Hi and welcome to Nursing School Explained. Today I'd like to go over
respiratory medications. This seems to be a topic that a lot of times is kind of
confusing to students but when we really think about the mechanism of
action of a medication really represents its physiology and the physiological
response that it will enhance or inhibit in the body. So I have written down here
some basic terms that hopefully will help you be able to dissect the
mechanism of action of these medications and then understand how they work and so
also how they're indicated and why they would be used in the treatment of
certain respiratory disorders. So first of all I just wanted to review
inflammatory mediators. You might remember from your physiology class all
the different cells that help us in providing inflammation when we are
battling infection, disease, allergies, any of those things in the body and some of
those mediators I have written down here so those are neutrophils you know those
are the number one defense and we also have mast cells, macrophages, leukotrienes,
T-cells, histamines. Now remember these are only a few of the inflammatory
mediators there's there's a lot of other ones but these are the most important
that we will apply here to the respiratory medications. And then other
principles here and this not only pertains to respiratory medications, this
pertains to cardiac medications as well. And so whenever you see the word
adrenergic think adrenaline, think sympathetic nervous system and
fight-or-flight response. So adrenaline, adrenergic response,
sympathetic nervous system, where cholinergic pertains to the
parasympathetic nervous system. Okay so whenever you see these
terms adrenergic a cholinergic you know that they are working either on the
sympathetic or parasympathetic nervous system. And then in addition medications
can be agonists or antagonists or they can be anti - against something. So an
agonist helps to promote the natural response by occupying the receptor site.
Remember that most of the physiological mechanisms that take place in our bodies
it's kind of like a key and a lock mechanism so only certain keys will fit
to certain receptor sites and be able to initiate a response. So an agonist is
basically a chemical or a pharmaceutical mediator or response that we're trying
to elicit. So when its agonist it helps to promote or agonize that response;
where an antagonist as you can imagine does exactly the opposite. So it blocks
the receptor sites so when we don't want something to happen, when we want to
inhibit certain things from happening that key and lock to match then we want
to give an antagonist because that pharmaceutical, that medication then will
block that receptor site as basically like a fake key so the natural response
cannot occur or is inhibited. And then there's also medications that started
with anti and that basically just means that it's against something, so
kind of similar to antagonists but almost like just a different terminology
that is used. Now another graph that I've drawn out here over here is basically
beta 1 and beta 2 and then alpha because there is beta-2 adrenergic receptor
blockers for example alpha adrenergic receptor blockers or beta cholinergic.
There's all kinds of different combinations but remember beta 1 we have
one heart so beta 1 always pertains to the heart. Now we have two lungs so
beta two always pertains to the lungs as I've drawn out here the heart is beta 1
beta 1 one heart beta 2 we have two lungs so that pertains to beta 2. And
then this here is an alpha turn on its side, alpha means blood vessel so this
would be the structures of the blood vessels flowing throughout the body in
this little graph here. So beta 1 - heart, beta 2 - lungs, alpha pertains to the blood
vessels. And that for the blood vessels it mostly means are they dilating or
constricting, are they having a sympathetic or parasympathetic nervous
system response and then the mechanism of action can be easily identified. So
back to our respiratory medications. So there are a variety of classifications
there, this mostly applies to asthma but they can also be used in conditions such
as chronic obstructive pulmonary disease, emphysema, maybe cystic fibrosis or for
acute respiratory disorders such as bronchitis where there might be some
acute inflammation, not chronic like in asthma when a patient might benefit
from a short course of one of these medications. So let's look at that. So
number one I've written out SABA and SABA
stands for short-acting beta-2 adrenergic agonist. Okay so very short
acting. So beta 2 - lungs, adrenergic - sympathetic nervous system. Okay so
basically this binds to the beta-2 adrenergic receptors
therefore it relaxes the airway smooth muscle and causes bronchodilation. Right?
When we have a sympathetic nervous system response, when we need to get
ready to fight or flight, when we need to get ready to run away, we need to be able
to dialate our bronchioles by allowing more oxygen exchange
because with our muscles we'll need that oxygen for the flight flight or fight
response. So therefore short-acting beta-2
pertaining to the lungs, adrenergic - sympathetic nervous system, agonist - it's
going to help to promote that natural response by relaxing the smooth air
muscle Airways and causing bronchodilation. And really the only
SABA there is is Albuterol. I'm sure you've heard about, it it's the most
commonly used inhaled medication. Now I've written down here O, P and D which
is onset, peak and duration because later we'll compare it to some of these other
medications. So Albuterol: the onset is 5 to 15 minutes, it's peak occurs at
two to three hours and it lasts for about four to six hours. So this is
something that we need to keep in mind whenever we're doing patient teaching
regarding these medications - how soon can they expect this to work. Now
classification number two is ICS which are inhaled corticosteroids. And you
might know that steroids always battle inflammation. So now looking back at
these inflammatory mediators so which ones in particular do those inhaled
corticosteroids inhibit? So for inhaled corticosteroids they decrease
airway inflammation but they work on multiple inflammatory mediators. So they
don't just pick out neutrophils or mast cells or leukotrienes, they work on
multiple mediators, which is why they are the most commonly used inhaled
anti-inflammatory medication because they work on a variety of different
cells therefore inhibiting that inflammatory response that causes
bronchoconstriction and then causes problems for the patient. And these
inhaled steroids just like any steroids usually end in -one so an example would
be Beclomethasone, Fluticasone, just like your corticosteroids, your PO would
be a prednisone for example. They all end in -one. And if you can remember these
endings of these medications and connect them to the classification, it will be
much easier for you to remember and kind of classify
them and then only memorize the drug category rather than memorizing all the
individual medications because there's just way too many out there. So number
