Full transcript
0:06what's up ninja nerds in this video
0:09we're gonna talk about antiplatelet
0:10medications this video is brought to you
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0:57so it's gonna get started alright
1:00engineers so let's go ahead and talk
1:01about these different antiplatelet
1:02medications and an order for us to
1:04really know all the different types of
1:06antiplatelet medications it's best to
1:07look at them based on their mechanism of
1:09action right so first thing we have to
1:13do before we really get into all these
1:14medications is just the most basic
1:16overview of hemostasis if you guys
1:19remember endothelial cells what was
1:21their function generally they were
1:23supposed to release specific chemical
1:25substances that keep the blood and Chi
1:28thrombotic right if you guys remember
1:29back from that video we had molecules
1:32like PGI two molecules like nitric oxide
1:35and if you guys remember what these
1:37little guys were doing is they were
1:39basically in activating the platelet
1:41right so they were keeping this little
1:43dude inactivated so that he doesn't
1:46attach to the endothelial lining and
1:48cause a clot that we don't want well if
1:51someone has let's say damage of the
1:54blood vessel lining right for whatever
1:56reason what's that going to do to the
1:58pgi2 and nitric oxide production it's
2:00going to decrease what's going to happen
2:03to the inhibition on the platelet it's
2:04going to be lost so what's the pletely
2:06going to want to do then it's gonna want
2:08to attach to the endothelial lining so
2:11let's say that there is damage and you
2:12guys know that
2:13never there is damage to the endothelial
2:14lining the underlying collagen becomes
2:17exposed this little blue stuff here
2:18right and what happens is there's a
2:21protein that binds within that collagen
2:23meshwork and if you guys look here I
2:25should be able to name it out
2:26it's called von Willebrand factor right
2:28it's made by the endothelial cells it
2:30can even be made by platelets what
2:32happens is this von Willebrand factor is
2:35like glue to the platelets the players
2:37love it they have a specific protein
2:39that allows for them to bind on to that
2:41von Willebrand's factor you know that
2:43little suckers called the little pink
2:44guy that is called gp1 B so these little
2:49pink proteins here are called G p1b
2:52proteins okay and what these allow for
2:56is they allow for this connection
2:58between the von Willebrand factor and
3:00the platelets so that's really important
3:02gp1 B is the connection between the von
3:05Willebrand factor and the platelet now
3:09when the von Willebrand factor binds
3:11with the platelet the platelet has to
3:13let other platelets know to come to this
3:14area of where injury is so that they can
3:17attach as well how does it do that if
3:19you guys remember we have little
3:21granules inside of these platelets
3:24different types of granules we're not
3:25gonna go into crazy detail there is
3:26alpha granules they release things like
3:28clotting factors and PDGF which is
3:31called platelet derived growth factor
3:32but the more important one is the delta
3:35granule or the dense granules in these
3:37Delta granules they release multiple
3:39different types of substances for
3:42example they can release three really
3:45important ones okay
3:47serotonin which is also kind of written
3:52as 5-hydroxytryptamine
3:545ht there's also another one called ADP
3:57and you can also release calcium but
4:01there is another one that's made by the
4:02membranes and we'll talk about that one
4:04and a little bit here called thromboxane
4:06a2 and if you guys remember from that
4:08hemostasis video
4:10these guys are platelet aggregate
4:12aggregation agents right so in other
4:14words they tell other platelets to come
4:16and come stick to this platelet but how
4:20does this platelet stick to this
4:22platelet there's got to be a way right
4:23well look here you see these little blue
4:25guys here
4:26these little blue guys here are called
4:29GP now hold onto your tail you to your
4:33seats these guys are long GP to be three
4:36a proteins ok so here's a GP to be three
4:40a protein on this platelet and here is a
4:44GP to be three a protein on this
4:48platelet what is this little stuff
4:50connecting between them this little
4:52stuff between them is called fibrinogen
4:55right so it's called fibrinogen
5:00fibrinogen is going to be like a little
5:03glue between these two proteins and it
5:06allows for the platelet plug to be
5:08stable so again platelet connect to
5:10platelet through there's GP 2 B 3 a
5:12proteins and again fibrinogen is like
5:15the glue between that so that's how they
5:18stick with one another how do you
5:19trigger their aggregation these little
5:21guys so we have medications that are so
5:24cool that you can block adp you can
5:27break down thromboxane a2 and you can
5:31block this protein from linking to one
5:34another let's talk about some of those
5:36proteins so the first one that I want us
5:38to talk about is this thromboxane a2 now
5:41if you guys remember I said that the
5:43thromboxane a2 is coming from this
5:44platelet it's not really coming from the
5:47granule it's actually coming from a
5:48different type of like acid they call it
5:51arachidonic acid let's do this guy here
5:54and purple so you have this guy here
5:57called arachidonic acid we're gonna put
6:00a a here arachidonic acid arachidonic
6:05acid is actually going to be broken down
6:08through a specific enzyme into it's
6:12called prostaglandin g2 then it's
6:16metabolized again into prostaglandin h2
6:19is actually going to be metabolized
6:22so he gets metabolized into two
6:24different components here right one
6:27component we're not super worried about
6:28it's like your PG e 2 PG f 2 PG d2 and
6:35there is another one called PG I
6:38those ones were not super super worried
6:40about right now the one that we do care
6:42about is called thromboxane a2 so it's
6:48made from arachidonic acid where does
6:50this arachidonic acid come from well you
6:53guys know within this platelet you have
6:55a phospholipid bilayer that phospholipid
6:58bilayer can actually get broken down
7:00into different types of fatty acids like
7:03a call this Anna Coast annoyed and that
7:05arachidonic acid from the membrane can
7:07get converted all the way into
7:09thromboxane a2 ain't that cool all right
7:11so what does thromboxane need to do well
7:13when it binds on to this receptor the
7:15star on boxing a chi receptor it can
7:17activate multiple different types of
7:19interesting in the pathways right so it
7:21has the ability to activate like a GQ
7:24pathway right so GQ if you guys remember
7:27will actually shuffle along the membrane
7:30and bind on to a specific membrane bound
7:32protein here which is called
7:34phospholipase C look at this cute little
7:37guy yo you know so phospholipase C is
7:42actually going to get stimulated by this
7:45GQ protein now down to this
7:47phospholipase C it's going to break down
7:50the specific membrane bound structure
