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?
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.
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
Are you clear about
Management is important.
The 2020 GINA Guidelines
recommend inhaled corticosteroid,
as the preffered
reliever for patients
who present with symptoms
less than twice a month
and for the prevention
Short acting beta-2 agonist can
be used in addition if needed.
Long-acting beta agonist,
Give me some.
what if you knock out the LOX?
What if you knock out the
receptors for leukotrienes? -kast.
things you’ve looked at, is that clear?
Which leukotrienes are you trying to
avoid in asthma, in bronchospasms?
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
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?
So, what do you think
theophylline might do?
well how do cyclic AMP break down?
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 to.
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?
If you can avoid giving medication
to your patient that is your answer.
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.”
you want to try to 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 intervened ASAP.
Let’s talk about
that acute flare,
so during the acute
flare in your head,
you should be thinking about
is that loop spirometry
which we saw a
Here, when you have an acute
flare what are you trying to do?
Immediately try to bronchodilate.
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?
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
Albuterol much more so.
What else? Oral or 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
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
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?
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?
Welcome to respiratory
acidosis and that is no joke.