welcome to another MedCram lecture we
were talking 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 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 a 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
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
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 air
reversible which we would see in COPD
where 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 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 glycated 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
so you have a nerve that come
down and 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
anti-inflammatories 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 gonna
be number two and the anti muscular
necks are gonna 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
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 asthma 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 so then post nasal
drip can cause asthmatic symptoms and so
whenever you see a patient with asthma
or you're asked about on a test you
should think about these things as
causing asthma so what we call coffee
variants asthma post nasal drip and
gastro esophageal 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
leukotrienes antagonists and we'll talk
about those
so just remember Sanders try it in your
patients with asthma
ask him if 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 we'll join us for part two where we
talk about the diagnosis and the
treatment of asthma
you