7:52here which is called pip2 when it breaks
7:57down pip2 it breaks it into two
8:00components right one is called ip3 the
8:05other one is called da G this is ina
8:09SCYTL triphosphate and diacylglycerol
8:12ip3 binds on to this little endoplasmic
8:15reticulum like Network and stimulates
8:18protein channels to allow for calcium to
8:23be shuttled out and then the calcium
8:26will do what the calcium will then come
8:29down here and stimulate these granules
8:31and cause these granules to start fusing
8:34with the actual cell membrane
8:36once it fuses with the cell membrane
8:38what happens it starts to release out
8:42these little molecules such as ADP such
8:45as serotonin such as calcium and again
8:50you're going to get more but
8:51ilysm of from boxing a to what's gonna
8:54happen that's gonna cause more platelet
8:56aggregation at the same time da G is
8:59also activated what can this little guy
9:01do da G can also activate protein kinase
9:05is like protein kinase C protein kinase
9:08C can then go and regulate this specific
9:13protein here which is that GP 2 B 3 a
9:15protein and what does that allow for it
9:18allows for this protein on this playlet
9:20to stick with this protein on this
9:22platelet through the fibrinogen glue
9:23that's a beautiful thing right so what
9:28do we need to block this whole action
9:31well we have a drug a very commonly
9:33utilized drug that basically inhibits
9:36one of the enzymes in this pathway right
9:39now watch you know arachidonic acid
9:42there's a specific enzyme called a
9:44cyclooxygenase that's shortened to Cox
9:47and there's different isomers there's a
9:49Cox one and a Cox - okay there's a
9:54specific drug that can inhibit both
9:55isomers okay and it's a beautiful drug a
9:58very commonly utilized drug and it's
10:00called aspirin or acetyl salicylic acid
10:03and what this guy does is if he inhibits
10:07he irreversibly inhibits this Cox enzyme
10:11let's follow this along if a rock anodic
10:14acid can't get broken down to PGG - it
10:16can't get broken down to PGH - and it
10:19can't get broken down to thromboxane a2
10:20if there is decrease thromboxane a2
10:24there's decreased stimulation of the
10:28phospholipase c there's decrease
10:30production of i p3 decreased production
10:33of d AG decrease calcium getting
10:36released from this little endoplasmic
10:38reticulum structure and decrease
10:41degranulation so decreased degranulation
10:44in other words if you decrease the
10:47degranulation you decrease the
10:49aggregation and activation of other
10:51platelets at the same time you decrease
10:53protein kinase C and you inhibit okay
10:57this actual there's no more stimulation
11:00so there's inhibition now and now this
11:02GP 2 B 3 a protein on this platelet boat
11:05act with the gp2 v3 a protein on the
11:07other platelet so there's no
11:08stabilization of that clot or that
11:11platelet plug that's a beautiful
11:13mechanism love that so darn cool okay so
11:16we got one one of the big ones here is
11:18throne box in a - what about the ADP how
11:22does that one important let's go over
11:24here
11:26so ADP what is this little guy do so he
11:31comes over here right you know you have
11:32a little protein here there's actually a
11:34very beautiful receptor here let's write
11:35this receptors name this receptor is
11:38called the p2 y12 receptor they call us
11:42a p2 y12 that ADP binds on to so what
11:49happens is ATP gets released right it
11:54binds on to this receptor now this
11:56receptor can go two different ways we're
11:58going to quickly fly through the pathway
11:59one of the proteins that it activates is
12:02called AG inhibitory protein that gene
12:05hibbett or e protein is going to do a
12:07couple different things it's gonna move
12:09along the actual cell membrane and it's
12:14going to inhibit this enzyme all right
12:17what is this enzyme here called it's
12:18called adenylate cyclase adenylate
12:21cyclase function is designed to be able
12:23to take ATP and convert it into cyclic
12:28AMP E and then cyclic AMP e will
12:31activate a specific enzyme called
12:33protein kinase a protein kinase a will
12:37then phosphorylate another enzyme let's
12:39think of it a really beautiful color for
12:41this one oh here's another one this is
12:44called vasodilator stimulatory protein
12:48vasp okay now what happens is vasp
12:52is going to get phosphorylated into
12:55what's called vasp
12:57p right so it's going to get its
13:00phosphorylation there here's what's
13:02really interesting with vas whenever it
13:06has that phosphorus group bound to it
13:08it's interestingly inactive
13:11and when it doesn't have that it is
13:14active here's what's really interesting
13:17what did we say ADP does it stimulates
13:20let's follow the whole process here it
13:22stimulates the gene hibbott or e protein
13:24which inhibits adenylate cyclase that
13:27means there's less ATP converted into
13:31cyclic A&P there's less protein kinase a
13:34and there's less of this vast P being
13:37formed okay when this is active what
13:41does it do it stimulates the GP to b3 a
13:49follow that gene Debra Tori protein less
13:52cyclic a and P less protein kinase a
13:55less phosphorylation of the vasp into
13:57vas P if this is active it's going to
14:00stimulate this protein now we just need
14:02a drug that can block that receptor and
14:04have the opposite effect an antagonistic
14:07effect what are some of those drugs I'm
14:11glad you asked guys so some of these
14:13drugs are called clopidogrel it's a very
14:18commonly utilized one brand name is also
14:21called plavix okay there's another one
14:24called prasugrel which is called eviant
14:28there's another one called Tyco a girl
14:30or which is called bRILINTA and there's
14:34another one that's not commonly used as
14:36much anymore because of some of the
14:38problems it has you know developed such
14:41as T TTP and we'll talk a little bit
14:43about that in a TRS but these drugs are
14:46basically inhibiting this receptor so if
14:51they inhibit this receptor what does
14:53that mean that means that there's less
14:54jane hibbott or e protein that means
14:57that there's less inhibition of
14:59adenylate cyclase so that means that
15:01instead of having decreased ATP there's
15:03actually a slight increase in ATP that
15:06means that a little bit more ATP is
15:08converted into cyclic AMP e that means
15:10you get a little bit more protein kinase
15:12a if there's a little bit more protein
15:15kinase a then more of this reaction is
15:17heading towards this direction and
15:19there's actually going to be more of
15:21this vast pia and less of the vast
15:24so now this is not going to be able to
15:26stimulate this anymore
15:27so what does that mean there's no
15:29stimulation if there's no stimulation
15:31then it's going to start to become
15:32inhibited and what does that mean that
15:34means that the GP to be three a protein
15:37of this politely can't bind to the GP to
15:39be three a protein of the other platelet
15:41it's a beautiful mechanism right there's
15:43also another thing that you would just
