Drug Families: Anticoagulants and Antiplatelets

One of the most common drugs we encounter in the field are various forms of anticoagulant and antiplatelet medications. These are relevant to our care both in their therapeutic role as well as in their adverse reactions and potential for harm.

Unfortunately, coagulation is a miserably complex process, and it has to be understood at least generally in order to understand these drugs. In the hope of making this less confusing, rather than throw a wall of text at you, the worker gnomes at EMS Basics have put together an illustrated video. View this, then read on — the drugs won’t make any sense if you don’t start with the physiology.

This form of teaching is a new frontier here, so any input or feedback is welcome. Due to both personal and technical failings, it didn’t turn out exactly how I’d hoped, but hopefully things will continue to improve in the future.


Now that we understand the process, we should talk about the drugs.

There are two major categories here: anticoagulants and antiplatelets. Antiplatelet drugs inhibit the initial step of platelet aggregation and adhesion, where they collect at the wound site in activated form and create a loose plug. Anticoagulants have no effect on this, but instead interfere with the production of fibrin, and therefore prevent a solid clot from growing.

As a general rule, the anticoagulants are rather more clinically significant, as far as their effects on bleeding.



First off, to be clear: tPA (tissue plasminogen activator) is not an anticoagulant of any shade. It is a thrombolytic; it attacks and degrades existing clots, dissolving their fibrin bonds. It has no role as a protective agent, and would be far too hazardous in such a role anyway; even its emergency use for acute events like ischemic stroke always requires careful weighing of benefit vs. risk — because the risks are significant.

With that said, there are two main anticoagulants we see frequently in the field.


Warfarin (Coumadin)

Coumadin is an old drug with an interesting backstory; one of its original uses was for rat poison. It’s given orally.

Nowadays, it’s mainly used for chronic anticoagulation of patients at high risk for embolic events. For instance, if you’re in atrial fibrillation at baseline, the blood in your atria isn’t being pumped downstream effectively, and tends to pool. We saw that brisk movement of the blood is one of the main ways we prevent clotting; A-fib is therefore a risk factor for hazardous clots. So when possible, these patients are covered by Coumadin or similar drugs.

The mechanism is interesting. Recall that for the activation of several factors, primarily in the extrinsic and common pathways (including thrombin and Xa), Vitamin K needs to be present. (For some factors, Vitamin K is also needed for the initial production of their inactive forms.) The process looks like this: in order for the factors to be activated, a second background process must also occur, where Vitamin K is changed into a form called Vitamin K epoxide. Once this is done, Vitamin K epoxide can be cycled back into Vitamin K, allowing it to be reused again for the next activation.

Coumadin prevents this second step. It allows the inital activation and conversion, but it blocks Vitamin K epoxide from being recycled to Vitamin K. So over time, as you use up available Vitamin K, it doesn’t get replaced, and you end up with less and less of it available. Less available Vitamin K means less activation of thrombin and its precursors, which means less fibrin, which means less clotting.

Obviously this process takes time. Since Coumadin has no effect on the active factors already present, if we start you on Coumadin today, it won’t have any effect for several days. We need to wait for currently circulating factors to degrade. So for newly anticoagulated patients, a more fast-acting drug is usually used to cover this loading period; heparin is common.

Other than its widespread use, warfarin is also famous for frequent misdosing. It has a narrow therapeutic index, where it’s very easy to give too much or too little, and depending on diet and other drugs, the appropriate dose can change daily. It therefore requires regular monitoring of the patient’s actual anticoagulation, which is done through a test called the prothrombin time (PT). This is a lab test that measures clotting time with an emphasis on the extrinsic and common pathways, and gives a result in seconds. Due to different PT tests available, a standardized result has been devised called the INR (or International Normalized Ratio). This is essentially a ratio of your clotting time over the standard clotting time; a normal result is therefore close to 1.0. Obviously, anticoagulated patients should have a longer clotting time, so 2.0–3.0 is more typical. Much higher than this puts one at high risk of bleeding — into the GI tract, into the lungs, into the nose and mouth, and if trauma occurs, the chance of significant bleeding is magnified. A too-low INR, of course, simply removes the benefits of protective anticoagulation.

In the event of overdoses that need reversal, patients can receive supplemental Vitamin K, as well as plasma (or concentrates) to replace the missing factors directly.



Heparin is another old drug. It’s actually a biological substance naturally present in the blood, one of the body’s own anticoagulants, and when extracted for pharmacological use it’s derived from sources like pig intestines. Lovely. You can’t take it orally, so as a rule it’s given by IV.

