Hematology | Hemostasis: Coagulation Cascade

all right nine nerds in this video we're going to talk about hemostasis first off what is hemostasis hemostasis well first off we can kind of break apart this term here hemo is blood stasis means stop so it's a localized blood stoppage right so that's what we're trying to do usually this occurs whenever there's some type of damage to our blood vessels right whenever they're either ruptured or lacerated and blood is actually leaking out and our desire is to be able to stop that from happening so there's a a sequence of five steps that we're going

to go over throughout this entire length of the blood vessel in order to understand how this hemostasis is occurring before we do that we really need to understand what is keeping the blood naturally thin what's keeping it from coagulating on its own naturally so now we need to go over that before we go into understanding how this coagulation how these actual platelet plug formations and all that stuff is occurring so let's come over here and let's understand exactly how the blood is keeping itself naturally thin and pring it from becoming thrombotic in other words trying

to form a clot all right first thing we have here our endothelial cells right so here's here's our endothelia cells here we have underneath it our subendothelial layer and you know the subendothelial layer is made up of connective tissue specifically collagen it's rich in rich in collagen and then down here we have some smooth muscle cells with some specific types of receptors and then over here these orange cells are going to be our no receptors or our pain receptors right all right so first thing our endothel I cells they secrete chemicals two really important chemicals

one is called nitric oxide and the other chemical that it secretes also is going to be pg2 which is prostacyclin all right so it secretes these two chemicals prostacyclin and nitric oxide what is the purpose of these chemicals well you know if with inside of our blood we have two things plasma and cells are form elements right and those formed elements are platelets when we're going to care about white blood cells and red blood cells so circulating through this area what are we going to have we're going to have these little tiny microscopic cytoplasmic fragments

which are called platelets and what happens is this nitric oxide and pgi2 it naturally inhibits the platelet and keeps the platelet inactive and prevents the platelet from being able to bind on to the endothelial lining that's what it's naturally doing so what is this whole purpose of this it's inactivating the platelet okay so you can think about these platelets as though they're sleeping right so they're sleeping they're catching some z's over here right so again that's the whole purpose of this nitric oxide prostoy inactivate the platet and prevent the plat from binding onto the surface

that's one thing to prevent the blood from clotting natur on naturally right next thing there's another Protein that's present on the membrane actually it's not a protein it's a proteoglycan or glycos aminoglycan I should be more specific it's a glycos aminoglycan and this glycos aminoglycan is called Hein Hein sulfate it's called Heparin sulfate and Hein sulfate is a natural anti-coagulant right so here's our Heparin Hein sulfate and what does Hein sulfate do Hein sulfate binds another protein which is called anti-th 3 so this is called anti- thrombin three not and tensin three antithrombin three okay

so again Hein sulfate is bound bound to the plasma membrane it activates antithrombin 3 and imagine antithrombin 3 having like a specific type of uh hand out here imagine it having like a specific type of cutter look at this it's got a little cutter here a little like blade or radula and there's specific clotting factors that are constantly circulating throughout your bloodstream naturally what are those clotting factors that this one degrades it degrades clotting Factor two it also degrades clotting Factor n and clotting Factor 10 so imagine these guys running through this this little grinder

what does it do it inactivates these these proteins so what proteins are inactivated then you inactivate two so two is inactivated all right nine is inactivated and 10 is inactivated so now these guys are inactive all right one more mechanism this one right here look at this protein right here this protein right here is called thrombo modulin this protein is called thrombomodulin so what does thrombo modulin do thrombomodulin binds another protein and this protein is called thrombin or we can also call it Factor two right so you can also call it Factor two and then

what does thrombin do imagine thrombin having its hand out here so imagine it has a hand right and what it does is there's a protein that's kind of circulating by in this area and just so happens to run into this guy so look at this protein right here this protein this green protein is called protein C and what happens is when protein C moves across the thrombin it becomes active so now we have activated protein C and then what does protein C do protein C degrades so again what is this protein protein C protein C

degrades two factors one is going to be Factor five and the other one is Factor eight okay so these guys are going to be degraded or inhibited so these are kept inactive okay so again what happens with these guys these are all the three natural mechanisms that are trying to be able to keep the blood naturally thin and preventing it from un undesirable clotting now that we know that let's go into the first mechanism so now well first off let's actually number them real quickly what are the what are the five mechanisms right here we're

