Chronic asthma is a common, reversible obstructive airway disease characterized by airway hyperresponsiveness, leading to symptoms like wheezing and shortness of breath. Effective management involves a stepwise approach guided by symptom severity, age, and adherence to treatment, prioritizing inhaled corticosteroids and personalized action plans.
Mind Map
Click to expand
Click to explore the full interactive mind map • Zoom, pan, and navigate
Okay. Well, welcome to this disease
state review on chronic asthma. I'm Dr.
Bust, your faculty for this lecture with
High Yield Med Reviews. You know,
asthma, it's a common obstructive lung
uh disorder that impacts many patients
of all ages. It's also known to
contribute significantly to healthc care
resource utilization. Well, thankfully a
number of professional organizations and
medical professionals have come together
nationally and around the world to
create guidelines to help in the
management of this disease.
Asthma is not very not only wellnown but
is also has a number of treatments that
have evolved over the past decade and
that are relevant to consider. We will
make sure to cover all of these points
on this important disease. And with that
let's go ahead and jump into chronic
asthma. Well, just like with other
disease states, we're going to hit the background,
background,
pathophysiology, you know, clin the risk
factors, how patients present,
diagnosis, and then jump into the
treatment plan, trying to point us to
some of the basic core aspects of the
guidelines. Um, this is not meant to be
uh every potential avenue angle on
asthma. Uh but I also want to say that
I'm going to try to put it in the
context of the other obstructive airway
disease which is known as COPD because
there is some degree of overlap and so
that's important. Um okay so with that
let's go ahead and jump into the uh
background. So asthma is a chronic
obstructive airway disease that is more
reversible. Um if you can remove the
antigen or allergen it can be u you know
symptoms can be controlled much easier.
uh that's different than especially
emphyma which is the later stage of COPD
that is irreversible in nature after the
you know remodeling of the airway has
already occurred. Now asthma is unique
not only in that it's not necessarily
being remodeled like emphyma. There is
some structural changes and anatomical
changes that do happen with chronic
uncontrolled asthma but it is a hyper
respponsive airway disease that
typically responds better to things like
bronco dilators. Um now but just like
other obstructive airway disease there
are uh a difficult ability for the
patient to get rid of um you know volume
of um their volume of air in their lungs
and that affects their expiratory flow
and that's usually what causes most of
their symptoms. But this is a pretty big
problem. 25 million in the United States
diagnosed. Um approximately 5 million of
these are children and adolesccents
below the 18 years of age. So it's a
very relevant um disease state. On top
of that there is a family connection
which seems to be correlated to genetics.
genetics.
Um so third uh you know a number of
cases so if you look at the number of
people that have asthma with one parent
uh about 25% recurrence of asthma with
two parents diagnosed is 50%. So there
seems to be a small correlation
uh to that as well. Okay, let's now jump
into the
pathophysiology and again putting a
little bit in the context of how does it
compare to other obstructive diseases
like COPD so that you keep it straight
in your mind because it we get to the
management side some of the drugs that
we use early on are very different uh in
these two dis obstructive airway
diseases. Okay. So most patients with
asthma again will have a trigger uh and
this trigger is what causes the
exacerbation or the hyper respponsive
component of their disease. Those
triggers can be exercise. The airflow
going in and out can be irritating to
the mucosal lining and the lung parinma.
Allergens certainly are a big one.
irritants like uh secondhand smoke, even
changes in the weather and yes,
obviously getting viral or bacterial
lower respiratory tract infections in
particular. Um but it can also overlap
with other diseases and that's where see
there is a some people have a what's
called overlap syndrome. uh and I'll
show you a vin diagram here in a minute
that kind of highlights that key point
because it does matter and this is where
some treatment options are available in
both diseases and the way we would use
them. Now I want to highlight we're
going to talk about allergic asthma
versus non-allergic asthma. Okay. And
the reason this is in part relevant is
um it does help us to understand who's
going to respond better especially to
those inhaled uh corticosteroids or who
look like patients who have an overlap
syndrome. So in allergic asthma, the
triggers often produce an innate immune
response and it's specifically with the
exposure of the agent that results in an
activation and progression especially of
what we call T-helper cells or TH2
um that end up producing local
recruitment of eocinophils but also the
production of IG antibodies which are
classically known known to be associated
with allergic reactions. We even have
drug therapy targeting that. So we have
drug therapy that the imino inhaled
cortosteroids targets these things to
help reduce the progression of this
particular type especially allergic
type. So over time though with chronic
inflammation and exposure to antigens
without adequate treatments you get this
increased mucus secretion. you get
airway narrowing as a result. This also
causes hyper respponsiveness to the
airway where it spasms and that's what
usually causes the wheezing but it
reduces flow distal to that point. Now
eventually cytoines can be released uh
from these TH uh 2 cells uh T helper
cells and they become the again like I
said the recruitment driver uh for the
eocinophils that show up. Remember with
asthma versus COPD eosinaphils are
predominant in asthma whereas neutrfils
are predominant in in COPD.