15:45briefly talk about here is that the gene
15:47hibbott or e protein is one of the
15:49pathways but this ABP receptor pathway
15:51can also activate another kind of like
15:54structure here and what is it
15:58it can also activate GQ and if you guys
16:04remember GQ will stimulate a specific
16:06enzyme called phospholipase C
16:09phospholipase C does what it breaks down
16:12pip2 into ip3 and D AG ip3 does what it
16:23binds on to these receptors and triggers
16:25the release of calcium and calcium will
16:28then try to cause degranulation in class
16:29platelet aggregation and D AG again we
16:32know that this will activate protein
16:33kinase C and protein kinase C will also
16:36regulate the activity of the gp2 b3a
16:39so if you give clopidogrel prasugrel
16:44Tyco haggler Tecopa dean what's it gonna
16:47do it's gonna inhibit GQ right if you
16:50inhibit GQ you get less ip3 less calcium
16:54less degranulation less aggregation and
16:56platelet activation if you get less d AG
17:00you get less phosphorylation of the gp2
17:02b3a
17:03which means less interaction between
17:04platelets awesome it's a beautiful
17:06mechanism right so we have aspirin we
17:09have clopidogrel pursue growth like a
17:11griller to Khloponin what else do we
17:13have what if we had something that
17:14directly bound and blocked these guys we
17:17do we do guys so what are these drugs
17:20that inhibit these their GP to be a3
17:23inhibitors so things like AB 6 and mad
17:28tyro fivin an app to FIBA tied okay now
17:43these guys will do what they will
17:46inhibit the GP to be 3a interaction if
17:52there is no interaction between the GP
17:54to be a to p3 a proteins what's going to
17:56happen less platelet interaction and
17:58less stabilization of the clot that is a
18:00beautiful mechanism so you have your GP
18:04to be 3a inhibitors you have your ADP
18:07receptor inhibitors you have your
18:09cyclooxygenase inhibitor like aspirin
18:12there's actually one more remember this
18:15we haven't talked about this little tube
18:16yet this little jheri curl like enzyme
18:19and this enzyme is called PDE okay
18:23phosphodiesterase it's actually a tight
18:25it's a type 3 if we really want to be
18:27specific so it's called
18:29phosphodiesterase 3 and there is drugs
18:32that are utilized to inhibit that enzyme
18:35and what are some of these drugs well
18:38you have a drug which is called salats
18:41dissol okay we're gonna put them over
18:43here and why not bring an arrow to them
18:46okay so you have another drug called SCI
18:49lost us all and diaper animal and what
18:56these drugs can do is is they have the
18:59ability to inhibit this enzyme okay now
19:04let's explain why that's important
19:05what does phosphodiesterase is do they
19:09break down cyclic A&P and whenever
19:12cyclic AMP is broken down can it get
19:14converted into protein can activate
19:15protein kinase a No
19:17so if you inhibit this enzyme you
19:20inhibit the breakdown of cyclic a and P
19:22if you inhibit the breakdown of cyclic
19:25AMP P what does that mean you get
19:26increased cyclic AMP E which means you
19:29get increased protein kinase a which
19:31means you get increased phosphorylation
19:34of vas P which means that this is no
19:37longer going to be able to stimulate
19:38this protein and so now it's going to be
19:41in
19:41tremely inhibited so there's going to be
19:43extra inhibition
19:45that's so darn cool so that's one of the
19:48mechanisms of these guys so they have
19:50the ability to inhibit this guy they can
19:54also through other mechanisms inhibit
19:57these degranulation as well but one of
19:59the big things is they they inhibit this
20:01gp2 b3a alright so the last thing i want
20:04to talk about with the losses all and
20:05die pretty MO which is a really cool
20:06action of them and that's why they have
20:08another indication that we'll talk about
20:09a little bit afterwards called
20:11peripheral artery disease is they can
20:13also cause smooth muscle relaxation and
20:15blood vessels that's really important
20:17because it can dilate the blood vessel
20:19and increase the blood flow around any
20:21type of like maybe plaque or even
20:24thrombi so that's what's really cool
20:26about this drug so go ahead and take a
20:27look at how they actually do that so if
20:29you remember we have the endothelial
20:32lining here right and just underneath it
20:35you're gonna have that tunica media so
20:36if you guys remember your Anatomy you
20:38have Tunica interna which is basically
20:41simple squamous epithelial tissue with a
20:43little bit of loose areolar connective
20:44tissue underneath it then you have if
20:47you really want to be specific and
20:49internally elastic lamina after that
20:51then you have your tunica media which is
20:53a smooth muscle layer right what happens
20:56is selasa Zahl and diaper animal what
20:58did I tell you they do they inhibit this
21:00little jheri curl like pac-man and again
21:03that is what's really important because
21:05this is a P D e3 inhibitor right and
21:10this is a PD III enzyme so if you take
21:12some loss dissol and diaper it Amol and
21:19again inhibit this enzyme that's
21:22important so how does that work
21:24basically if you guys remember another
21:26thing for these particularly diaper
21:28animal is you have another molecule
21:30called adenosine an adenosine can
21:35actually bind onto these receptors they
21:38can activate a g-protein like G
21:40stimulatory protein which will then
21:42activate a dental aid cyclase adenylate
21:44cyclase when it's stimulated again we
21:47know that it takes ATP and converts it
21:50into cyclic A&P and cyclic AMP II
21:53then activates protein kinase a protein
21:55kinase a then acts on what's called
21:59myosin light-chain kinase and what's
22:01interesting is that whenever you take
22:04myosin light-chain kinase and
22:07phosphorylate it it's actually inhibited
22:12so in the phosphorylated form it's
22:15inhibited and so it's actually not going
22:18to be able to do what it's not going to
22:20be able to cause smooth muscle
22:22contraction so if we give a drug okay
22:27like selasa salt or diaper at a mall
22:29it's going to inhibit PB III that means
22:32that this enzyme is no longer going to
22:35be able to break down the cyclic AMP II
22:37right so that's gone so cyclic A&P
22:41production will start to rise protein
22:44kinase a production will start to rise
22:47increase phosphorylation of myosin
22:50light-chain kinase will increase and now
22:53the ability to cause smooth muscle
22:56contraction is inhibited so now what
22:58happens to this crossbridge formation
23:00there's not gonna be any phosphorylation
23:02of myosin there's not going to be any
23:04cocking and pulling or any of those
23:05reactions so because of that you get
23:08smooth muscle relaxation and that cool
23:17and that the smooth muscle relaxants
23:18what happens to the blood vessel it
23:20dilates so these kind of have like a
23:22little dual function they can inhibit
23:24platelet activation and aggregation as
23:26well as causing smooth muscle dilation