going to go one is the first one we're going to go into is called vascular spasm the second mechanism is called platelet plug formation and the third is going to be the bear of it all which is coagulation this is a beast and then the fourth one is clot retraction and repair and then we'll finish up with fibrinolysis these are the five steps of hemostasis and that's what we're going to go into in specific order so first one we have to go into is vascular spasm well how do you classify vascular spasm whenever there's damage

to the blood vessel lining so look here let's say that we damage these endothelial cells right here they're damaged so look at them they're damaged and maybe we damage some underlying tissue also so these guys are damaged now whenever these tissues are damaged what can happen blood can leak out right well we don't want the blood to leak out into this area because then if we start losing blood volume that can lead to a lot of problems right so we don't want to lose a lot of that blood so what we want to do is

we want to be able to prevent this blood loss from occurring so we want to contract or constrict the blood vessels and by constricting the blood vessels we decrease the amount of blood that's being lost that's what we want to do that's vascular spasm what causes these smooth muscles here to contract let's go into that first thing whenever these smooth muscles are injured I mean whenever these endothelial cells are injured they secrete a chemical and this chemical is called I'm going to put it with an E Endo thylin so what is this chemical called it's

called Endo thin and what does endothil do you see this purple receptor down here in the smooth muscle look what he does he comes over here and he binds onto that purple receptor and he activates an inter cellular mechanism and that intracellular pip2 calcium signaling mechanism will cause contraction and whenever that smooth muscle contract so again what's happening here there's going to be contraction that's the overall effect and what is contraction going to do it's going to cause vasil constriction which is going to decrease the diameter of the blood vessel and try to prevent the

blood loss that's one mechanism second mechanism so again what's the first mechanism here for vascular spasm so we have vascular SP spasm this is our first event the first event is endoth while we're at the muscles let's do one more mechanism so endoth um effect right the second thing is there's what's called a myogenic mechanism so whenever you have direct contact or injury to the blood vessel wall and it it actually causes direct injury to the smooth muscle whenever there's direct injury or contact with the smooth muscle there's a protective mechanism in response to that

and it's called a myogenic mechanism so if there's direct injury or contact the smooth muscle will contract so again what's the second mechanism this is called a myogenic mechanism okay so it's whenever there's direct injury or contact with the smooth muscle it contracts third event you see these orange receptors here these orange neurons whenever there's inflammation you release specific types of inflammatory chemicals so there's a lot of inflammatory chemicals within this area area a lot of INF inflammatory chemicals like maybe some histamines and some lucrin and some prostaglandins what are they going to do they're

going to stimulate these actual orange orange uh neurons right these noio spors and whenever they're stimulated they're going to initiate pain but that pain reflex can cause Vaso constriction so whenever these neurons are stimulated these no acceptors due to local inflammatory chemicals or mechanical trauma so other words you they're direct injury to them as well they're going to initiate a reflex that causes contraction so so again what will happen here he can initiate contraction onto this actual smooth muscle cell and whenever there's contraction that will cause the vascular spasm also so again what's the third

effect noio sceptor Activation so three mechanisms that trigger this vascular spasm event right so that's that's that part now let's go into the second event because we've already gone over how we're trying to prevent this from happening let's go over here and do the second event what's the second event now all right so now when there's damage to these endothelial cells right damage to the endothelial cells maybe damage to the collagen maybe damage to the smooth muscle what happens is there's a protein there's a protein produced by the endothelial cells look at this see this

protein right here this protein is called Von Wilder bronze Factor Von Wilder bronze Factor so again what is this protein called it's called vau will debron Factor so this protein it's secreted by the injured endothelial cells right and what happens is normally the platelets love to bind to the collagen because it is Von Wilder Bron's Factor if these cells are injured can they release nitric oxide can they release prostacyclin no so then the plet is not kept inactivated so that plet is actually going to bind and on top of that if we don't have Hein

sulfate because maybe it's damaged and there's Hein sulfate right here can we keep some of those CLA factors inactive no and if we have thrombomodulin right there and that was damaged can we actually keep the blood thin from Factor five and factor 8 no so this would trigger that coagulation Cascade right but but first we need to do playlet plug so again nitric oxide and prosy is inhibited and then the platelets will come and bind here so look here's a platelet right here and here's a platelet right there they'll bind but on the Von W