three medications would be a LABA so you can see it's very similar. The only
difference is it's a long-acting beta two adrenergic agonist. So it's exactly the
same thing is up here except that it's longer acting so the mechanism of action
is the same as a SABA but it's longer acting. The example here would be
salmeterol, again ending in -ol, which is pretty typical for these adrenergic
agonists. Now we already know that beta 2 applies to lungs, adrenergic -
fight-or-flight adrenaline pertains to the sympathetic nervous system. So it
does exactly the same as the Albuterol, where it binds to those beta-2
adrenergic receptor sites, relaxing the bronchial smooth muscle and allowing for
bronchodilation so the pro patient can breathe easier. Now looking at onset, peak
and duration over here so onset is one hour you can see it's short it's
longer than up here, the peak is 1 to 5 hours, and the duration up to 24 hours. so
it's long acting, right, long acting 24 hours compared to short acting four to
six hours for duration up here. Now number four would be anticholinergic
medications. And we already talked about cholinergic meaning that it pertains to
the parasympathetic nervous system. I'll move back over here. So cholinergic
pertains to the parasympathetic nervous system and anti means against now why
would we want to block or counteract the parasympathetic nervous system? Now think
about it if we again are in a fight-or-flight response we want that
sympathetic nervous system to kick in. Cholinergic or parasympathetic nervous
system is in charge of rest and digest, right? When we need to flee from a danger there
is no need for rest and digest. All the blood flow needs to go to the important
organs, the heart and the lungs and the muscle so that we can run away from the
danger. So anticholinergic medications anti- meaning it inhibits the
cholinergic receptor sites in the Airways so now we are inhibiting the
parasympathetic nervous system from kind of slowing everything down and
constricting the bronchioles so we can rest and digest. And when we inhibit the
cholinergic response it also brings us bronchodilation. So bronchodilation here
is the end effect in SABAs, LABAs as well as anticholinergics but they work
in different ways. So anticholinergics working on the parasympathetic nervous
system basically just blocking those receptor sites so they don't have a
chance to cause bronchoconstriction because that's what they would do for
rest and digest response. And an example for an anticholinergic respiratory
inhaled medication would be Atrovent or Ipratropium. You probably have heard that
before as well. Now in comparison the onset, peak and duration for
anticholinergic - so onset is 1 to 3 hours, the peak is 1 to 2 and duration 4 to 6.
So you can see it's very similar to the Albuterol in terms of the duration so
it'll last about the same time. Now there are certain medications that can be
given to patients that are used in combination. And one of the the ones used
very frequently in the emergency department is called a duoneb, so duo -
two medications by nebulizer. And that's always a combination of Albuterol, a SABA,
and the atrovent, the anticholinergic. So they both combine to work together to
agonize the sympathetic nervous system and antagonize the cholinergic system so
that bronchodilation can occur on both pathways. Remember that every organ has
innervation from sympathetic and parasympathetic nervous system receptors
so that they can work either to speed things up also slow things down. Now
number five here leukotriene antagonists. So you can see here leukotrienes are one
of those inflammatory markers we reviewed earlier and they are basically
a very specific, they respond to very specific inflammation response and so
these leukotriene antagonists, they do just that. They block the receptor sites
for the leukotrienes so which which usually would cause inflammation and
therefore they antagonize that so they decrease the effect of the leukotrienes
and cause decreased inflammation and that would be specifically a desired response
in patients with asthma where there's a lot of underlying inflammation and other
respiratory conditions that have inflammation at their at their core. And
an example of a leukotriene antagonist would be Singular or Montelukast as the
other, the generic version of it. Now then further we have mass cell stabilizers.
Again mast cells are different inflammatory mediators and when we
stabilize the mast cells then again we decrease inflammation so they are again
very specific to those specific inflammatory markers. And an example
would be Cromolyn sodium. And then in addition as if this wasn't enough
already, we have certain combination medications. And these combination
medications usually are consists of an ICS, an inhaled corticosteroid and a LABA,
a long-acting beta adrenergic agonist. The most commonly used one is Advair
that's that purple discus that you might have seen in the clinical setting and it
consists of salmeterol, which is our LABA, and Fluticasone,
you know our -ones, are our inhaled corticosteroids. And then inhaled
corticosteroids also come in low, medium or high doses so depending on the
severity of the patient's asthma, they'll be on the strength basically the
more severe the asthma, the higher strength or the higher of a dose the
patient will need. Let's see so I hope this has clarified the medications for
you. Now when we think about asthma, think about that the patient will always need
a SABA, which is also called a rescue medication, rescue. So this is something
that the patient should have with them at all times. And depending on the
severity so maybe all they have is allergies in the springtime and when
everything is in bloom, when they go outside they need that Albuterol with
them otherwise they get short of breath because this inflammation starts. But if
this is somebody who is let's say allergic to dust mites or dogs and now
they have a dog, or they have some other allergen that's
basically year around that requires the inflammation in their lungs to be
controlled on a more regular basis, then they'll be on an inhaled corticosteroid
in addition to a rescue medication. Now if this is somebody who let's say has
COPD, emphysema, one of those other chronic lung disorders where now we need
to have longer-acting bronchodilation then they will usually be on a LABA
and an ICS so they'll be on something like Advair now this is definitely
nothing that nurses need to worry about in terms of prescribing because it will
always be up to the provider to find the most fitting medication for the patients
but keep in mind it is very important to understand the mechanisms and how they
work and if you know the mechanism of action you will always know how they
work, what they what response they initiate in the
physiology and then you can apply it. So I would recommend that you memorize this:
adrenergic, cholinergic, agonist, antagonist as well as the receptors: beta
1, beta 2 and alpha that way you can kind of combine these terms and know what's
going on to kind of dissect the meaning of these respiratory medications. Thank
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