How to put a downloadable pdf on squarespace

This gives journalists some quick background info for short mentions but also provides deeper insight for more in-depth articles. OptinMonster presents some basic facts in the form of a webpage and outlines some of its staff members.

They also list some of the different areas of their press kit, including press releases and other media coverage. Reporters can get stats for the site in real-time. HappyFox puts their logo and wordmark right at the top of their press kit page so they are easily found by users.

Squarespace opens with its most recent press coverage. They then offer tabs in their navigation bar that let people download press releases and images or get brand and logo guidelines.

For journalists feeling out a story idea about their company, the details on this page offer a lot of insight into advances within the company. There are also links to learn more about the company and to get images and contact info. Starry has a page dedicated to members of the press looking for information on their brand.

This internet service startup company has a kit you can download, but they also list an email address in case you have additional questions. Under the kit, linked are press releases ordered from newest to oldest. Take a look at how Worldwide Supply draws interest. They have two columns: one with press releases and one with mentions of them in the news.

Evernote does a good job of adding a headline for press people and explaining the purpose of their page. There is no confusion over what people will find in the digital press kit on this page.

Zendesk creates an interactive experience for their press kit. As the user clicks on animated text, they are taken to a new page with more information.

The press site is engaging for users. Treehouse offers its press kit in an easy-to-download PDF document. Embedded links take you to their resources, such as logos and images.

Mailchimp places everything on a single page, including some loose guidelines to using their images and brand name.

Close does something kind of unique with their online press kit by offering screenshots to show examples of their logos and name in use.

Visitors can also download a logo page with files in both PNG and EPS formats, which work for both online publications and printed materials.

Dropbox starts their online press information with a listing of their appearances in the news. Bench offers a list of news and press releases. However, they also place a reminder at the top that they are happy to work with reporters on stories about Bench and invite them to contact the brand for more information.

This provides an opportunity for a customized press kit for each journalist. Intercom offers assets at a glance by placing logos to the right of the download link. Who actually needs prophylactic anticoagulation? You may find yourself here when deciding to give prophylactic or therapeutic doses of an anticoagulant. It's pretty much impossible for me to give you a clear answer. Like most other things in medicine, it's a gray area with wiggle room for clinical judgement. There's also room for common sense here.

If you have a cancer patient with a history of DVTs that presents to the ER with a GI bleed, prophylactic anticoagulation probably shouldn't be on your immediate "to do" list.

In some areas, it's common to perform a thromboprophylaxis risk assessment to help guide the decision on prophylaxis or not. Here's a helpful sample calculator to give you an idea of what criteria goes into the decision. Another point to mention is that the doses we use for prophylaxis are usually but not always much lower than the doses we use for treatment.

This changes the need for monitoring we almost never monitor prophylactic dosing. In some of the cases above, patients will get full therapeutic dosing of anticoagulants as prophylaxis. Often times, this is used as secondary prevention after a clot has developed. But not always. As an example, cancer patients with any history of DVT or PE usually require lifelong prophylaxis with therapeutic enoxaparin.

Another example is any patient on warfarin therapy there isn't really a "prophylactic" dose of warfarin. So here you'll see patients with a-fib, APS, mechanical heart valves, and the like. So just think of prophylaxis on a case by case basis. Assess the risk factors for clotting, as well as the bleed risk for the patient.

As a quick disclaimer, before moving on to the reason you're reading this article. All of the following medications have a potential side effect of bleeding. They're anticoagulants. It's just what they do. They don't wanna hurt nobody but a bee has got to sting. I'm going to cover the most important pharmacology and therapeutic info below. But again, I'll stop just shy of providing dosing which in some cases is going to be institution-specific anyway.

It's loaded with common doses, dosing adjustments, clinical pearls, and a whole lot more. Unfractionated Heparin UFH is one of the oldest and most widely used anticoagulants. It binds to and activates antithrombin III. So what is antithrombin III? It floats around your blood and inhibits thrombin Factor IIa and Factor Xa from propagating the coagulation cascade.

That's pretty easy to remember, right? Antithrombin inhibits thrombin. So here's the thing with heparin. Its kinetics are horribly unpredictable. It seems to affect everyone a little differently, and the only way for us to get around this is by monitoring. But you may come across some that monitor the anti-Xa level.

Whether aPTT or anti-Xa is more accurate is actually the subject of ongoing debate. It seems like you can safely use either. However, at least at the time of this writing, aPTT is used more commonly.

So use that as your launching point for test questions while you're in pharmacy school. When used for treatment usually dosed IV , heparin is very closely monitored.