bronze Factor so let's say here's the Von Wilder bronze Factor there's a specific receptor on the platelet that binds with the Von Wilder Bron's Factor what is this glycoprotein called and the only reason I mention it is because it's important because we have to understand certain diseases and drugs that protein right there is called that black protein is called glycoprotein 1B so again what is that protein called right there it's called glycoprotein 1B and it binds with the Von wild Bron's Factor so the playlets bind here right and then what happens once the platelets are

actually going to be like activated because of this binding their granules start actually releasing specific chemicals what are those chemicals that it secretes three chemicals it secretes one of these chemicals is called a DP right that's one really really important one another chemical is called thromboxane A2 and another chemical that secretes is called Sarah tonin or five hydroxy tryptamine what do these chemicals do well I told you before that there's platelets just kind of naturally circulating within this area right here right so maybe here's a platelet Maybe here's a platelet Maybe here's a platelet here's

a platelet right these platelets are just tiny little cytoplasmic fragments they're super super tiny they're derived from a mega Cario site right so what happens is ADP and thromboxane A2 these guys work to be able to stimulate this these actual uh platelets so they have receptors on their membrane that specifically bind the ADP and the thrombo A2 so when ADP and thrombo A2 bind on to these playlets it activates the playlets and causes these playlets to want to come to that site of injury so then what's going to happen these plets are going to start

aggregating to that site of injury so they're going to undergo what's What's this called whenever they come here it's called platelet aggregation that's the first step all right so now the playlets are going to start binding here so look at what's happening here so playlist bind here they bind here they bind here and they start forming this nice plug right here but then there's one more thing that we have to do before we keep going on with this right so the playes are binding but how are they binding to each other we know how they

bind with Von Wilder Bron's Factor let me draw a platelet right here so here's one platelet and here's another platelet so we know that they can join with the Von Wilder bronze Factor right so here's the let's say here's a Von Wilder bronze Factor protein they bind with that with the glycoprotein 1B right so here's our glycoprotein 1B that's how they bind this but how do they bind to each other well here's another there's these proteins here on each one's surface and then there's a thing called fibrinogen that actually leaks links them together this protein

right there is called get ready glycoprotein 2 B 3 a holy goodness right so that's a it's a crazy name right there but it's important because we have to know these proteins because they're drug targets okay so again glycoprotein 2B and 3A with fibrinogen between them link the platelets together so that's what you'll see linking them together but now look we got a nice platelet plug okay we're not done yet what is thron box2 and what else does serotonin do well you see these actual pink these purple receptors down here thr oxan na2 and serotonin

love to bind to the smooth muscle and when they bind onto the smooth muscle they cause contraction so again what would they cause let's come down here they cause contraction right and what does contraction cause contraction leads to Vaso constriction and then again what will that Vaso constriction do enhance the vascular spasm effect so again ADP and throx na2 cause platelet aggregation which leades plet plug but throx A2 and serotonin cause vasal constriction to enhance the vascular spasm response that is the second step so what is this second step right here that we've done it's

called platelet plug formation not bad right all right so again we've done the Second Step so we done first step second step now let's go on to the third step okay so now real quick recap this this will be right so again there's damage to this endothelial lining we already know what happens Von water bronze factor is going to be right here right and it's going to have its specific proteins there what's going to bind platelets and they're going to bind with their glycoprotein 1 B they're going to bind to each other through their glycoprotein

2 B 3A with the fibrinogen in between them they're going to start becoming activated and secreting ADP and thrombo and A2 which causes platelet aggregation and then they're going to secrete serotonin and then throx and A2 also will cause vasil constriction to enhance vascular spasm right so now we got this beautiful platelet plug here now we go into the be of it all all right now we're going to go into coagulation okay so now we're talking about the coagulation Cascade so first off these playlets so they've already undergone a aggregation and the plug formation and

they just continue to keep pulling more playlists at that site but once this has happened we go into this next step right so there's these things called phospho tialing groups that are going to be on present on the platelet's membrane and it creates these negative charges right here so these negative charges on the actual platelet cell membrane and this is again caused by phospho talerine there's going to be proteins you know your liver your here's your liver right here so your liver is const stantly making tons of clotting proteins tons of clotting proteins and these