Compared to warfarin, heparin has a more direct mechanism. Recall that one of the antagonistic factors that works to deactivate thrombin (as well as a few other factors) is antithrombin. Heparin, when taken in therapeutic doses, multiplies the effects of antithrombin by several thousand times. It therefore deactivates far more factors, which are then unable to produce fibrin. Thrombin and factor Xa are two of the factors most affected.

You can already imagine that heparin will probably work much faster than Coumadin. Aside from being given intravenously, it’s not simply stopping the influx of new Vitamin K and waiting for the old factors to degrade; it’s actually going in and deactivating them directly. In fact, heparin takes effect within half an hour or so. However, its half-life is short, so it’s often given as a continuous drip. Obviously, its usage is typically for acute events, such as acute coronary syndromes, or the bridging to Coumadin we mentioned.

However, there is another version of heparin that’s available. To briefly describe the chemical structure of heparin, it’s a polysaccharide, or a repeating chain. When we cook this stuff from pig parts, we end up with a collection of heparin chains in widely varying lengths. The problem is that only chains of a relatively long length will deactivate thrombin. So depending on the actual size of our heparin molecules, unaltered heparin — known as unfractionated heparin — can be fairly unpredictable in its effectiveness as an anticoagulant.

Even very short chains, however, will deactivate factor Xa, and since Xa is a necessary precursor for thrombin, this has the same effect. So if we can produce an artificial product that only includes short heparin chains, then it will mostly affect Xa rather than thrombin, and its effects will be more predictable. This is called low molecular weight heparin, and it has several advantages. It’s easier to manage, it requires less close monitoring, and it has a longer half-life. In fact, it can be given once a day by subcutaneous injection; for instance, post-operative patients can be taught to inject themselves and sent home with the ability to manage their own anticoagulation. Most of these LMWHs end in -arin: enoxaparin (Lovenox), dalteparin (Fragmin), and tinzaparin (Innohep) are common. Fondaparinux (Arixtra) is also used; although technically not a LMWH, it’s very similar in all respects.

Heparin can be monitored by testing the partial thromboplastin time (PTT), which focuses on the intrinsic and common pathways. LWMH can, if necessary, be monitored by testing levels of factor Xa. Overdose leads to bleeding complications, and in a few cases heparin can induce a disorder called heparin-induced thrombocytopenia (HIT), causing a paradoxically elevated chance of clotting. Super-therapeutic levels can be reversed by protamine sulfate, which binds to heparin and prevents its utilization.


Dabigatran (Pradaxa)

A few brief words on this relatively new drug, only made available over the past year or so.

Dabigatran is an anticoagulant from a wholly different class known as direct thrombin inhibitors. Unlike the somewhat roundabout pathways of warfarin and heparin, these drugs inhibit thrombin directly, and may therefore be somewhat more predictable and easily managed.

In the case of dabigatran, it’s being marketed as a replacement for Coumadin. Although supposedly just as effective for chronic anticoagulation, its claim to fame is that it requires no monitoring of INR, which would be a huge burden lifted from patients and caregivers.

Still very new, it remains to be seen how widely it will be adopted. The main concerns about it are: 1. Cost, and 2. Reversal. Unlike warfarin, which in the case of hazardous events (the proverbial bonk-to-the-head with an epidural bleed) can be readily reversed by Vitamin K and fresh frozen plasma, there is no easy or clear method of reversing dabigatran. Some ideas are out there, but clinical experience remains scarce at this point. In any case, this drug isn’t too common yet, but you may start to see it more often.





Aspirin is probably in your medicine cabinet somewhere. It has widespread uses from analgesia to antipyretic effects, but also plays a role in platelet adhesion. It’s taken orally, although IV aspirin does exist, and is used both for chronic risk-reduction and acute treatment of coronary syndromes. This stuff is good enough that nearly everybody you know with wrinkles on their face probably takes it every day.

As platelets are activated and degranulate, one of the chemicals they release is thromboxane A2. It has several effects, including vasoconstriction of the immediate area and stimulating further platelet activation. However, it also promotes platelet adhesion by a pretty neat mechanism.

Remember fibrinogen? The inactive precursor of fibrin? Unlike some of the other inactive factors, this one has its own chance to be the star of the show. Fibrinogen can form a bond between activated platelets, attaching at their glycoprotein IIB/IIIA receptors and creating a link. This isn’t anywhere near as strong as a fibrin bond, but it’s enough to make platelets stick together and clump. Thromboxane activates glycoprotein IIB/IIIA receptors and allows the formation of these fibrinogen bridges.

