pathway_Of_Hemostasis
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Coagulation (also known as clotting) is the process by which blood changes from a liquid to a gel, forming a clot. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion, and aggregation of platelets along with deposition and maturation of fibrin. Disorders of coagulation are disease states which can result in bleeding (hemorrhage or bruising) or obstructive clotting (thrombosis).[1]
LIKE ON FACEBOOK :
The coagulation factors are generally serine proteases (enzymes), which act by cleaving downstream proteins. There are some exceptions. For example, FVIII and FV are glycoproteins, and Factor XIII is a transglutaminase.[7] The coagulation factors circulate as inactive zymogens. The coagulation cascade is therefore classically divided into three pathways. The tissue factor and contact activation pathways both activate the "final common pathway" of factor X, thrombin and fibrin
Tissue factor pathway (extrinsic)[edit]
The main role of the tissue factor pathway is to generate a "thrombin burst", a process by which thrombin, the most important constituent of the coagulation cascade in terms of its feedback activation roles, is released very rapidly. FVIIa circulates in a higher amount than any other activated coagulation factor. The process includes the following steps:[7]
Following damage to the blood vessel, FVII leaves the circulation and comes into contact with tissue factor (TF) expressed on tissue-factor-bearing cells (stromal fibroblasts and leukocytes), forming an activated complex (TF-FVIIa).
TF-FVIIa activates FIX and FX.
FVII is itself activated by thrombin, FXIa, FXII and FXa.
The activation of FX (to form FXa) by TF-FVIIa is almost immediately inhibited by tissue factor pathway inhibitor (TFPI).
FXa and its co-factor FVa form the prothrombinase complex, which activates prothrombin to thrombin.
Thrombin then activates other components of the coagulation cascade, including FV and FVIII (which activates FXI, which, in turn, activates FIX), and activates and releases FVIII from being bound to vWF.
FVIIIa is the co-factor of FIXa, and together they form the "tenase" complex, which activates FX; and so the cycle continues. ("Tenase" is a contraction of "ten" and the suffix "-ase" used for enzymes.)
Contact activation pathway (intrinsic)[edit]
The contact activation pathway begins with formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and FXII (Hageman factor). Prekallikrein is converted to kallikrein and FXII becomes FXIIa. FXIIa converts FXI into FXIa. Factor XIa activates FIX, which with its co-factor FVIIIa form the tenase complex, which activates FX to FXa. The minor role that the contact activation pathway has in initiating clot formation can be illustrated by the fact that patients with severe deficiencies of FXII, HMWK, and prekallikrein do not have a bleeding disorder. Instead, contact activation system seems to be more involved in inflammation.[7]
Final common pathway[edit]
The division of coagulation in two pathways is mainly artificial, it originates from laboratory tests in which clotting times were measured after the clotting was initiated by glass (intrinsic pathway) or by thromboplastin (a mix of tissue factor and phospholipids). In fact thrombin is present from the very beginning, already when platelets are making the plug. Thrombin has a large array of functions, not only the conversion of fibrinogen to fibrin, the building block of a hemostatic plug. In addition, it is the most important platelet activator and on top of that it activates Factors VIII and V and their inhibitor protein C (in the presence of thrombomodulin), and it activates Factor XIII, which forms covalent bonds that crosslink the fibrin polymers that form from activated monomers.[7]
Following activation by the contact factor or tissue factor pathways, the coagulation cascade is maintained in a prothrombotic state by the continued activation of FVIII and FIX to form the tenase complex, until it is down-regulated by the anticoagulant pathways
SUBSCRIBE
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WATCH AGAIN
https://www.youtube.com/watch?v=LVYmV5mK6QI
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CHECK OUT NEWEST VIDEO: "Nucleic acids - DNA and RNA structure "
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- published: 22 Oct 2015
- views: 902633