clotting proteins are normally circulating within the blood plasma right but they're kept inactive but now we're going to activate them so the first clotting protein that just so happens to be walking through this area and then boom interacts with a playlet is called Factor 12 so what is the first protein called it's called Factor 12 or hegan's factor right so there is Factor 12 Factor 12 will interact with those negative charges on the playlet and then convert itself into an active form so it's a precursor or a pro-enzyme we can call it a pro-enzyme right

or even we can call them zymogens they're just inactivated right well we're going to activate them now so now here's Factor 12 he's activated what happens next is Factor 12 activates Factor 11 so here we have Factor 11 Factor 11 is going to get activated ated by Factor 12 so now he's activated and then Factor 11 is going to go and activate factor nine so here's another one so here's going to be factor nine so factor nine right here is going to interact with Factor 11 and he'll be activated and then what happens factor nine

interacts with another protein that just happens to be walking by all right and that is going to be be called factor8 so over here is actually going to be factor8 and factor8 is going to interact with factor nine and they're going to form a complex right but they're going to need two other things present for this to happen they're going to need what's called platelet Factor 3 and calcium so they need calcium as a co-factor and then need they need the membrane of the platelets or platelet factor three in order for this complex to occur

then there's another protein here and this protein is called Factor 10 and Factor 10 so these guys are actually going to combine together and they'll form one complexing pathway right here that will drive the conversion of the inactive form of 10 into active form of 10 and now the active form of 10 is going to react with another protein I know this is a lot of proteins here but it's going to react with Factor five so Factor five will actually react here you'll also have platelet Factor 3 and calcium driving the step also and what

this will do is this will activate another protein and this protein is called the pro thrombin activator so this is called the pro thrombin activator okay now what the proin activator does is it has look at these ears look at these ears what it does is there's another molecule kind of circulating within that area and that molecule is called Factor 2 but in this form it's called prothrombin it's in the inactive form so what the prothrombin does is look it reacts with the ear of pro thrombin activator reacts with him and when it does it

converts the prothombin into thrombin the activated form so Factor two is also called thrombin okay know that factor two is also called thrombin thrombin then does what okay here's where we get to the good stuff thrombin reacts in two ways one there's a molecule which is called look I'm going to draw it like a circle here they're kind of just hanging out in this area these little circle circles what are these little circles called these little circles are called fibrinogen so this is called fi brinogen and fibrinogen is a plasma protein if you remember from

the hematocrite that is actually counting for some of the the 4% of the plasma proteins right and it's circulating through the blood soluble Wise It's soluble within the blood plasma but then what happens is Factor 2 or thrombin polymerizes them starts linking them together and if you starts linking them together look at what they're going to look like now so now how many do I have 1 2 3 4 5 six seven so I have to have seven of these together over here so three four five 6 7 what is this molecule here called This

is called fibrin and fibrin is insoluble in the blood plasma so this is going to help to turn the blood for more of a liquid into a jelly-like substance that's the purpose of coagulation because we want it to be more jelly like so that it will slow down the blood flow beyond that area because we don't want to keep losing our red blood cells so it slows that flow of the red blood cells through there and turns it into more of a jelly-like substance all right so now it's insoluble one more thing it reacts with

another protein over here and this protein is called Factor 13 also called the fibrin stabilizing factor and look what he does he becomes activated and you need calcium also for this step to occur so what else do you need for this step to occur you need calcium Factor 13 will then take these fibrin strands and cross link them together so then it'll take another fibrin strand that it might have over here somewhere that thrombin's polymerized and look what it's going to do it's going to cross link them so it's going to take this one cross

link it this way and then it might cross link another one over here what's the purpose of crosslinking this the purpose of crosslinking it is to create a nice fiber mesh so that when we lay this over the platelets it prevents the platelet thrombus from dislodging and going into an area and causing animalism right we want to keep this taught nice and held down so that we don't have any blood loss from here but we also don't let it break off that's important so again fiber and stabilizing Factor will cause this crosslinking so again what