23:29so that is one of the beautiful things
23:31about these medications so there's a
23:33couple groups of medications that i want
23:34you guys to remember big one aspirin
23:37this is a really really important one
23:40okay second group is your antiplatelet
23:44medications particularly they call these
23:46themö pyridine derivatives okay don't
23:49worry about that I just want you to
23:50remember clopidogrel
23:51pursue 'grill Tyco haggler de clippety
23:53okay
23:54those are your adb receptor inhibitors
23:57your GP to be 3a inhibitors is ab 6mm
24:01Tyrel 5n and f2 v tide and the last one
24:05that i want you to remember which is
24:06your PD
24:07three inhibitors which helps to inhibit
24:08platelet activation as well as cause
24:11smooth muscle relaxation via
24:13vasodilation is selasa zahl and diaper
24:16animal okay so we covered their
24:17mechanism of action we covered what
24:19groups there and now let's talk about
24:20what we use them for all right guys so
24:23now that we talked about the mechanism
24:24of action and how it's basically
24:26designed to inhibit clot formation
24:28that's one of the big things is that
24:30it's thrombo embolic basically anti
24:33thromboembolic okay so we're trying to
24:35be able to prevent that so what are some
24:37different thromboembolic conditions that
24:39we have to protect these people from and
24:41that's why they should go in these
24:42medications well one of the big big big
24:46ones that you guys got to remember is
24:48acute coronary syndrome now if you guys
24:50remember acute coronary syndrome we can
24:52actually break down into three
24:54components right so we call it acute
24:56coronary syndrome or ACS we have
24:58unstable angina we have in STEMI and we
25:07have STEMI okay so unstable angina and
25:11stemming which is your non-st segment
25:13elevation myocardial infarction and
25:15STEMI which is your ST segment elevation
25:16myocardial infarction these medications
25:20are commonly utilized in ACS but more
25:24particularly a combo usually you're
25:27giving something like aspirin plus
25:31something like maybe clip it a grill or
25:36prasugrel or you're giving something
25:40like Tyco a girl or and in rare
25:45situations you might use something like
25:46a GP to b3a inhibitor specifically like
25:50AB 6m AB okay but really the only time
25:55where you're really going to want to use
25:57this one as if the patient has are
25:59extremely high risk so what I mean you
26:02might be used this to the patient's like
26:04greater than 75 so like okay well here
26:06we write down a couple reasons if
26:07they're greater than 75 if they're a
26:09diabetic if you see ST segment changes
26:14ST segment deviations on the EKG if you
26:17see really height rope levels
26:20if they have if you do an echo and their
26:23left ventricular ejection fraction is
26:25like less than 40 percent or if they
26:29have a lot of pulmonary edema okay then
26:33that would be reasons of why you want to
26:35use that six and that the reason why you
26:37don't give up six amount commonly for
26:39people who are going to be getting PCI
26:41because they have it acute in mine is
26:43because it has a very high bleeding risk
26:45okay you got to remember that the GP to
26:48be three inhibitors have the highest
26:50bleeding risk next thing how would I
26:53determine which one to use between
26:55clopidogrel pursue grow and Tyco haggler
26:57all right so with utilizing these
26:59medications and knowing which
27:01combinations to give to these patients
27:02whenever they're having an acute
27:03coronary syndrome it comes with kind of
27:06learning about the clinical scenario so
27:08and also their bleeding risk you got to
27:10remember their level of potency okay so
27:13when we talk about these starting with
27:14the most potent at one ab six a map is
27:18extremely potent as a high bleeding risk
27:21okay so all of your GP to b3 inhibitors
27:24are gonna be extremely potent the most
27:25potent the second one is going to be out
27:28of these pursue growth so it actually
27:30has a blackbox warning and you got to be
27:32careful because of its bleeding risk
27:34after that you have Tyco a girl or and
27:38then after that you have clopidogrel and
27:43some will even say that these are pretty
27:45much equal and in that ability but then
27:47the last one here which has the least
27:49amount of bleeding risk is aspirin so we
27:51have to realize here when we're talking
27:52about potency if you have someone in a
27:55cute coronary syndrome they're not
27:57extremely complicated other words not
27:59greater than 75 they're not a diabetic
28:01they don't have chest pain that's been
28:02lasting for more than twenty minutes
28:04they don't have any ST segment
28:05deviations the tropes aren't super
28:08elevated they're left ventricular
28:09ejection fraction isn't super low they
28:11don't have any pulmonary edema you don't
28:13really need to give up six in that okay
28:15well then what about the other ones
28:16pursued rule again you got to be careful
28:19whenever you're giving this medication
28:20it is a high bleeding risk so you're
28:22going to want to chance that now so we
28:24don't really do that one unless we
28:25absolutely need to it comes down to
28:28really complete Capital Grille and Tyco
28:30haggler these are kind of more commonly
28:32utilized ones
28:33okay tyke Aguilar is a little bit more
28:35effective and more utilize a little bit
28:37more just because there is the risk with
28:39clopidogrel of what's called TTP we'll
28:41talk about that also with Capital Grille
28:45another thing you have to be careful of
28:47is that there is certain individuals who
28:50are poor metabolizers so they have
28:52what's called a cyp2c19 mutation they're
28:56poor metabolizers of Capital Grille and
28:58in those situations pursue grow or tyke
29:00a grower would be the more likely option
29:02so ACS is going to be one indication and
29:06it's usually a combo what else well so
29:10again if someone has an acute coronary
29:12syndrome any of these things so any
29:14blockage so if they're having any type
29:16of thrombus which is including the
29:19myocardium this is going to be a good
29:21good and good drugs to give another
29:25thing that we want to remember is that
29:26these are usually medications that you
29:28can give pre and post ACS so you can
29:31give these medications both pre so we
29:34talked about giving these medications
29:35pre PCI so in other words before they go
29:40to the cath lab and they get angioplasty
29:42they balloon up the vessel and they're
29:44good post PCI okay
29:48and again it's usually a combo of
29:50aspirin and something else more likely
29:53than not it's aspirin and clopidogrel
29:54long term aspirin and Tyco a girl or for
29:58the pre PCI and then super needed
30:00situation aspirin in that six of Matt if
30:03needed pre PCI but usually post PCI a
30:06spring clip integral okay what about
30:09some type of CVA so certain situations
30:13where there's actually blood clots that
30:15are actually going to be going to
30:16different types of structures within the