Aspirin inhibits thromboxane release. Fewer fibrinogen bonds are formed, and less platelets adhere. Coagulation itself proceeds unimpeded, but there are fewer platelets in the clot to be married by fibrin.

Due to the widespread effects of aspirin, overdose is a complex subject. Altered mental status, neurological and cardiovascular signs, sensory disturbances (blurred vision or ringing of the ears), and GI problems are all possible. However, there are typically no obvious bleeding abnormalities. Treatment of acute toxicity can include attempts to limit the dosage (such as gastric lavage and activated charcoal), bicarb, supportive care, and if necessary hemodialysis.


Glycoprotein IIB/IIIA inhibitors

This mouthful of a name is another class of drugs from the antiplatelet family. They’re typically not used chronically like aspirin; one reason is because they’re given intravenously, with oral forms rarely seen. (Another reason is because they’re simply stronger drugs). We see these most often used during and after known coronary “events,” such as a STEMI, NSTEMI, or a coronary catheterization, at which times they can help prevent reocclusions.

Their mechanism is similar to aspirin. As we saw, fibrinogen binding to glycoprotein IIB/IIIA receptors helps bind together platelets and allows them to adhere and aggregate. GBIIB/IIIA inhibitors block these receptors by competitive binding, and hence prevent the fibrinogen bonds.

We rarely see these in the field, but common ones include: abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Adverse effects mainly involve bleeding.



Although there are a few drugs in this class, by far the most common is clopidogrel (Plavix). Think of these as an alternative, somewhat more powerful aspirin; they work similarly, have similar effects, and are used for similar purposes. Like aspirin, some people use it chronically and it can be given in acute events as well. It can “stack” with aspirin for a synergistic effect, or be used in its place for those who cannot tolerate aspirin.

Once again, the mechanism will sound familiar. One of the pathways that activates glycoprotein IIB/IIIA receptors requires the binding of adenosine diphosphate, or ADP. (ADP is more famous as the product of ATP once energy is released, but it has its fingers in a lot of cellular pies.) The thienopyridines block ADP binding and hence discourage platelet aggregation. Prasugrel (Effient) is another drug in this class.

Adverse effects generally involve bleeding diatheses.

More Drug Families: Stimulants and Depressants; Steroids and Antibiotics; ACE Inhibitors and ARBs

Drug Families: ACE Inhibitors and ARBs

Understanding the renin-angiotensin-aldosterone system is like following one of those dotted-line Family Circus cartoons — not just long and tortuous, but seemingly designed just to be obnoxious.

Here’s the basic idea. The RAAS is the basic system your body uses to control blood pressure, as well as related values like fluid volume and sodium levels. The most important thing to understand is that the activation of this system causes an increase in blood pressure. Following the trail:

First, renin is released by the kidneys. Renin attacks circulating angiotensinogen, turning it into angiotensin I. Angiotensin I is attacked by circulating angiotensin converting enzyme (or ACE), which turns it into angiotensin II. Angiotensin II has various effects, one of which is to stimulate the release of aldosterone.


But this isn’t as complicated as it looks. Renin has no real effect. Angiotensinogen just makes angiotensin I. Angiotensin I’s main role is to make angiotensin II. The real money here is in angiotensin II, as well as aldosterone.

Angiotensin II has the primary effect of vasoconstriction. It tightens up the vasculature, increasing blood pressure and systemic resistance. It also produces vasopressin (aka ADH, or anti-diuretic hormone) and aldosterone, which cause the kidneys to downregulate urine production — more fluid will be returned to the circulation rather than discarded into the bladder. Vasopressin also helps angiotensin II to induce further vasoconstriction.

To make a long story short, the activation of the RAAS system causes an increase in blood pressure via both vasoconstriction and a decrease in kidney output. It is always active, playing a key role in maintaining homeostasis; if you sweat out a liter of water running a marathon, or bleed out a liter from a gunshot wound, the system simply upregulates itself to maintain your blood pressure using the remaining volume. (Unlike the sympathetic and parasympathetic systems, which also play a major role in regulating blood pressure, regulation via the RAAS is captained mainly at the kidneys, where low pressure and throughput induces increased renin production.)

Cool? Cool.

Okay, so the role of ACE, or angiotensin-converting enzyme, was to transform the useless angiotensin I into the powerful angiotensin II. What do you think a drug called an ACE inhibitor would do? Indeed: it inhibits the activity of ACE, thus reducing the production of angiotensin II, which then causes reduced production of aldosterone and vasopressin.