will it cause here it'll lead to cross-linking of fibrin and this produces the fibrin mesh so what is this molecule now called it's a fibrin mesh Network right now what does this fi mesh do this fibr mesh is going to be laid over this so now imagine here I'm just going to draw it as lines now look look at this we're holding this down now and here's our cross linking there's our fiber and mesh and that's holding that platelet plug in place place so that it doesn't dislodge and go somewhere else right and also it's

keeping the blood as it's circulating through this area right here more jelly-like more thick more viscous so that slows the blood flow down so we don't continuously have blood loss right all right so what have we gone over then so basically let me let me tell you real quick here we have two Pathways an intrinsic pathway and an extrinsic pathway I haven't talked about the extrinsic but I will it's a very quick pathway but intrinsic is the ones that we just talked about where we started with 12 right and we went from 12 down to

11 and then 11 down to 9 and then nine with eight and then eight combined with nine to activate another one which is that factor 10 right and here let me tell you one more thing Factor 10 getting activated this is the common pathway so now what we just went over here is the intrinsic pathway right in the intrinsic pathway is the pathway that's occurring inside of the blood independent of the extrinsic pathway what do I mean if you take someone's blood out of their you take someone's blood and you put it in a tube

that's not heparinized so it doesn't have heper coding it right the the glass has a roughen surface and charged surface so what does that do it activates Factor 12 so the intrinsic pathway can occur inside of a test tube independent of the extrinsic pathway however the extrinsic pathway which you're going to talk about does depend on some of the factors and proteins within the intrinsic pathway all right but before we do that again know that what we covered intrinsic is 12 11 9 8 and then activating the common pathway which is 10 that's going to

be super important because now you see how there was tissue damage here whenever there's damage to any of our tissues our tissues release a protein which is called tissue factor or factor three factor three now factor three will come over here and look what it will react with it will react with another protein over here and this protein is called Factor 7 so this protein is called Factor 7 when Factor 7 reacts with this factor three it becomes active and look what it can do now it can do two things one thing is it can

stimulate this step you see how it can actually push factor nine into becoming activated well look what else it can do it can also converge right here onto the common pathway it can converge right onto the common pathway right so now what do we know out of this then so what do we know is we know that factor three can be secreted by damaged tissue cells and those tissue cells will then actually activate they produce tissue factor factor three factor three will react with react with Factor 7 and then Factor 7 can activate Factor 9

and it can come into this common pathway that is the extrinsic pathway so what is this pathway here again let's write it up over here so again what is this pathway called This is the extrinsic pathway and again how does this pathway occur what is the protein produced by the damaged tissue cells this is factor three factor three will react with Factor 7 Factor 7 will be activated and Factor 7 can drive the activation of factor 9 as well as he can also Drive the activation of the common pathway so what is the big what's

the big thing about this look how much longer it takes for the intrinsic Pathway to occur versus the extrinsic pathway the extrinsic pathway can occur in about 30 seconds it's very fast whereas the intrinsic pathway might take about four to six minutes to occur so it's a little long right so now now that we understand that we understand the activity of the intrinsic and extrinsic pathway how the ex transic tries to drive either Factor 9 activation or it can act try to activate Factor 10 and then the intrinsic pathway is the sequence of cascade that

also desires to activate Factor 10 which is again the common pathway all right so I know coagulation is a is a pretty big beast it takes a lot to remember all these proteins so I wanted to give you a little trick to help you you to remember it all right so here on the left we're going to have the intrinsic pathway here on the right we're going to have the extrinsic pathway it's just a little trick you can take it if you want it so what I do is x marks the spot so I put

that it's the first thing I do I put it right in the middle then after that I count downwards starting with 12 skipping 10 so in other words I I put x x marks a spot that's 10 and I work backwards from 12 12 11 skip 10 9 8 and then I go to 10 right so look here 12 to 11 11 to 9 9 to 8 and then 8 to 10 guess what pathway this is this is the intrinsic pathway right so this is the intrinsic pathway again what do I do x marks the

spot so 10 and then again I count backwards from 12 just skipping 10 12 11 skip 10 9 8 and then I get to 10 how do I remember the extrinsic pathway extrinsic you can remember 3 + 7 = 10 that's easy right so again count backwards from 12 and then 3 + 7 equals 10 now how do I remember the common pathway and then the formation of throm and the fiber mesh so in order to make 10 right because this this is going to go downwards but in order for me to remember this I