30:18brain that could be another indication
30:20for givingness so again remember that
30:22cerebrovascular accidents this is also a
30:25good combo to give on things like
30:28aspirin and things like Klaipeda Grill
30:33another important thing here with CVS is
30:37sometimes if someone is getting a stent
30:39in the carotid artery so another thing
30:41to remember about is if someone's
30:43getting what's called carotid
30:45artery stenting you can actually give
30:50aspirin and clopidogrel you can give it
30:55pre and sometimes even post carotid
30:58artery stenosis okay so it helps with
31:00that process so if someone has a CVA or
31:03post CVA ask for a nickel pretty girl or
31:06good combinations to give if someone's
31:08getting carotid artery stenting where
31:10they're putting a little stint into the
31:11carotid artery it's also good to have
31:13these anti thrombotic agents as well
31:15okay another thing is if someone has
31:19already had an mi all right let's say
31:22that they have already had an mi they
31:24have heart failure something of that
31:25nature right there's also some risk
31:28sometimes so sometimes if someone has a
31:30already have been diagnosed with
31:32coronary artery disease okay so someone
31:35has already been diagnosed with coronary
31:37artery disease it's been shown that
31:38aspirin has the ability to reduce the
31:42significance of any other comorbidity so
31:44aspirin is also a really good indication
31:45for individuals with chronic coronary
31:48artery disease and it's just good
31:50prophylactic treatment so prophylaxis so
31:54basically preventing them from having
31:55another myocardial infarction or another
31:57CVA okay another really interesting
32:01indication for these medications
32:03specifically aspirin is in certain
32:06individuals who get what's called giant
32:08cell arteritis you know there's a vessel
32:13here called the temporal artery and what
32:15happens is the temporal artery it gives
32:18off some different branches so you have
32:20the Tim poor artery which can actually
32:23supply it parts of the forehead right
32:24the temples and but it also has these
32:27branches off the internal carotid artery
32:29called the ophthalmic artery and you
32:31also have vessels that are going to the
32:32muscles of mastication in certain
32:34situations people with giant cell
32:36arteritis if they have inflammation of
32:38those vessels they call it a vasculitis
32:40and you got to remember that vasculitis
32:42is a risk factor for developing clots
32:44and sometimes it can cause clots that
32:47develop within the ophthalmic artery or
32:50clots that develop within the vessels
32:51going to the mouth right to the jaw
32:53muscles and this can cause jaw
32:55claudication it can cause even
32:58vision loss and a lot of pain on the
33:00temporal region so a good medication
33:03that they give to individuals to prevent
33:05them from actually you know having some
33:07of these symptoms is aspirin
33:10so aspirin is another good medication
33:13that's utilized for peace by patients
33:14with giant cell arteritis so we have
33:17acute coronary syndrome
33:18whenever someone's having it in line and
33:20they're going to PCI post PCI we talked
33:22about that CVA same thing a spring clip
33:26integral whoo one thing I remember when
33:29because we don't give if people having a
33:31stroke
33:32within the first three to four and a
33:34half hours we don't give aspirin and
33:36clopidogrel it's after that time what do
33:38you give generally before the three to
33:39four and a half hours you give TPA so
33:42you got to remember that this for the
33:43CVA stuff it's actually particularly
33:46when it's greater than three to four and
33:48a half hours okay that's when you're
33:51really actually giving someone aspirin
33:53and clopidogrel combination so I want to
33:55make sure that we're perfectly clear on
33:56that okay
33:57giant cell arteritis again we talked
33:59about it syndication and if someone has
34:01diagnosis of coronary artery disease and
34:03it's a chronic condition you give them
34:05this aspirin to prophylactically prevent
34:07them from having another heart attack or
34:09having any other type of cardiac event
34:10okay another indication sometimes
34:14aspirin and clopidogrel can be used for
34:16PA D but remember there was a nice drug
34:19we talked about remember with PA D you
34:22have vessels here that run through the
34:23legs right okay and sometimes what can
34:27happen is they can actually develop
34:31plaques or thrombi or maybe different
34:34types of clots that can develop within
34:36these vessels and that includes the
34:38blood flow to the surrounding tissues
34:39it's like it's such as the muscles into
34:41the feet what can happen as a result of
34:43that you can get ulcers around that area
34:45of the body you can start getting a lot
34:47of what maybe even gangrene okay because
34:51you're not getting enough oxygen and
34:52nutrients to the tissues and so they
34:53start dying what else the muscles need
34:56oxygen order to contract so you can get
34:58tightness and pain within those muscles
34:59they call that claudication so this is
35:02common symptoms of someone who is
35:04struggling with what's called peripheral
35:06artery disease or PA D peripheral artery
35:09disease
35:11when we give medications we can give
35:13medications like aspirin
35:14so aspirin has a good medication to give
35:16to someone with peripheral artery
35:17disease but what else is another
35:19medication that we can give guys we
35:20already talked about its elasticity mall
35:24so I lost is also lost is always going
35:26to be a big one okay that is the more
35:30commonly utilized one so selasa is all
35:32and aspirin are good medications to give
35:34to patients with peripheral artery
35:36disease beautiful thing right what's
35:39super interesting and I found extremely
35:41interesting when I was actually doing
35:42some research is that aspirin has a
35:46prophylactic protection from colorectal
35:48cancer so whenever you're giving
35:51somebody aspirin they've shown that this
35:55can actually decrease the risk of
35:58colorectal cancer particularly a type of
36:02colorectal cancer called Lynch syndrome
36:04and if you guys know a little bit about
36:06Lynch syndrome it's basically a tumor
36:09that can actually form within multiple
36:11tumors that form with the multiple areas
36:12of the body like colorectal endometrial
36:14ovarian renal pancreatic so a lot of
36:18different things can happen with this
36:20and there's very different variants like
36:21Turco syndrome and Gardner syndrome so
36:24again they've shown that aspirin has the
36:27ability to decrease the risk of
36:28colorectal cancer significantly okay the
36:31last thing I'm going to talk about we're
36:32not gonna go into a ton of detail on it
36:34but diaper rhythm all remember I told
36:37you that it causes vasodilation right
36:38they use it as a specific test so I'm
36:42people who have maybe coronary artery
36:44disease and you want to diagnose it they
36:46do stress testing right so they do