However, when you have patients with
non-allergic, which we'll come to in a
minute, you'll see that that the
neutrfils show up. So, over time, the
mucous glands get enlarged. The smooth
muscle of the bronchioles hypertrophy
and grow in size, and so you have a very
thick muscle that's able to spasm even
greater, and that overall reduces air
flow and is the common reason you hear
wheezing sounds on the exam. Now the
patient with non-allergic where the T-H
helpper 2 cells are lower um these
patients do have a trigger but the
triggers are typically produce a
macrofase initiated response that then
stimulates other cytoines and
inflammatory mediators like interferon
TNF alpha and other inolucans that are
not as prominent in the allergic type
and that's why you know they break these
two down in these these main categories.
So, it's important to to recognize, but
this is where those neutrfils eventually
start to show up and that can cause a
remodeling of the airway that mimics a
pattern similar to COPD. So, they have
some shared effects. They're both
obstructive airway diseases, asthma and
COPD, but there's cell lines that are
predominantly present are different. So
asthma is predominantly eocinophils not
doesn't mean only said predominantly
COPD is predominantly neutrfils but even
COPD patients with more moderate to severe
severe
disease can have more eosinaphils which
typically leads to more symptoms and
those are the patients in COPD that
benefit benefit from inhaled steroids.
Um so when you look here you see
hyperreactive component to as is is a
characteristic of asthma and the airway
activity whereas it's not very
responsive in COPD broncoil response
therefore is much more prevalent and
beneficial in asthma with hyperreactive
airway disease than with COPD and also
the because of the einophils in
particular um and their effects on the
um hyperresponsive nature of the airway
it held steroid roids are not only ear
used earlier on but become one of the
mainstay of treatments at the very very
early stage even before we would
consider using short acting kind of
bronco diilators like albuterol because
historically we would give everybody
those drugs but sometimes what happens
is they they use those preferentially
and they're not using the thing that's
going to help prevent them from ex
corticosteroid so I mentioned the
overlap that kind of syndrome. That's
the asthma COPD overlap
ACOS. So remember this is COPD right in
different stages. Chronic bronchitis
typically occurs earlier, emphyma
typically occurs later. There's this continuum.
continuum.
They're all ob obstructive airway
diseases because you have asthma and CBD
and then there's these in the ven
diagrams are nice because they give you
that visual perspective of that there is
this small percentage of patients who
have an overlap syndrome and that's why
we have to keep those subsets of people
in the back of our minds. Now there are
other types that the literature and some
of the guidelines and resources will
cover you might hear about. I mentioned
this at the beginning of the lecture
that exercise with that increased air
flow and minute ventilation can cause
irritation to the airway. So there is
exercised induced bronco constriction
which these patients would then use an
agent commonly like for motorol with a
quicker onset longer acting betagonist
and then right before they exercise so
that they can continue to be physically
active but not have an exacerbation of
their um disease. There's also irritant
induced asthma and also reactive airway
dysfunction syndrome. sometimes are a
little hard to differentiate. These are
like sub subclasses that you know break
down to minutia. Not really as common,
but I wanted you to be aware that these
these other things exist. And then
aspirin and exacerbation exacerbated
respiratory disease has to do with the
way aspirin works. So remember aspirin
is an irreversible inhibitor of psycho
oxygenase. And so therefore when
arachidonic acid is released from the
cell membrane it only has one of two
pathways that it can go down to generate
pro-inflammatory mediators in most
cases. It can go the cycle oxidase
pathway and form thromboxane A2 as well
as the prostaglandins or it can go down
the five lipooxygenase pathway and form
lucotriins. And unfortunately what
happens when you give aspirin in some of
these patients is that you shunt
arachidonic acid towards the lucotrien
and these patients develop a common
pattern of exacerbation and the samp
triad is the patient population who most
commonly is going to experience this.