remember 5 * 2 * 1 = 10 so what is we have Factor five right that activ uh reacts with 10 and then 10 and five activate two which is thrombin right so two is thrombin and then two activates one what is one fibrinogen so again how do I do it x marks the spot 10 count backwards starting with 12 skipping 10 so TW 10 12 sorry 12 11 9 8 and then he had 10 how do you remember the x transic 3 + 7 = 10 and then how do you remember the formation of

uh the the thrombin so you have remember 5 * 2 * 1 equals 10 right so five is going to be who Factor five two is going to be thrombin and then thrombin is going to be activating fibrin so you can remember that again 10 with five activates two two activates one so that's a very quick easy little trick to be able to remember the coagulation Cascade okay so again what have we done then we finished this third step which is coagulation Cascade so we finished the third step coagulation Cascade now let's go to the

fourth step so again what do we have over here we had damage to the endothelial lining right it's just a constant review of this guys so again damage here then what do we have on Wilder bronze Factor here then we have our platelets here here's our plet plug the platelet plug is releasing tons of different chemicals right causing the platelet aggregation causing the plet plug formation vascular spasm then we have the coagulation Cascade which is leading to the production of the fibrin mesh with the intrinsic and the extrinsic pathway now we go to our fourth

step what is the fourth step the fourth step is called clot retraction and repair hair so you see these plets they have contractile proteins within them it's called actin and myosin so what they do is Imagine imagine my arms are the platelets right so imagine I'm the platelet right here what I'm going to do is I'm going to take one arm over here and I'm going to grab I'm going to grab the endothelial cell on this side and then I'm going to grab the endothelial cell on this side what I'm going to do is I'm

going to pull the edges of the endothelial cells closer together right by doing that I'm bringing those ruptured edges of the blood vessel closer together so again what does the platelet do within this step the first thing that's going to happen is platet contraction and that will pull the ruptured edges of the blood vessel closer together second thing that's going to happen it's going to secrete a chemical these platelets nearby are going to secrete a chemical which is called platelet derived growth factor so this chemical is called platelet derived growth factor what does this PL

deriv growth factor do the pl derived growth factor comes down here and if these smooth muscle cells were damaged so let's say that the smooth muscle cells were damaged right here there was damage to these smooth muscle cells the plet derived growth factor is going to trigger trigger the mitosis or proliferation of the smooth muscle lining and on top of that if there was any damage to these connective tissues here it's going to cause connective tissue patches to be formed to regenerate those collagen fibers so it's going to help to produce connective tissue patches to

repair the collagen maybe even produce connective tissue patches over this endothelial cell area and it's going to help to proliferate the smooth muscle to renew that lining so again what is this chemical here called This is called platelet derived growth factor what is the third thing that happens there's one more chemical and that chemical is called vascular endothel growth factor and again the pl will secrete that chemical so again what is this chemical called This is called vascular endothelial growth factor what do you think it does it says it within its name the vascular endothelial

growth factor is going to regenerate the new endothelial lining so any of the endothelial lining that we damage it's going to help to regenerate that okay so again CLA retraction repair it's going to contract pull the pl ruptured edges closer to one another secrete p dgf to proliferate the smooth muscle and produce connective tissue patches here and then it's going to release vascular endothelial growth factor which is going to replenish the new endothelial lining and it can lead to what's called canalization but we're not going to do that here that's the fourth step all right

so this last step here this last step the fifth and final step for this process is called fi breno Lis so you remember here that we had that clot right now this area can get pretty big and sometimes it can get so big that it can actually olude the blood vessel flow beyond that area and lead to aeia right so we don't want that so what we want to do is is we want to be able to get rid of that clot we want to bust that clot up so there's natural proteins present here on

the cell membrane here so what is this protein called right here this protein right here is called they have two names for you can call them tissue plasminogen activator sometimes they even call it strepto but we're going to just call it tissue plasminogen activator so what is the tissue plasminogen activator do there's a protein naturally present within your bloodstream again and this protein is called plasminogen it's called plasminogen and plasminogen will react with the tissue plasminogen activator and get converted into what's called plasmin and imagine plasman as though he's like a hungry little eater here