36:48stress tests to see how good the
36:50perfusion is to the myocardium so you
36:52have them exercise well in certain
36:53individuals where they can't exercise
36:55for whatever reason they give them a
36:57drug called diaper animal and what
36:59diaper animal does is is it dilates the
37:01vessels going to the myocardium so that
37:03you can see the perfusion on the imaging
37:06techniques that you're utilizing but it
37:08increases the blood flow through the
37:09normal vessels but not very much through
37:12those actual fixed or stenotic vessels
37:14so that's why diaper animal is also good
37:16for stress testing if you wanted to
37:18remember that as well one of the big
37:20things with all these drugs is that some
37:22people say what about knowing the dosage
37:24is important but you know you can always
37:27look those things up and it's important
37:29to make sure that you do look those
37:30things up so that you don't make a
37:31mistake whenever you're giving someone
37:33the medications obviously knowing
37:35someone who is having some type of acute
37:38coronary syndrome is important to know
37:39that you should give them 325 milligrams
37:41of aspirin have them chew it and then
37:43swallow it but more for your daily
37:46prophylaxis it's more along the lines of
37:48like 81 milligrams per day clopidogrel
37:52the big thing that you should know
37:54dosage wise of this one is if you are
37:56giving it to someone who's going to be
37:57going to get a PCI or some type of
38:01carotid artery stenting or they have had
38:03a CVA that's been greater than this is
38:04the period of you know three to four and
38:06a half hours then you can give a loading
38:08dose of 300 milligrams and then from
38:10that point on you give them 75
38:12milligrams every day but what I want you
38:14guys to remember is that these
38:16medications are basically designed to be
38:19able to prevent from what conditions or
38:20treat acute coronary syndromes CVAs
38:24outside of the range of receiving TPA
38:26people who are going to be getting
38:28carotid artery stenting or they're
38:30utilizing this basically as an adjunct
38:33to stenting CA D prophylaxis preventing
38:36them from having another myocardial
38:37event again aspirin for giant cell
38:40arteritis which is at a particular type
38:42of vasculitis pa D the good ones so
38:45losses all and decreases the risk of
38:47colorectal cancer significantly and
38:49again diaper at a mall it's used for
38:51specific types of cardiac stress tests
38:53to look at myocardial perfusion imaging
38:55alright so those are the indications of
38:57these medications alright guys so let's
38:59talk about the last two things here
39:01which is going to be the adverse drug
39:02reactions that can happen sometimes
39:04whenever you're taking these medications
39:05you got to be you know you got to watch
39:07out for as a clinician it's important
39:09for us to be able to recognize what is
39:11some normal side effects but what are
39:13the things that we don't want to miss so
39:15when you're putting people on these
39:16medications these antiplatelet
39:17medications there is a couple things
39:20that we do really have to be aware of
39:21and we have to watch out for so you have
39:25to think about these things one of the
39:27big things that you want to watch out
39:28for is you're putting some people on
39:29antiplatelet medications anti thrombotic
39:32medications you're trying to stop blood
39:34clots so sometimes if maybe you receive
39:37too much of the then
39:38you give them too much of the medication
39:39or they have some type of just severe
39:41adverse drug reaction where there are a
39:43rapid metabolizers of the drug they can
39:46have excessive bleeding and we want to
39:49watch out for that so what are some of
39:50the things that we could see that
39:52actually elude us - oh they might we
39:54might have them on too much of this
39:55medication we got to watch out we got to
39:56discontinue this medication so things
39:58like this would be bleeding bleeding
40:01from orifices are bleeding into the
40:02surfaces of tissues so one of the big
40:05ones that you got to watch out for is if
40:07someone is bleeding from their nose what
40:08do you call that epistaxis right so you
40:11want to watch out for what's called
40:13anterior epistaxis so that could be one
40:18type of indication it's letting you know
40:20oh they might have there might be
40:23bleeding too much and I need to
40:24discontinue this medication one is if
40:28they're bleeding from their gingiva from
40:30their gums so what if somebody shows
40:31signs of gingival bleeding so you start
40:33seeing bleeding from their gums okay
40:37that could be an indication so if you
40:38see gingival bleeding that could be an
40:44indication saying move they might be on
40:47too much of this medication we got to
40:48discontinue what if you see little
40:51pinpoint bleeding like little dots
40:53little pinpoint hemorrhaging little
40:56suckers on the skin what could that be
40:59indicative of they call this petechiae
41:02so if you see petechiae eye or you see
41:06very large types of heme pinpoint
41:09hemorrhaging that could be indicative of
41:11some type of purpura or maybe they're
41:14really large bruising and that could be
41:16ecchymosis so if you start seeing a lot
41:18of bruising on the skin
41:20petechia preparer ecchymosis that could
41:23be indicative or if there's blood that's
41:26actually coming out through their mouth
41:28hole right so if there's someone is
41:31actually vomiting up blood so if they
41:33have um if someone is having hematemesis
41:39right that could be an indication so
41:41someone's vomiting up blood or they're
41:45having Malena so they're having blood
41:47coming out through their stool maybe
41:49it's a dark type of blood
41:51and that could be indicative of an upper
41:53GI bleed or maybe it's bright red blood
41:56which is called hematochezia and that
41:59could be indicative of maybe a lower GI
42:01bleed so those are things that we want
42:03to watch out for okay another thing is
42:07that sometimes there could be excessive
42:09vaginal bleeding or uterine bleeding so
42:12we would want to watch out for any type
42:13of abnormal vaginal or uterine bleeding
42:16so these are some of the things that we
42:19want to be aware of when patients are on
42:21these medications look for any signs of
42:23bleeding sometimes you might not have
42:25any blood that's visible so what should
42:27you do if someone you think is on this
42:29medication they might be bleeding they
42:31have iron deficiency anemia whenever you
42:33take their a CBC go ahead and do a
42:36hemoccult okay so check to see if there
42:38is any blood inside of the stool as well
42:40again so whenever someone's on these
42:41medications do a very good physical exam
42:43look at their oral cavity look at their
42:45skin look just ask if they've had any
42:47recent nosebleeds ask if they've had any
42:49dark stools if they vomited up any blood
42:50do a hemoccult
42:52check a CBC ask if their periods have
42:54been heavy have they had any bleeding