Less angiotensin II means less vasoconstriction; the systemic circulation opens up, reducing blood pressure. Less aldosterone means less fluid is retained at the kidneys, so urine output is increased, reducing circulating volume, and again, reducing blood pressure. Handy!

A secondary role of ACE is to degrade, or break down, bradykinin. Bradykinin is basically just another vasodilator. If ACE is inhibited, then less bradykinin will be broken down, hence more bradykinin will be available. The result is more vasodilation — once again, reducing blood pressure.

Readers who can recognize patterns will probably have deduced that ACE inhibitors are used primarily to reduce blood pressure. Obviously, this includes the typical patient with primary hypertension that needs to be managed to reduce long-term morbidity. But it also means other things:

  • Reduced afterload — the resistance the heart has to push against when it pumps blood — means less work for the heart. This is beneficial for patients with heart failure, whose hearts aren’t pumping very well to begin with; or with coronary artery disease, whose hearts need to manage their workload to match the oxygen they’re able to bring in. It reduces “remodelling,” where the heart and the arteries thicken and change shape to better pump hypertensive volumes, with harmful results. And it reduces the damage following myocardial infarction.
  • Reduced preload — the amount of blood that passively fills the heart during diastole — — also means less work for the heart. Greater preload causes greater filling and hence greater contraction, which all means more work, more oxygen demand, and more remodelling. In heart failure, where the heart is unable to fully expel its contents, reduced preload also means less “extra” fluid to back up into the lungs and circulation, and therefore less edema.
  • Better renal function. This is a desirable effect in patients with various forms of kidney disease.

Angiotensin receptor blockers (ARBs) are a closely related family of drugs. Instead of interfering with the conversion of angiotensin I to angiotensin II, they simply prevent angiotensin II from binding with its receptors. The effects are therefore largely the same: vasodilation; reduced aldosterone production, with corresponding greater urine output; and reduction in hypertension with less work for the heart.

The main difference between ACE inhibitors and ARBs goes back to bradykinin. If you remember, ACE plays two roles: converting angiotensin I to angiotensin II, and degrading bradykinin, a vasodilator. Since ARBs have no effect on ACE, bradykinin is broken down normally. This may result in slightly less vasodilation, but it also reduces the side effects of elevated bradykinin, which can include edema and a nasty cough. ARBs are most often used in patients who can’t tolerate ACE inhibitors.

Overdose on ACE inhibitors is generally unremarkable. The main effect is hypotension, but it is rarely severe.



Generic names of ACE inhibitors and ARBs are very, very easy. Trade names are harder, but do have some common elements.

ACE inhibitors

  • Drugs ending in -pril are invariably ACE inhibitors (enalapril, ramipril, captopril, lisinopril, etc.)
  • Drugs ending in -ace are often trade names of ACE inhibitors (Altace, Tritace)
  • Drugs ending in -tec are often trade names of ACE inhibitors (Vasotec, Renitec, Novatec)


  • Drugs ending in -sartan are invariably ARBs (losartan, valsartan, candesartan, etc.)

More Drug Families: Stimulants and Depressants; Steroids and Antibiotics; Anticoagulants and Antiplatelets

Polypharmacy in the Elderly

A tremendously valuable Educational Pearl from the wonderful UMEM mailing list, courtesy of Amal Mattu, emergency physician extraordinaire.

We already know that polypharmacy is a big issue in the elderly, but here are a few key points to keep in mind:

  1. Adverse drug effects are responsible for 11% of ED visits in the elderly.
  2. Almost 50% of all adverse drug effects in the elderly are accounted for by only 3 drug classes:
    a. oral anticoagulant or antiplatelet agents
    b. antidiabetic agents
    c. agents with narrow therapeutic index (e.g. digoxin and phenytoin)
  3. 1/3 of all adverse-effect-induced ED visits are accounted for by warfarin, insulin, and digoxin.
  4. Up to 20% of new prescriptions given to elderly ED patients represents a potential drug interaction.

The bottom line here is very simple–scrutinize that medication list and any new prescriptions in the elderly patient!

Samaras N, Chevalley T, Samaras D, et al. Older patients in the emergency department: a review. Ann Emerg Med 2010;56:261-269.

The value of this is inestimable. We know that polypharmacy is a big deal, but it’s such a big deal that it can be hard to shrink down the problem enough to really consider it when an elderly patient presents themselves. Could their problem involve something on this med list that’s as long as your arm? Certainly, but where to start?