so look he's got nice little teeth in here right and he's ready to eat what he's going to do is he loves to eat fibin okay so he loves to eat fibrin all right I love fibrin right so what he does is he's going to come over here and he's going to start digesting that fibr mesh he's going to start cutting that fiin mesh up and what is he going to do then by degrading the fibrin mesh he might release a little bit of fibrinogen out here which remember was the precursor and he also might

release a very very important chemical called a d peptide or a d dier why is this important when they run specific blood tests to determine if someone's had some type of clot formation they run a d dier it's really important because we run a d dier and we see elevated D dier levels that can help us to understand maybe this person has had some type of clot form so dmer is very important for Diagnostic uh procedures within differential diagnoses right so again what is this going to do plasma into plasma it's going to digest the

fibrine and bust that clot up right and by busting up that clot that helps to be able to prevent uh e clusion to the blood vessels right one more thing why is this TPA important we give this to people who have some type of a a stroke so if they have some type of transin es schic attack that's blocking the uding the blood flow to the cerebral vessels the TPA we're going to give that to them in the acute response within hours you needan you need to give it within hours because they also give aspirin

in response to this too but TPA what is it going to do when you give it to them it's going to make plasmine what's plasma going to do it's going to start breaking down that fiin mesh to get rid of that blood clot right and that's important because we don't want to have too much blood blood loss to a specific area within the brain because it can lead to cytotoxicity and that what leads to the the damage to some of the neurons within that area and it can lead to limb weakness and problems with that

right all right so that covers our fifth step which is fibron analyis let's come back over here do a quick recap of everything and talk just really really briefly about a couple drugs all right so again what was that first thing that we wanted to go over again what keeps the blood naturally thin the nitric oxide the prostacyclin and activates the platet the Heparin sulfate the anti-thrombin 3 and activate some of these coagulating proteins Pro coagulating proteins and then thrombomodulin thrombin and protein C and activate other procoagulants so again this is all our step one

but it's again it's what keeps the blood naturally thin now what kind of drug could we use here to enhance this process if someone needs to be able to prevent themselves from having a cloth well you know antithrombin 3 we can give a molecule called Hein and what does Hein do if we give more Hein it's going to enhance antithrombin reactivity if you enhance antithrombin re activity what are you going to do you're going to destroy a lot of these procoagulants keeping the blood naturally thin all right what's this first step here that we went

over vascular spasm what's the whole purpose of it just to be able to keep blood from uh prevent blood from continuously being lost right by how vasoconstricting the blood vessel and preventing as little blood as possible from leaking out into the tissue spaces right and causing hematomas and other damage severe blood loss right that's important there Second Step plet plug formation again what was the whole purpose here the plets love to bind with the Von Wilder Bron's Factor there okay now one more thing here when these playlets aggregate right how can we prevent the aggregation

well you remember ADP ADP there is a a drug that can actually block ADP this drug is called cigil so what does it do it inhibits ADP that's one drug that you can give another drug that you can give inhibits the formation of thromboxane A2 which it's a Cox 2 inhibitor and this is called everybody usually knows this one this is called aspirin and an aspirin inhibits thromb boxy A2 you can also give a drug to block this glycoprotein 2 b3a protein right and this is called ab6 aab and ab six amab inhibits the activation

of the glycoprotein 2b3a connection so a lot of things that you can do you can also give direct uh proteins in here you can actually give some some specific Inhibitors you can actually give a direct bromen Inhibitors you can give uh I'm sorry direct Factor 10 Inhibitors and you can give Factor 2 Inhibitors uh common factor 2 Inhibitors are like the botran or praxa as the brand praxa or deigan etexilate that can inhibit this enzyme right there okay so there's a lot of different drugs that you can give here to be able to treat some

of these conditions right you can also give warrin and what is the purpose of warrin warrin is a vitamin K oxide reductase inhibitor what the heck does that even mean you know there's specific proteins like Factor 2 Factor uh seven factor nine Factor 10 protein C protein s whole bunch of different proteins they require vitamin k What warrin does is it inhibits the enzyme that actually uh pushes that vitamin K into these enzymes making them functional so if you don't have vitamin K what's going to happen to these procoagulants they're going to be inhibited and

not functional that's another drug that you can give someone to be able to inhibit the clot formation so again that's in a nutshell everything we're going to need to know about hemostasis and just a very basic amount of drug information that we can go to understand a little bit more about that pathway