It is usually given as a continuous infusion and the aPTT or anti-Xa levels are monitored every 6 hours. I have never seen this in practice, and I strongly suspect you won't run into either. But at least you know there's labeling for it now. Practicing Pharmacists: If you have used the subcutaneous treatment dosing of heparin in your practice, please email me at mail tldrpharmacy.

I'll update this article with the knowledge you drop my way. Despite the erratic kinetic profile, heparin is still a drug of choice in a lot of situations for treatment or prophylaxis.

It has a very short half life, and heparin can be used in any stage of renal failure including dialysis. That's an important fact, because many of our other anticoagulants cannot be used in the later stages of renal failure. Another benefit of heparin is that it has an antidote; protamine sulfate. Protamine has a max dose of 50 mg. It's also derived from fish, so it should be used with caution or avoided altogether in patients with a fish allergy.

Heparin has a number of "weird" side effects that you wouldn't necessarily think about for an anticoagulant. For starters, it can actually block the synthesis of aldosterone , which basically makes it an aldosterone antagonist. As you might suspect, this can lead to hyperkalemia. Through an unknown mechanism, heparin also seems to increase osteoclast activity, and decrease osteoblast activity. So you can end up with osteoporosis after prolonged use.

Heparin: Origin Story Image. Heparin is porcine in origin. So if your patient has a pork allergy or even if they prefer to avoid pork products for cultural or religious reasons then you need to look elsewhere.

In the case of pork allergy, administering heparin can lead to anaphylaxis. As the name implies, HIT is a situation where your platelet count drops in response to heparin therapy. HIT Type I , for all intents and purposes, is the "better" one to have if you're the patient. It's also known as heparin "associated" thrombocytopenia. It's a transient, usually mild drop in platelet count that happens within the first couple of days of initiating heparin. Platelets rarely drop below k, and the effect is reversed within 3 or 4 days after stopping heparin.

There's actually a group of clinicians proposing to change the name from HIT Type I to "non-immune heparin associated thrombocytopenia" to reduce the confusion between Type I and Type II. This time, there's an immune response associated with the drop in platelets. Effectively, heparin binds to your platelet and undergoes a conformational change that makes it immunogenic. Your immune system doesn't like this, so it goes to the scene to bust up the offending platelet like a bouncer at a night club.

Your platelet counts will drop accordingly. But in a weird twist, your immune system actually activates the platelets before it clears them out. So, ironically, even though platelet counts are dropping, patients with HIT Type II are at risk for developing clots pretty much any and everywhere in the body.

This article does a nice job at summing up the pathophysiology. This reduction in count should also coincide with heparin administration. So if the patients platelets were k on Monday, then heparin was started and the patients platelets were k on Wednesday, that's the beginning of a HIT diagnosis. It's not the full HIT diagnosis of course.

You also want to evaluate if there are any thromboses or any other reason for thrombocytopenia maybe the patient just received chemotherapy? Since HIT Type II is immune mediated, we would also run an antigen test to confirm the presence of heparin antibodies. Obviously, you don't wait around for the results of HIT antigen testing to intervene clinically here.

In the acute setting, you'll usually transition the patient to either fondaparinux or argatroban I'll have more on each of them below. Once you're gearing up for a transition to the outpatient world, you can use pretty much any oral anticoagulant on the market.

Warfarin , or any of the NOACs are a fine choice here though it is recommended to wait until the platelet count recovers before initiating. If the HIT antigen test comes back negative, you could consider rechallenging with heparin depending on your institution's protocol and everyone's comfort level with re-challenging. These all end in the suffix "-parin. But for the sake of completeness, there is also dalteparin and tinzaparin.

As the name implies, these are low molecular weight versions of heparin. But something weird happens with the smaller size of LMWH. But it inhibits Xa a lot more. For starters, the kinetics are much more predictable. Unlike heparin, LMWH is pretty consistent with its anticoagulation effect. The upshot of this is that we don't routinely need to monitor levels even with therapeutic dosing.

I italicized "routinely" above Namely, we might monitor in renal disease like heparin, LMWH is renally cleared , extremes of body weight because it's not extensively studied in very under or overweight patients , and pregnancy because you just have to be careful in pregnancy. If someone experienced a treatment failure or a bleed while on therapeutic LMWH, you'd probably also want to monitor levels going forward.

To recap that in bullet form! I'd consider that the 'gold standard' of monitoring that should be your starting point on any test question. You may even have some institutions with a special LMWH assay.