Start with the above. Over half of your problems will involve anticoagulants, antidiabetics, and easily misdosed drugs. Those are the usual suspects; they should jump out at you from the list. But we can do even better, because nearly half of those will involve one of three particular serial offenders: insulin, warfarin (aka Coumadin), and digoxin. And let’s add a fourth one: any new or recently modified prescriptions. If any of these are present in a patient with an appropriate complaint or presentation, it should be strongly considered as being part of the problem if not the actual smoking gun.

Insulin is easy, especially if you have access to finger-stick glucometry; diabetic emergencies (especially hypoglycemia), including iatrogenic ones, are so common that you might as well assume anybody with an altered mental status is diabetic — even if they aren’t. Definitive treatment is obviously oral glucose or IV dextrose, as appropriate.

Warfarin is still an extremely common anticoagulant, although a couple new alternatives are now available, and it requires close and frequent monitoring of levels in order to maintain a therapeutic dose. (The usual standard is a measure of clotting speed called INR; the test can be performed in the lab, but nowadays can also be done right at the bedside.) Various medication interactions and even dietary changes can shift this range. Overdose is associated with, no surprise, bleeding — in all forms. If necessary, supertherapeutic warfarin levels can be antagonized with Vitamin K or IV clotting factors.

Digoxin is seen less today than in yesteryear, but once upon a time everybody and their mother was on “dig,” and it’s still used with some regularity. Its most common application is for rate control of atrial fibrillation patients. Although other antiarrhythmics are now more common, dig has the peculiar magic of reducing cardiac rate while actually increasing contractility (negative chronotropic but positive inotropic effects). However, its therapeutic range is narrow and is easily shifted by pharmacological, renal, and other issues; as a result, dig toxicity is famously common. Overdose symptoms include GI problems and neurological complaints such as visual disturbances and changes in mood or energy level. It can also present prominently on the ECG, with the most classic sign being degradation of AV conduction with an increase in atrial and ventricular ectopy — for instance, slow A-fib or atrial tachycardia, a third-degree AV block, and a junctional escape with PVCs. (As a result, the atrial fibrillation patient controlled on dig may present with an unexpected “regularization” of his pulses, due to a junctional or ventricular escape taking over from the usual A-fib. This is a clue even the BLS guys can catch.) Treatment is supportive for arrhythmias and heart failure; severe cases can be managed with Digoxin Immune Fab (aka Digibind or Digifab).

Drug Families: Steroids and Antibiotics

When things go wrong
as they usually do —


There are a lot of bad things that can happen to your body. Homeostasis, as we like to call it, is that smooth state when all your bits and pieces behave just as they ought to; and “bad things” are anything that knock this out of whack.

And what’s funny is that, no matter what that insult is, you can pretty much count on the body to respond with inflammation. Other, more specific things too, but inflammation will be there. It’s physiological duct tape: your basic, one-size-fits-all solution for any physical calamity.

Inflammation is caused by a complex blend of chemical mediators, but physically, the result is usually some combination of five classic signs.

  • Heat [calor]
  • Redness [rubor]
  • Swelling [tumor]
  • Pain [dolor]
  • And sometimes included, a general loss of function [functio laesa]

Try the Latin if you’re trying to impress someone at the bar.

Suppose you fall and bang your elbow, causing minor soft tissue damage. The body reacts immediately by activating a local inflammatory cascade, whereby numerous processes swing into gear. Local vasodilation occurs, bringing more blood into the area, to support faster healing; this increased bloodflow (hyperemia) produces the redness and warmth associated with injury. Vascular permeability is also increased, allowing fluid to leak into the surrounding tissue, which results in edematous swelling; this not only conveys healing factors into the damaged area, it also physically limits movement around the affected joint by “self-splinting.” Other chemical mediators increase your local sensitivity to pain, which further discourages you from movement; a decrease in the joint’s function is the result.

All of which is part of the inflammatory package. Neat!

The inflammatory cascade in soft tissue damage

Now suppose you catch a cold. Viral particles enter your mouth or nose, whether by direct contact or by inhaling them as an aerosol, and lodge somewhere in your oronasopharynx. Our response: inflammation! Your immune system recognizes the intrusion and responds with an influx of infection-fighting white blood cells, such as neutrophils and monocytes, along with the same cocktail of general inflammatory mediators (bradykinin, cytokines, etc.) that we saw with the injured elbow. The result? Swelling; excess mucus production; pain (as in sore throat); a general discomfort and sense of crumminess; and in more systemic cases, a fever to make the environment less hospitable for the virus.

It’s all the same story. When things go wrong, the body responds in various ways, but it’s almost always accompanied by some sort of inflammatory response to facilitate and assist the repairs.

