welcome to another MedCram lecture we're going to talk about asthma and
specifically the causes the pathophysiology diagnosis and treatment
of this very common disease I want to kind of show you what's going on at the
bronchial level you remember if you look at our pulmonary function test
discussion we looked at a flow volume loop and what happens when you blow out
air very quickly your your forced expiratory volume or flow rate goes up
very quickly and then comes down and then you take a inhalation in and thus
obstruction that occurs in asthma and in COPD occurs in this area here which is
the small Airways and as that obstruction gets worse you see a
decrement in the flow rates especially later on in blowing out and the point
here I want to make is that these are the small Airways so this is where
asthma is occurring it's obstruction of these small Airways not the large ones
but the small ones and as such I want to diagram what it is that's going on so
you've got the airway and this is a very simplified version of what it is that's
going on you've got this lumen of the airway that's here and as you may know
it is lined with smooth muscle when that smooth muscle contracts this lumen gets
smaller okay so there's two major things that are occurring in an asthma or
obstruction of these small Airways is you've got some sort of an inflammatory
process for whatever reason that's going on here this inflammation stimulates
certain cascades that occur and it causes smooth muscle constriction and as
a result the inflammation causes the lumen to get smaller and smaller and
smaller until finally there's wheezing there's obstruction and the primary
problem is that you can't get air out of these small Airways and that is why in
an asthma attack you will see that this flow volume loop comes down
and the flow rates in these small Airways is almost non-existent that's
when you run into asthma attacks now the severity of this contraction is
going to give you the severity of the asthma attack and how we affect this and
what the pathophysiology is of this is going to determine how this is treated
so let's talk about that a little bit once again I want to emphasize that in
asthma what we have is reversible airway inflammation that is opposed to
irreversible which we would see in COPD where there's really this airway
inflammation has occurred and this constriction has occurred in COPD it's
kind of irreversible in asthma we can actually reverse it back to almost
completely normal this inflammation and constriction can sometimes be mediated
by IgE so sometimes you will see elevated IgE levels and that fits into
the pathophysiology and the treatment what is IgE it's an immunoglobulin
specifically it's an immunoglobulin E and that's important because
immunoglobulin E affects a cascade that releases histamine which causes swelling
which is going to make the area in that Bronco even smaller IgE uses the
basophils and mast cells
you
these release histamine there are ways of preventing these cells from releasing
histamine and that is sodium chromo gleich 8 you'll see for instance
medications like Chrome illan sodium criminal Glock 8 is used to stabilize
these mast cells and basophils and prevent histamine so sometimes we
actually use that in the treatment of asthma ok so again I want to review the
bottom line here is is that we've got a situation where you have inflammation
which causes constriction of the smooth muscles in the bronchioles so let's talk
a little bit about this smooth muscle then okay we've got nerves that affect
this smooth muscle two types of nerves specifically and they have receptors the
first one I want to talk about is the beta receptor okay so you have a nerve
that comes down and it releases compound which hits this beta receptor and this
causes relaxation and there's another receptor which is the muscarinic
receptor
and that causes constriction and so in both asthma and COPD as it turns out we
want this muscle to be relaxed that's the goal we want relaxation and so what
we're going to actually end up doing is activating this receptor and blocking
this receptor and so what you see is pharmacologically we're going to be
using anti muscarinic s' and we're going to be using beta agonists that's how we
get to the treatment now the other thing that we're going to see
pharmacologically and we'll talk about this is inflammation inflammation is
going to cause constriction because of inflammation
so what we're also going to use is an T in flama tories so what I've just shown
you here are the three cornerstones of asthma treatment some of them are going
to be used first because they're much more effective than others and you could
probably guess which one is going to be most effective because inflammation is
starting everything off the anti-inflammatories are gonna be number
one the beta agonists are going to be number two and the anti muscular Nick's
are going to be number three okay so we'll get into the pharmacology of that
let's talk about the pathophysiology about perhaps clinically where this
inflammation may be coming from so asthma there's there are lungs
things that can trigger problems in our Airways based on a number of things
first of all because of the stuff that we breathe in so that's a trigger the
air that we breathe what else could trigger a spot what else
could be causing it well there's a tube that sits right next to the trachea
which goes down to the stomach called the esophagus and sometimes stuff in the
stomach can reflux up and irritate the airway that continues up so another
thing that can cause this is gastroesophageal reflux disease that can
sometimes cause symptoms of asthma now if we go up here we have the nasal
passageway sometimes you can have allergies that drip down and cause
irritation in there and that so that post nasal drip can cause asthmatic
symptoms and so when I ever I see a patient with asthma and whenever you see
a patient with a sore you're asked about on a test you should think about these
things as causing asthma so what we call coughing it's asthma post nasal drip and
gastroesophageal reflux disease some of the other things that can contribute to
all of these think about down feather pillows
pets in the bedroom
these are places that you spend a good six seven eight hours a day and could
affect some of the treatment symptoms so these are some of the things that by
getting rid of we might improve asthma there's also environmental things and
things from work for instance from your occupation there's something called
isocyanates or cotton dust wood dust
solvents all of these things can by breathing the men set off asthma
exacerbations there's one other thing that I should make you aware that they
might ask you on a test they love to ask things that are uncommon in asthma that
could be very unique or make you think of something and there's something
called samplers triad where you see number one aspirin sensitivity number
two asthma and number three nasal polyps
now when these people take aspirin or any type of NSAID what can happen is
that these medications inhibit cyclooxygenase and as a result they're
going to have increasing compounds that are going to set off asthma
exacerbations the key here is that within hours of taking aspirin they're
going to start to feel flushed and they're going to go into an asthma
exacerbation these patients who are typically sensitive to aspirin or NSAID
products are also going to have nasal polyps the key here is that they need to
stop using aspirin and NSAID products and find an alternative these patients
by the way and we'll talk about treatment also respond very well to
leukotriene receptor antagonists and we'll talk about those
so just remember samplers try it in your patients without
I'm asking that they've had a history of aspirin sensitivity or if you've noticed
that their symptoms have gotten worse after taking aspirin or NSAIDs and then
ask them about a history of sinus problems maybe even sinus surgery or
nasal polyps okay will join us for part two where we talk about the diagnosis
and the treatment of asthma
you