42:56after sex anything like that is
42:57important to make sure that we look for
42:59that stuff the big thing that I really
43:03wants you guys to be aware of and you
43:04have to be careful of whenever you're
43:06putting someone on things like
43:08particularly clip integral and another
43:10one called tickle pitting that's why
43:12they don't use tickle budding as much
43:14anymore but clopidogrel you also have to
43:16be careful of with this one it's called
43:18TTP so you have to watch out for what's
43:21called T T P thrombotic thrombocytopenic
43:27purpura so what happens in this
43:32condition basically you have platelets
43:35right and what these platelets do is
43:38they're designed to be able to stick
43:40with the von Willebrand factor that's
43:42basically stuck in that collagen
43:44meshwork so let's go ahead and draw some
43:46von Willebrand factor molecules what
43:49happens is here's your von Willebrand
43:50factors here these little pink guys
43:52right now normally von Willebrand
43:54molecules are these little monomers
43:56they're just one little single protein
43:58but what can happen is they can actually
44:01start fusing with one another and this
44:03is a normal physiologic process
44:04where they confuse with one another and
44:06they can go from a monomer to a multi
44:10mer okay and you have a specific enzyme
44:15thank goodness that basically prevents
44:18this from happening and breaks these
44:20multimers down back into monomers okay
44:23and that enzyme is called atoms T 13
44:27it's called atoms T 13 so this enzyme is
44:34designed to be able to stimulate the
44:36multi more break down into monomers
44:37that's important but in certain
44:41situations there might be a decrease of
44:46atoms T 13 what could be an indication
44:48of that what could be a reason
44:50antiplatelet medication such as
44:51clopidogrel to Khloponin it could even
44:54be a conditions like lupus or some
44:57sometimes a radiotherapy meta
44:59chemotherapy medications like gem try
45:01said threatenin Jen try Center beam
45:03cyclosporine some of those medications
45:05could also be reasons why there's a
45:07deficiency in this enzyme if that enzyme
45:10can't break down the multi mer into
45:12monomers what happens they just
45:13auto-populate and guess what they do
45:15guess what loves to stick to von
45:17Willebrand factor platelets and so then
45:20what do you get you'd get this huge
45:23platelet mess here and all these
45:26platelets start sticking to these
45:28multimers and what happens then the
45:31platelets start getting consumed but
45:33they start forming lots of clots so two
45:36things happen as a result of this you
45:38get a decrease in platelets they start
45:40getting consumed because you're making
45:42tons of clots so you're get an increase
45:47in clots because these multimers of von
45:50willebrand factor are binding tons of
45:52platelets and you're getting big clots
45:53but you're using so many of the
45:55platelets that you have a decrease in
45:57platelets so thrombocytopenia along with
46:00widespread clotting this is TTP and
46:03that's what you got to be careful of so
46:05what are some of the signs that if
46:06someone's coming in with you have to
46:08make sure that you recognize it and
46:09treat them accordingly if someone's
46:11coming in and have a fever okay so if
46:14they're fib Rao if anybody comes in and
46:16they're presenting with a fever
46:18that would be an indication okay maybe
46:21it's greater than 100 point 4 degrees
46:23Fahrenheit right or you get a CBC and on
46:29that CBC it shows signs of hemolytic
46:32anemia okay because again you're also
46:36within this process you're gonna start
46:38having red blood cells come through this
46:40area so there's also gonna be breakdown
46:42if your red blood cells hemolytic anemia
46:43so you'll be able to see that whenever
46:45you check because when the of these red
46:47blood cells are busted open you're get
46:49an increase in what's called LDH and
46:52enzyme inside of the red blood cell
46:54you get an increase in bilirubin which
46:56is a component of hemoglobin and there's
46:59another enzyme that loves to bind to
47:01hemoglobin and whenever hemoglobin is
47:04released onto the blood this enzyme once
47:06this protein binds to it and that's
47:08called half de globin so the amount of
47:10free haptoglobin will go down because
47:13it's bound to hemoglobin instead of free
47:15okay
47:16the other thing is you're using up your
47:18platelets so the platelets are going to
47:20decrease you're gonna thrombocytopenia
47:23another thing is that there's going to
47:26be damage to the kidneys so there can be
47:28renal insufficiency if there's kidney
47:31damage the ability to excrete out things
47:34like creatinine and a lot of blood urea
47:37nitrogen products decreases so what
47:39happens to that there's an increase in
47:41creatinine there's an increase in the bu
47:44n if you take and do a BMP and on top of
47:49that there's also certain types of
47:51neurological damage so they start might
47:53start experiencing things like headache
47:55they might have things like confusion
47:58okay and that's some of the things that
48:00we have to watch out for as well okay
48:02you can remember this through the
48:03montana monic that are in fat RN so fat
48:09RN you remember fever anemia
48:12thrombocytopenia renal insufficiency and
48:15neurological damage okay when someone
48:19has this what do you treat them with the
48:21best thing to do is to do what's called
48:24plasmapheresis okay and what
48:27plasmapheresis is is you're basically
48:28taking out all of these different types
48:30of structures that are in
48:32side of the blood and cleaning the blood
48:34okay so you're gonna do plasmapheresis
48:37they can also do what's called steroids
48:39cortical steroids and the reason why is
48:41we're trying to reduce the inflammatory
48:43response and sometimes they can use
48:45other medications like rituximab and
48:48again we'll talk about that in another
48:49video when we specifically go into it
48:50but right now if you notice it you got
48:53to treat it
48:53plasmapheresis steroids those are
48:56usually the main treatment
48:57contraindications to utilizing these
48:59medications there's a very very
49:02important one G you got to remember if
49:05the kid comes in the basically they say
49:09anything less than 19 years of age so
49:11less than 19 years of age the kid comes
49:16in less than 19 years of age and they
49:18have a fever you never give them aspirin
49:22okay you never give them aspirin and you
49:24want to make sure that the parents know
49:26that as well the reason why is and again
49:29the mechanism isn't completely like rock
49:31solid but this is what they think inside
49:34of your liver you have mitochondria
49:37right and the mitochondria are
49:39responsible for taking free fatty acids
49:42and breaking them down through a process
49:45called beta oxidation into what's called
49:47acetyl co a and then acetyl co a goes
49:51through the Krebs cycle and it generates
49:54some molecules like nadh fadh2 all these