Sometimes, however, this process becomes maladaptive. Whether it’s an immune response to infection or a local response to injury, short, appropriate, and effective inflammatory activity is a valuable part of our defenses — but if becomes too severe, lasts too long, or serves no purpose, then it can become part of the problem. For our bumped elbow, inflammation will promote healing, but if after a few days we find that the area is still swollen, this is no longer valuable; it’s impeding our ability to use the joint, which is what we need to do in order to circulate blood and encourage further healing. Our body’s response was excessive. So we apply ice to vasoconstrict the area, elevate the extremity, and take anti-inflammatory drugs, all to reduce that local edema and tamp down our inflammatory freak-out.

Key players of inflammation in sepsis

Numerous illnesses and injuries exhibit this sort of excessive, harmful inflammatory response. For example:

  • Traumatic brain injury is deadly because swelling within the cranium has nowhere to go, resulting in a self-feeding cycle of increased pressure and increased damage.
  • Sepsis occurs when an infection becomes widespread enough that it causes a system-wide inflammatory response, resulting in organ damage and vascular disruption — this cascade is self-feeding and can quickly become more harmful than the infection itself, even causing death long after the initial infection has been eradicated.
  • COPD and asthma are caused, in part, by inflammation of the lower airway (due to prior damage or various dysfunctions).
  • Shock kills early by hypoperfusion, but if that is survived, it kills later by an uncontrolled inflammatory cascade resulting from that hypoperfusion. If not managed early, this cascade can continue to spread independently of the original shock state.
  • The entire spectrum of autoimmune diseases is characterized by an inappropriate immune response to the body’s own tissues.
  • Allergic reactions, including lethal anaphylaxis, are hypersensitive immune responses to benign foreign agents like dust or foods.

To make a long story short, sometimes, inflammation sucks.



Steroids are modern medicine’s answer. Steroids are a large class of molecule, including the anabolic steroids that “pump you up” and sex steroids like testosterone and estrogen, but what we’re interested in are glucocorticoids (sometimes called corticosteroids, which is actually a broader category, but the terms are often confused). Glucocorticoids are interesting hormones with numerous effects; as a matter of fact, they’re part of the “fight or flight” stress response we talked about before. (Put simply, catecholamines like adrenaline give you a boost to help deal with danger right now; glucocorticoids, on the other hand, give you a slightly more delayed “second wind,” so you’ll still have some juice a few hours later.) And fighting infections and healing injuries is a real waste of energy when we’re running from wild tigers. The result? Glucocorticoids inhibit the inflammatory response.

They can therefore play a role in the management of all the problems we just mentioned. Maintenance-type inhalers for asthma and COPD are often steroids. Anti-allergy nasal sprays too. Appropriate steroid use can be complex, because we must be careful not to over-inhibit our inflammatory system; for instance, although they would seem like an obvious answer to sepsis, their use for those patients is unclear and has long been controversial. Or how about using steroids to treat epiglottitis, an infectious swelling of the epiglottis that can obstruct the airway? We would expect the steroids to combat the swelling, but also to impair our ability to fight the underlying infection. So finding the balance can be difficult.

Corticosteroids can be administered locally, when a local effect is desired, such as via metered-dose inhaler for asthma. Or they can be administered globally for systemic conditions, such as by IV or oral routes for autoimmune conditions.



Of course, sometimes the body is fighting for a reason.

As we’ve seen, the body responds with inflammation to a wide range of insults, but one of the most common is infection. And in the many cases of infection when our primary goal is simply to eradicate the source, pharmacological support can be beneficial.

Antibiotics are generally well-recognized as agents that kill bacteria. The terminology has become somewhat clouded nowadays, as the word “antibiotics” is sometimes used to strictly mean anti-bacterial agents, and sometimes to mean all anti-microbials, including anti-fungals and anti-virals. But the general idea of immunosupport is the same.

These agents generally work in one of two ways: either by directly killing the microbe, or by impeding its ability to replicate. They’re tuned so that they affect the bad guys without harming (not too badly anyway) our body’s own cells.

It’s therefore natural to think of antibiotic therapy as the natural opposite of steroids, and this has some truth to it. In the case of infection — which, remember, is not the only cause of inflammation — steroids do inhibit the immune response. But bear in mind that antibiotics do not, as a general rule, actually support or promote the body’s inflammatory response; rather, they work independently by attacking the infection directly along their own pathways. The result is that some pathologies (such as the contentious cases of sepsis and epiglottitis) may respond both to steroids — to manage the excessive inflammatory response — and antibiotics — to help eliminate the source infection.



