Now, the asthma treatment therapy. We’ll
go from what’s known as relatively mild
to severe. First and foremost you always take
history and with the history you’re looking
for.. What’s the most common type of asthma?
Extrinsic. Go step by step. Exposure to the
external world and that’s called atopy,
right? Atopy. So, maybe your patient needs
to then remove himself or herself from that
environment. That’s your first step of management
if that’s the case. Next, short-acting bronchodilator.
So what does that do? Albuterol as needed,
puff whenever they’re
having an attack or bronchospasm. And so
therefore, relieves that obstruction. Next,
what about inhaled steroids, ICS, corticosteroids
low to mid. Remember, inhaled corticosteroids
is it going to do what? It’s going to then
help you with some of that bronchoconstriction
perhaps, and whenever you deal with your corticosteroids
you tell me what enzyme is it knocking out?
Is it LOX? Is it COX? Or is it phospholipase
A2? Good, it’s phospholipase A2. You’ve
knocked out the leukotriene and prostaglandin
pathway, haven’t you. And by knocking out
some of that leukotriene pathways especially
C4,D4,E4, then you may then avoid bronchoconstriction.
Are you clear about that pharmacology? Management is
Continue. Long-acting beta agonist, leukotriene
modifier. Give me some. Well, what if you
knock out the LOX? Zileuton. What
if you knock out the receptors for leukotrienes?
-kast. Montelukast, Zafirlukast, things
you’ve looked at, is that clear? Which leukotrienes
are you trying to avoid in asthma, in bronchospasms?
C4,D4,E4. About theophylline. Theophylline
will help you, well this goes back to biochemistry,
you should be liking this. This beta 2 that’s
a receptor on the bronchial smooth muscle,
what does it work through? What second messenger
from biochemistry? Good, GS. What’s GS
mean to you? A-A-A-A-A… what does that…
what do I mean A-A-A? Well, that’s your
adenylyl cyclase, that’s your ATP to cyclic
AMP. That means protein kinase A.
What does that mean? I am knocking out
my myosin light chain
kinase because I phosphorylated. Remember
all this? If you don’t then this would
be a good time to go back and take a look
at your biochemistry with smooth muscle mechanics.
So, if you knock out the myosin light chain
kinase, guess what happens to the bronchi?
Relaxation. So, what do you think theophylline
might do? Theophylline, well how do cyclic AMP
break down? Phosphodiesterase. What if
you inhibit some of that phosphodiesterase?
Voila! You knock out the phosphodiestrase,
your cyclic can’t be forevermore. Isn’t
that what you want with Beta2? Yes you do.
Now, I’ll tell you right now the two major
approaches for smooth muscle relaxation especially
for the bronchi. Either Beta2 you look for
that mechanism in pharmacology and biochem
and you take a look at NO, nitric oxide please.
Those are two that you want to pay attention
Let’s continue, you have anti IgE therapy,
alright so with IgE therapy you’re
thinking about well some of those
drugs that inhibit what? Your breakdown
of your mast cell. So anything that
then inhibits the degranulation of your mast
cell is always important. Hence you’re looking
at things like this, anti IgE therapy.
Alright now in terms of severity we’re just
going to move from top to bottom which is
just the severity in the beginning will be
quite minimal and then as you go through your
severity and it gets worse then obviously
as far as management, things become a little
bit more complicated. Prevention in all.
So how do you educate your patient?
Important. If you can avoid giving medication
to your patient that is your answer. So therefore,
educate your patient. “Oh, hey doc, my child
is having coughs episodically”…“Oh,
okay”… “And well, I can hear kind of
wheezes and such”… “Okay”…”and
he goes and plays, he plays in this particular
park and every time he comes back after he
plays, oh, he doesn’t seem so well.” Okay,
so, you want to try and figure out as to what
was the child exposed to in that park that
makes him feel like this?
Now after this, mild intermittent, Mild persistent,
moderate persistent and severe. Remember we
start getting to severe and such and even
at night if there’s coughs, not a good
sign, you need to make sure that you’re
Let’s talk about that acute flare, so during
the acute flare in your head you should be
thinking about that loop spirometry which
we saw a scalloped portion. Here, when you
have an acute flare what are you trying to
do? Immediately try to bronchodilate.
Nebulizer. So, what does that mean? That means
that you have a gas mask. I call it as such.
Which is then attached to a machine which
is then exerting or expressing what? Albuterol.
Ipratropium, keep in mind there are two ways
you can approach this, right? Either you could
stimulate the Beta2 receptors. I just walked
you through that in great detail, or you could
block your parasympathetic. Two methods, albuterol
much more so.
What else? Oral or IV steroids? IV steroids.
What’s my problem? Acute flare. Oxygen if
hypoxia is present. Antibiotics if there is
infection keep that in mind as well. Often
times with these flares there is going to
be some type of upper respiratory tract infection
that is involved. Acute flare, well the
magnesium just keep that in mind. Magnesium
is a big deal for your medicine though, okay?
Remember with magnesium two major things,
number one seizures if it’s hypomagnesemia,
also if it’s hypomagnesemia you’re thinking
about long QT syndrome. So those are major
things you want to think about when dealing
with magnesium. Close monitoring, make sure
chronic treatment are being used correctly.
By chronic we’re talking about well is the
patient on the right bronchodilator?
Is it a Beta2 agonist? Is it a leukotriene
inhibitor of the right type or maybe it’s
even a type of corticosteroids. So those
are things you want to keep in mind.
Now, what I wish to bring to your attention
that you will be asked, is if there is an acute
flare especially when you have a child that
has an asthma attack, not only is this child
breathing really quick and the diaphragm obviously
is being used but then the accessory muscles
of breathing are also being used, do you
remember this conversation? So, look for this
and don’t forget. If you find a patient
come in and they’re breathing,
the sternocleidomastoid is working and the
intercostal muscles are working, this is
a child who, at some point, those muscles
are going to fatigue and tire. And the
child starts quieting down and maybe
it’s an intern who didn’t know any better
and feels as though that he or she has treated
the child and the child is quieting down,
thinks that he or she is managing the child
properly. But why is the child quieting
down? The muscles are getting tired, the child’s
not breathing anymore. What’s your
next step of management? Intubate. Break a
few teeth rather than have your child die
on the table. Is that clear? That is a big
deal. So, what are you going to measure? You
tell me, use common sense. What are you going
to measure in the blood? This will tell you
that the child’s acute flare is actually
getting worse? The pH, of course. Because
if the child’s muscles are tiring and the
child’s not breathing, what’s the child
retaining? Carbon dioxide, good. What will happen
to your pH? Decreased. Welcome to respiratory
acidosis and that is no joke.