49:59little suckers and that stimulates the
50:02electron transport chain to make ATP
50:06well what they know is is that there's
50:10two things one is when someone takes
50:12salicylates it's actually metabolized by
50:15specific enzymes in the actual
50:18mitochondria and their metabolites can
50:20actually affect this process of fatty
50:23acid oxidation so here's what I want you
50:25to remember so if someone is actually
50:27taking aspirin alright
50:31dope taking absorbed it has the ability
50:35to alter the metabolism of these free
50:39fatty acids so the metabolites so the
50:41metabolites
50:43of the aspirin has the ability to
50:46inhibit the free fatty acid oxidation
50:48process okay so that means what less
50:51acetyl co a less nadh less fadh2s and
50:55less ATP well guess what if someone is
51:00infected let's say that they have a
51:01virus okay let's say here we have a
51:04virus whenever someone is infected these
51:11viruses have the ability to increase the
51:15actual metabolism of these South's iliac
51:19salicylic acid metabolites so there's
51:21going to be more metabolites of aspirin
51:23whenever someone is having a viral
51:26infection so this virus has the ability
51:28to potentiate and increase the number of
51:30salicylic acid metabolites that means if
51:33you have increased salicylic acid
51:34metabolites you have increased
51:36inhibition of free fatty acid metabolism
51:38less acetyl co a metabolism less NADH is
51:42in left
51:42LS fadh2s and less ATP if you don't have
51:47ATP with inside of this cell what
51:49happens all the functions of the cell
51:51start to decrease in this cell will
51:54start to die its ability to perform its
51:56functions will decrease what is one of
51:58the big things that the liver does it
52:00filters out different types of toxins
52:03you know there's a process where you
52:05take amino acids and you rip off a
52:09specific molecule called ammonia and
52:11ammonia is supposed to go through a
52:14process inside of the mitochondria
52:16called the urea cycle okay well if the
52:20liver is failing are you gonna be able
52:24to metabolize that ammonia no what
52:27happens to the ammonia then it starts to
52:29increase in the bloodstream as ammonia
52:32levels increase in the bloodstream it
52:34actually moves its way into the central
52:36nervous system and affects little cool
52:38little cells here called astrocytes and
52:41it actually gets inside of the
52:43astrocytes okay and binds with a
52:47molecule called glutamate and turns into
52:48glutamine and this causes the astrocytes
52:52to become osmotically active and pull a
52:54lot of
52:55water into them and they start to swell
52:58what can this result in this can result
53:01in encephalopathy in cephalopoda which
53:08it will show up as signs as maybe
53:10vomiting then they can then progress
53:13maybe to fatigue and then maybe they'll
53:17progress from there into seizures and
53:20maybe even into a coma as well as till
53:24they can have delirium as well so when
53:26someone has a fever particularly maybe a
53:29viral infection they're less than 19 you
53:32give them aspirin you're gonna lead to
53:34this liver damage that liver damage will
53:37result of increased ammonia hyper M
53:39anemia which result in encephalopathy so
53:42what is the Triad you have a patient who
53:45has a febrile illness liver failure or
53:48liver damage how will you determine
53:49liver damage
53:50what's the markers whenever the livers
53:53damaged it releases ast alt all of these
53:58will be increased as well right so
54:00you'll have signs of liver damage you'll
54:02have vomiting fatigue seizures delirium
54:05coma signs of encephalopathy and a
54:07patient less than 19 years old with a
54:09fever what do they call this they call
54:11this Reye's syndrome so this is a
54:13contraindication you do not give
54:15somebody who is less than 19 with a
54:20febrile illness aspirin okay that's one
54:25of the contraindications another thing
54:29that we have to talk about really
54:30briefly here is what are some other
54:32reasons why you would not want to give
54:34someone some of these anti thrombotic
54:35agents what if they already have really
54:38low platelets so what if their platelets
54:41are extremely low especially one of the
54:43big ones is AB 6 map your GP to be 3a
54:48inhibitors they really can drop down
54:50your platelets so if someone has less
54:52than a hundred thousand platelets you do
54:54not give them GP to b3 inhibitors so it
54:57can cause thrombocytopenia so you don't
55:03want to give someone these drugs if they
55:05are extremely thrombocytopenic
55:07especially like less than
55:09100,000 platelets per centimeter cubed
55:12of blood millimeter cubed sorry another
55:16reason what if someone has
55:18uncontrollable hypertension so their
55:20their actual blood pressure their
55:21systolic blood pressure is extremely
55:23high that's one reason another reason
55:25why is is because with high blood
55:28pressure there's risks of tearing
55:30through that Tunica intima layer and
55:33whenever you do that what can that cause
55:35that can cause a ordered dissections so
55:39then with this happening if someone has
55:41uncontrolled hypertension and they have
55:44a ordered dissection a history of aortic
55:46dissection they're at high risk of
55:48bleeding if you give them any of these
55:49medications so be careful if someone has
55:52a history of an aortic dissection or
55:55they have uncontrollable high blood
55:58pressure well that's another reason why
56:00you wouldn't to give this if they're
56:01already bleeding if someone has maybe a
56:04perforated peptic ulcer so what if they
56:07have a perforated peptic ulcer or some
56:09type of GI bleed all right so this could
56:11be a problem if someone is having a GI
56:13bleed whether it be an upper GI bleed or
56:16be a lower GI bleed or if someone's
56:19having an intracranial bleed so if
56:22someone's having some type of
56:23particularly maybe like a subarachnoid
56:25hemorrhage you don't want to give them
56:26that medication or if there's some type
56:29of trauma so maybe they were stabbed or
56:33maybe they went under the knife for some
56:35type of really intense surgery that's
56:37another indication of where you're not
56:38gonna want to give this medication all
56:40right so that should cover all of the
56:42things that we should need to know about
56:44antiplatelet medications I engineers in
56:47this video we talked about antiplatelet
56:48medications I hope it made sense I hoped
56:50you guys did enjoy it if you guys did
56:52please hit that like button comment down
56:54in the comments section please subscribe
56:56also as a reminder please go check out
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57:00down in the description box or it's the
57:02great courses plus comm slash an
57:04engineered science they have a lot to
57:06offer and it can definitely further your
57:08knowledge of multiple different topics
57:09so go check that out
57:10as always ninja nerds we love you and
57:13until next time
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