Once again, remember that common drug suffixes are usually only applicable to generic drug names. Trade names tend to be unique.


  • Drugs ending in -one (prednisone, hydrocortisone, clocortolone, etc.)
  • Drugs ending in -ide (fluocinonide, budesonide, desonide, etc.)
  • Drugs with pred in the name (prednisolone, loteprednol, prednicarbate, etc.)
  • Drugs with cort in the name (fluocortin, Cyclocort, Entocort)


  • Drugs beginning with ceph- or cef- are antibiotics of the cephalosporin type (cefixime, cephalexin, cefepime, etc)
  • Drugs ending in -illin are antibiotics of the pencillin type (penicillin, methicillin, nafcillin, etc.)
  • Drugs ending in -cycline are antibiotics of the tetracycline type (doxycycline, methacycline, etc.); not to be confused with the -tyline of tricyclic antidepressants.
  • Drugs ending in -azole are generally from a large family that can have antibiotic, anti-fungal, and anthelmintic (anti-parasitic) effects (metronidazole, fluconazole, miconazole, etc.). However, this does not include the -prazole drugs (omeprazole, pantoprazole, and others) which are actually proton pump inhibitors, with no antimicrobial effects.
  • Drugs ending in -floxacin are antibiotics of the quinolone type (levofloxacin, ciprofloxacin, etc.).
  • Drugs ending in -mycin are antibiotics of the macrolide type (azithromycin, erythromycin, etc.)
  • Drugs beginning with sulf- are antibiotics of the sulphonamide type (sulfamethoxazole, etc.)
  • Drugs ending with -adine are antivirals of the adamantane type (amantadine, rimantadine)
  • Drugs containing vir are generally antivirals (acyclovir, oseltamivir, ribavirin, efavirenz), including antiretrovirals for HIV treatment
  • Drugs ending with -vudine are antivirals (lamivudine, telbivudine, etc.)

More Drug Families: Stimulants and Depressants; ACE Inhibitors and ARBs; Anticoagulants and Antiplatelets

Drug Families: Stimulants and Depressants

There are many, many, many, many, many, many drugs.

And I think it’s noble and wise for a sharp EMT-B to learn as much as he can about as many of them as he can. General mechanism, typical routes, notable adverse effects and contraindications. The most common meds are encountered so frequently that you can’t help but become familiar with them.

But what about all the rest? (You remember those — many, many, many, etc.) Memorize them all? Maybe, but that’s a task on par with memorizing the map of London. I’ll freely admit that my own mental encyclopedia of pharmacology is weaker than it should be.

Use a reference? These are certainly handy; printed quick-books are available, as are digital versions you can access with a smartphone (Epocrates and Medscape are a couple good ones — see the Droid Medic for guidance). But we really ought to have at least a surface recognition of most drugs we come across, without having to consult an Ouija board.

Fortunately, 80-90% of the drugs you’ll encounter can be broadly categorized into a few major types. If you understand these types, and their basic physiological behavior, you’ll understand most of what’s relevant to your care; and it’s easy business to memorize which type a drug belongs to. So let’s go over some of these categories.

Some of these groups seem to fall naturally into matched opposites. So today, let’s discuss…


Stimulants and Depressants

Basically, it’s all about speeding up, or slowing down.

Most of us have heard of the “fight or flight” response, our body’s instinctive ability to step on the gas in times of need — an acute stress response that lets us climb trees, hunt mammoths, and escape from tigers. It’s the get-up-and-go state, and its physiological trigger is known to laymen as adrenaline. This is partly correct; in actuality, your body creates this high-output condition through a variety of hormonal mediators (including adrenaline, more commonly known in the US as epinephrine, but also dopamine and norepinephrine). Overall, this functionality of your autonomic nervous system is known as the sympathetic system.

Some of us have also heard of the reverse state of fight-or-flight, often called “rest and digest” (or sometimes “breed and feed”). This is the slow down, recover, repair, rebuild, and relax state; this is the brake to the sympathetic’s gas. Although slowing down is the last thing you want when escaping from sabre-toothed tigers, it’s just the ticket when you’re enjoying supper or having a snooze. This side of things is known as the parasympathetic system.

(How to keep these two straight? Try this mnemonic: the s in sympathetic is for “stress,” because this is your fight-or-flight stress response. The p in parasympathetic is for “peace,” because this is your peaceful, resting state. Thanks to Mark O’Brien for this one.)

