👉📝WANT STUDY NOTES FOR THIS PRESENTATION? 👉Join Patreon at
So let’s get right into it anticoagulants and antiplatelet agents which can lead to heart attack or stroke action let’s quickly review the clotting process so in the absence of injury the chemical mediators such as nitric oxide and prostacyclin now nitric oxide job is platelets this binding triggers certain reactions which ultimately prevent blood vessel let’s say due to
Skin cut well suddenly we have less nitric oxide activated but first things first with the adhere to exposed collagen which in turn causes them to change shape next these chemical mediators such as adp thrombin thromboxane a2 serotonin and platelet site of injury now the final step involves activation of the glycoprotein binds to these receptors on two separate platelets
Thus cross-linking platelets plug formation collectively we call them platelet aggregation inhibitors this class is aspirin in order to understand how aspirin works let’s take a arachidonic acid is released from the membrane phospholipids then it gets cox-1 finally prostaglandin h2 is further metabolized to thromboxane a2 well promote their aggregation so what aspirin does
Is it irreversibly next we have platelet aggregation inhibitors that work by blocking the action of adp receptor specifically p2y12 subtype drugs that belong to this mentioned before activated platelets release chemical mediators one of them is glycoprotein 2b/3a receptors which are required for fibrin mediated platelet inhibit platelet aggregation and thus clot formation
Eptifibatide and tirofiban these agents simply inhibit platelet platelets thus preventing fibrinogen from binding to platelets and making glycoprotein 2b/3a inhibitors are administered only intravenously now the discuss are phosphodiesterase inhibitors two agents inhibit enzyme called phosphodiesterase that is responsible and cilostazol increase intracellular levels of
Cyclic amp which in turn leads activation furthermore these agents inhibit phosphodiesterase in the for that reason cilostazol in particular is often used to treat symptoms of to legs when it comes to side effects bleeding is a major risk associated with due to their vasodilating properties can produce headaches now platelets acting like a plug is usually not enough to
Secure the site of injury involves cascade of enzyme reactions that transform various mesh now there are two pathways involved with a clotting cascade the intrinsic extrinsic pathway which is activated by trauma to the vascular wall as well as is activated when blood comes into contact with a collagen in the damaged sets a series of reactions that leads to activation of
Factor 11 activated factor 10 then converts prothrombin to thrombin and finally platelet plug now let’s take a look at the extrinsic pathway so extrinsic circulating blood it starts with an activation of factor 7 which then into a common pathway which again results in formation of fibrin clot description of coagulation cascade and many details were intentionally omitted
Work by disrupting this coagulation cascade let’s begin by discussing one of the most widely recognized and anticoagulants that is heparin and low- these agents bind to our natural anticoagulant circulating in blood called and thrombin so what heparin drugs do is they bind to antithrombin and by doing results in rapid inactivation of both factor 10a and thrombin however
Unlike thrombin and instead they selectively accelerate inactivation of factor 10a of factor 10a is fondaparinux however unlike low-molecular-weight heparins on thrombin when it comes to side effects bleeding is a major risk used to treat excessive bleeding caused by heparin drugs protamine sulfate stable inactive complex fondaparinux on the other hand doesn’t have any
Particularly associated with the use of heparin agents is heparin induced making antibodies to heparin when it’s bound to platelet-derived protein called platelet factor-4 complexes they begin to causing formation of unwanted clots and fall in platelet count now let’s move on agents that belong to this group are apixaban and rivaroxaban the the active side of factor 10a thus
Preventing it from converting anticoagulants that we discussed is that they are available in oral formulation not available now let’s move on to the next group of anticoagulants that is molecule agents in this group can be subdivided into two classes first we active site example of drugs that belong to the second class are bivalent direct thrombin inhibitors which bind to
Both bivalent binding contributes to their high affinity and high specificity for now one of the biggest advantages of direct thrombin inhibitors over platelet factor-4 which makes them very useful in treatment of heparin induced risk and there is no specific antidote available at this time now there is one of the oldest anticoagulants that’s still on the market and it has
Its own important to first understand the role of vitamin k in the coagulation cascade coagulation factors are biologically inactive until they are carboxylated by vitamin k available in this reaction reduced vitamin k is oxidized to the last step of this reaction oxidized vitamin k is recycled back to the this is where warfarin comes into play as it inhibits this enzyme
And thus factors as well as some other regulatory factors now one of the biggest associated with many drug-drug and drug-food interactions for these reasons international normalized ratio measurement also known as inr and adjust clotting fortunately in the event of bleeding anticoagulant effects of warfarin to 24 hours therefore in the event of emergency infusion of fresh
Frozen in this lecture are thrombolytics while antiplatelets and anticoagulants prevent existing clot causing it to dissolve and the way they do this is by directly or turns into plasmin now plasmin is an enzyme that breaks cross-links between alteplase reteplase and tenecteplase which are produced by recombinant dna another example is an agent called urokinase which is a
Naturally occurring agent called streptokinase which is derived from streptococcal bacteria now fibrin-bound plasminogen versus free circulating plasminogen so while acts to dissolve the fibrin in the thrombus streptokinase and bleeding into any organ system these bleeding complications from thrombolytic tranexamic acid these two agents can stop fibrinolysis by inhibiting
Plasmin and with that i wanted to thank you for watching i hope you enjoyed this
Transcribed from video
Pharmacology – ANTICOAGULANTS & ANTIPLATELET DRUGS (MADE EASY) By Speed Pharmacology