Just be aware that these exist, so you're not completely thrown off if you see them in practice. And remember, for most patients, we can give therapeutic doses LMWH without monitoring. Those therapeutic doses are given as subcutaneous injections twice daily and in some cases only once daily.

Compare that to the IV drip of heparin with monitoring every 6 hours and LMWH looks pretty attractive in the right patient population. Even better, enoxaparin syringes are pre-filled in a variety of strengths. Patients can self-administer therapeutic doses at home and don't need to stay in the hospital, providing another benefit of LMWH to heparin.

We run into an issue with LMWH in renal disease. Remember from above that we can give heparin no matter what your kidney function is. Even in dialysis. Unlike heparin, LWMH has a pretty long half life that's why we can get away with dosing it once or twice a day. It will accumulate in renal disease and predispose the patient to bleeding. So, if your patient has bad or even just unstable renal function, I'd recommend heparin.

As for other side effects, remember that LMWH is like a little cousin to heparin. The potential side effects are similar, but the likelihood of those side effects is less frequent with LMWH. LMWH does have a risk of hyperkalemia. However, this older and smaller trial says there's no risk at all. When you run into contradictory situations like this, my recommendation is to go with a "guilty until proven innocent" policy. I'm not saying you should empirically put a LMWH patient on kayexalate or anything.

Just that you should be mindful of potassium levels and watch out for synergistic drug interactions. As for Osteoporosis Some think we're chasing a red herring just because LMWH is similar to heparin. The jury is still out , but again I'd consider it a possibility worthy of monitoring until proven otherwise.

So it's much less likely. LMWH is also contraindicated in patients with neuraxial anesthesia i. It can cause a spinal hematoma which can lead to paralysis. So, umm. Don't do that. As for a reversal agent. There is conflicting data are you noticing a trend here?

Some sources that say you can use protamine as a reversal agent for LMWH. The reversal is considered "incomplete," but if you have a patient with a serious bleed I think most clinicians would take that over nothing. Just keep in mind that not everyone is on board with the using protamine for LMWH train. It's not a clearly defined choice like it is with heparin. The dose is 1 mg of protamine to neutralize 1 mg of LMWH.

Just like with heparin, the max dose of protamine is still 50 mg and don't forget about that fish allergy thing. You will often incorrectly see fondaparinux grouped with the direct factor Xa inhibitors we'll cover these in a bit.

That's because fondaparinux only inhibits factor Xa. I mentioned above that LMWH is just a trimmed up version of heparin. Think of fondaparinux as being trimmed up even further.

It is literally the precise 5 pentasaccharide sequence that binds to AT-III so you could say that it's binding is pretty specific. Clinically, this means that it only inhibits factor Xa.

There is no significant IIa inhibition here. I think this is why it often gets grouped with the direct factor Xa inhibitors. In general, monitoring is not required for fondaparinux. The special patient populations in which you would monitor are less clearly defined than they are with LMWH. However, what you should monitor is pretty clear: anti-Xa. So that's renal disease, extremes of body weight, pregnancy, and history of bleeds or treatment failures.

The package insert even goes so far as to recommend monitoring in patients who are less than 50kg, as fondaparinux is associated with a higher risk of bleeding in these patients. The neat thing with fondaparinux is that it's not really associated with those "weird" side effects from above like osteoporisis and hyperkalmia.

Additionally, and this is important , it has no association with HIT. Remember from above that fondaparinux is one of the two preferred options in the acute setting for patients who develop HIT. In my experience, that's been the most frequent reason for using fondaparinux. So why don't we use it more? Like most decisions in modern medicine, cost is certainly a factor. Fondaparinux is considerably more expensive than LMWH, and even more so than heparin.

Its other big strike is in renal failure. Fondaparinux has a solid 17 - 21 hour half life even longer than LMWH. So its risk of accumulating and causing a subsequent bleed in renal failure is even more probable. Making matters worse for renal accumulation, there is no specific reversal agent for fondaparinux. Protamine is not recommended. So you really have to use caution when selecting patients for fondaparinux. Argatroban is a direct thrombin inhibitor DTI.

Refer back to the clotting cascade earlier from this post there's also one included in our anticoagulant cheat sheet. You'll see that Thrombin Factor IIa is the thing that activates fibrinogen to fibrin which is then the material that cross-links the clot. So you inhibit thrombin, you inhibit fibrin and cross-linking. Make sense? The earlier DTIs hirudin, lepirudin, and bivalirudin are used so rarely anymore that I'm not going cover them in this article. You can read a neat timeline on the history of DTIs here if you're interested.