Together, these two systems keep your body tuned like a guitar string. It’s a mistake to think that when one is active, the other is switched off; actually, they’re both active at all times, merely to different degrees. Although their combined results are directly antagonistic, they’re independent systems, which means that you can have a mixture of a little sympathetic, a lot of parasympathetic, vice versa, a lot of both, or any combination thereof.

Think of it like the hot and cold knobs on your sink. You adjust them separately, but the result is a single water temperature. A little hot and a little cold will give you warm water, but so will a lot of hot and a lot of cold. And if you want to cool it down, you can either turn up the cold, or turn down the hot. Simple.

Well, the secret is that many of the drugs we use in medicine function primarily by adjusting this balance.

A drug that turns up the sympathetic system (thus “speeding you up”) is known as a sympathomimetic. A drug that turns down the sympathetic system is known as a sympatholytic.

A drug that turns up the parasympathetic system (thus “slowing you down”) is known as a parasympathomimetic. A drug that turns down the parasympathetic system is known as a parasympatholytic.

Okay, so those are mouthfuls. But the important thing to remember is that, while they’re not identical, the result of both a sympathomimetic and a parasympatholytic will be to support your fight-or-fight responses (run from the lion!), and the result of both a parasympathomimetic and a sympatholytic will be to support your rest-and-digest behavior (take a nap!). So whichever end you approach it from, there are still only two important end results here — up and down.

Virtually the entire body is controlled by these systems. If you can keep track of how each organ system is affected when you nudge this balance one way or the other, you’ll be able to understand a great deal of how drugs do their work.

For instance, consider epinephrine itself, which we use in auto-injectors to treat severe anaphylaxis. The life-threatening effects of an allergic reaction are primarily shock, due to vascular dilation, and respiratory distress, due to bronchial constriction. Epinephrine is a sympathomimetic (okay, “mimetic” means “mimick,” and epinephrine is actually one of the body’s own sympathetic hormones, so it’s not really mimicking anything — but bear with me here). So it produces a fight or flight response. What is the sympathetic effect on the skin and peripheral vascular system? Vasoconstriction (to pull blood away from the periphery into the core). What is the sympathetic effect on the lungs? Bronchodilation (to allow for greater air exchange during exertion). So the entire cocktail of epi’s beneficial results in anaphylaxis comes from stimulating sympathetic tone.

What if I shoot some heroin? My breathing will become slower and weaker. My level of consciousness will decrease. I will become generally slowwww, because heroin (like all opiates) is fundamentally a depressant. And my pupils, pleasantly parasympathetic, will constrict — the third hallmark sign of opiate use. Who needs light when we’re relaxing?



Now, not all drugs from the same neck of the woods are identical, of course. The effects of the same neurotransmitters can be radically different depending on where they bind. An important distinction should be made between non-selective drugs like epinephrine, which binds with all of the primary adrenergic receptor sites (alpha-1, beta-1, and beta-2), and selective agonists like albuterol, which primarily binds only at certain receptors (beta-2 in that case). In brief:

  • Alpha-1 (properly styled, α1) receptors are mainly in the blood vessels, and cause systemic vasoconstriction. Alpha-1 blockers, or antagonists, therefore cause systemic vasodilation.
  • Beta-1 (β1) receptors are mainly in the heart, and increase heart rate and contractility. Beta-1 antagonists therefore slow and reduce cardiac output. (Mnemonic: you have 1 heart.)
  • Beta-2  (β2) receptors are mainly in the lungs, and cause bronchodilation. Beta-2 antagonists therefore cause bronchoconstriction. (Mnemonic: you have 2 lungs.)

Naturally, none of these categories tell the whole story of a drug. (If they did, we wouldn’t need so many different ones.) Caffeine, atropine, and crystal meth are all very different drugs, even though they all fall roughly into the category of stimulants. But you can keep track of a good deal of their shared effects by understanding their common nature.



  • Drugs ending in -zepam (or sometimes -zolam — eg. diazepam, triazolam) are benzodiazepines, which have broad sedative effects.
  • Drugs ending in -alol (or -ilol, -olol — eg. atenolol, labetalol) are beta blockers, which have a sedative effect, usually localized to the heart via beta-1 antagonism.
  • Drugs ending in -erol (e.g. albuterol, clenbuterol) are beta-2 agonists, or bronchodilators; they are stimulants that primarily cause bronchodilation via beta-2 receptors.

Most pain killers, sedatives, and anesthetic agents are depressants.

Note: most common suffixes are only applicable to generic drug names. Trade names are usually unique.

More Drug Families: Steroids and Antibiotics; ACE Inhibitors and ARBs; Anticoagulants and Antiplatelets