You can probably surmise this from the name "Direct Thrombin Inhibitor," but argatroban directly binds to thrombin Factor IIa and inhibits it. Clever, no?

It is not used very often, but it does have its niche in therapy. As previously mentioned, it is the second of the two "go to" drugs for patients that develop HIT. Far and away, this is the most common reason that argatroban is used. Should you use argatroban or fondaparinux for HIT? It depends on why the patient was on heparin in the first place. Argatroban has a super short half life about 45 min compared to the 17 - 21 hour ordeal for fondaparinux. So if the patient is getting surgical procedures or has renal failure, you'd lean towards argatroban.

Obviously, a drug with a 45 minute half life is going to have the need for an IV infusion, and it's usually going to be titrated to therapeutic effect which means monitoring. Argatroban and bivalirudin are the only two drugs in somewhat regular use that are monitored with ACT that I'm aware of Again, that glorious 45 minute half life makes argatroban pretty useful for short-term anticoagulation during a procedure.

There is no reversal agent for argatroban, but this usually doesn't matter. It should also be noted that argatroban has to be used carefully if at all in patients with liver failure. Everything we've talked about up to this point has been renally cleared, so this is an exception worth remembering.

Argatroban interferes with the assay we use to monitor warfarin therapy the INR. Specifically, it falsely elevates the INR by several points. That seems like crazy talk, but remember, it's a falsely elevated INR. Argatroban's effect will wear off fairly soon after stopping the infusion, at which point you'd adjust the INR to the "normal" range for the patient's indication. DOACs are not tied to a specific mechanism.

I'm going to discuss the DOACs all as one group even though they have different mechanisms of action. The reason I'm doing this is because they're pretty much all approved for the same indications with some minor variances. It'll be easier to talk about the pros and cons of using one over another in a single section instead of making you scroll back and forth. I'll also make sure to highlight some relevant clinical pearls for each of the DOACs individually. The big "draw" of the DOACs is that none of them require the cumbersome monitoring that warfarin requires although that does keep pharmacists employed.

And although all of them have drug interactions via the P-gp pathway and some have interactions with CYP as well , DOACs have considerably less drug interactions than warfarin. And they have basically no interactions with food. On the down side, in many ways the frequent monitoring associated with warfarin can be considered a plus in many cases.

Monitoring is the only way to be sure you're not over or under anticoagulating your patient. We can use Praxbind to reverse dabigatran and Andexxa to reverse most of the Xa inhibitors fun fact: Andexxa is NOT indicated to reverse edoxaban. And on top of that, several DOACs carry a higher bleeding risk than warfarin in certain patients or for certain indications.

All of that is to say that while DOACs have a definite place in therapy, they do not yet spell the end of warfarin. If you want more info, here is an excellent read that gives a more detailed comparison of the NOACs. Alright, so let's get into the nitty gritty of this. Notice how all of the Xa Inhibitors end in "-xaban. I said "in general" because the above is a pretty big generalization. You may see a couple of them used for DVT prophylaxis in patients who just had hip or knee surgery.

Rivaroxaban, for example, is approved for both of those indications. Also notice that DOACs are specifically approved for non-valvular afib.

And then, literally as I was writing this article, the FDA had to go all fancy on me and approve betrixaban [Bevyxxa]. So now we've got another Xa inhibitor in the mix. I'll probably write up a new FDA approval post to cover it in more detail and I'll update this post later.

But here's where we're at right now with betrixaban. Its trials compared it to prophylactic enoxaparin at VTE prevention. The benefit of betrixaban is that it can be given orally. In terms of preventing VTE in patients that do not have a history of VTE, this is the only oral option we have unless you believe in the silly orthopedic recommendation of aspirin mg BID. Spoiler alert: I do not. Betrixaban has the same P-gp interactions as other Xa inhibitors.

It's also recommended to avoid use in patients with reduced liver function. Finally, it has not yet been studied in pregnant patients or in patients with mechanical heart valves once again, your options there are warfarin, warfarin, and warfarin. I suspect that the makers of betrixaban Portola Pharmaceuticals will be going after more indications because right now it's only approved for prophylaxis, not treatment.

Again, I'll dig in more with a new FDA approval post and will update this article and our anticoagulant cheat sheet as more info becomes available. Alright, now that that's out of the way. Let's continue with our "painting DOACs with a broad brush" generalization From there, a good place to start is renal function.

Check to see if the DOAC has a dose adjustment or contraindication based on your patient's renal function.

The dose recommendations change by indication and renal function, so I won't list them out comprehensively here. Instead, I'll give you some general cutoffs:.