Those are patients who have underlying
asthma symptoms, nasal polyps present,
and then they usually have attopic
dermatitis or some sort of
allergies. So the triad, all three of
those things typically are there and
have classically referred to as Sam's
triad. So just those are important small
little factoids that people will
sometimes test on or throw out there or
you might read about. I just wanted you
to be familiar that they they do exist. All
All
right. Now, we're going to move on to
the risk factor evaluation before we
then jump into the clinical presentation
workup and then get into the diagnosis
so that we can merge over to the
treatment. So, risk factors obviously I
mentioned a little bit about family
genetics. the more uh members of the
family that have one, the um the greater
the chance that the child will have that
exposure to environmental and also
occupational allergens. Obesity mainly
because you're not having good uh lung
capacity because of the weights in the
way. um other allergic conditions like
attopic dermatitis and then obviously
having more exposure to frequent lower
respiratory tract
infections when you have a a
predisposition already. Um so this would
be kids sometimes that go to daycare. Um
even you know we see this in in any
school system when kids go back to
school uh they come in close contact
with each other and there seems to be
this bump and exposure and that can
cause some kids to have an exacerbation
of their underlying
asthma. All right. Now there are some
other things that are important as it
relates to risk factors and these are
related to the increased risk of
exacerbations with asthma. Okay. So
these are people with poor outcomes.
These are reflective of people that
increased risk of exacerbation. One is
daily use of a reliever medication like
aluterol short acting betagonist and
that's where I think that attention over
time has been neglected and so as the
guidelines have evolved they have
shifted a stronger attention to the
preventative stuff because it was
mentioned but I don't think clinicians
because sometimes when we you know as
clinicians we're busy u we study things
we like tables charts summary summaries
and sometimes those tables, summaries
and charts can't provide every angle and
aspect of the context of the guidelines.
So that might be described somewhere in
the text, but a lot of times people
don't read all those things and
unfortunately they memorize those boxes
and they think everything is encompassed
there. Remember guidelines are meant to
be a guide. They're not absolutes. So
even within these recommendations and
issues, they're not 100% perfect. So
don't treat them that way. Don't be
dogmatic about it. But at the end of the
day, also we know that people that
preferentially use short acting beta
agonist to control their symptoms,
they're not controlling it. They're
finding out that they're they're doing
worse. They have bad outcomes.
Inadequate inhaled corticosteroids. That
goes just to the opposite. So that's why
this one is now truncated. You know, the
first one is patients who are not on
them when they should be uh don't do as
well. Other conditions obesity gird
because they can aspirate and they get aspiration
aspiration
pneumminitis allergic
rhinocyitis these are patients who have
post-nasal drip and they aspirate so
those are risk food allergens u
exposures to environmental pollutants
obviously um psychosocial psychological
problems certainly isn't going to help
lung functions especially when they're
FEV1 it shows a more severe obstruction
where it's FEV1 less than 60% of the
predicted as it relates to response to
broncoilator therapy. That's typically
not good. High eocinophil counts. Okay,
again remember those are the primary
cells that show up and especially in the
allergic type where those TH2 cells are
predominantly recruiting more and more
of those. If they have exacerbations,
especially where they've been intubated,
that's a red flag. Okay. Um, and I ask
that when, you know, I practice
emergency medicine, so I see these
patients come in all the time. But one
of the questions I'm looking for is it
as it relates to especially when they're
breathing a little faster and harder and
I see, you know, accessory muscle use.
Am I going to admit this patient? Have
they ever been admitted before? And
certainly if they've ever been
intubated, they are hard harder to
manage on a ventilator. So we do need to
be cognizant of that.
Okay, let's now move on to the clinical
presentation and some of the ways that
these patients present whether it's in
the you know ambulatory care clinic or
acute care
settings. Most commonly they feel chest
tightness, they're having a cough and
certainly they're having shortness of
breath and most commonly wheezing.
Sometimes you can even hear the wheezes
without a stethoscope.
The other complaint you'll mainly hear
from the parents is that the kid is
waking up all throughout the night
coughing sometimes even gets up
physically and comes to the room wakes
up the parents you know that's classic
symptoms. Now it will vary um over time
and in intensity is what you'll see and
that's usually due to exposure issues.
Again the symptoms typically worsen at
night. there is a circadian kind of
pattern that seems to be with it. But
also when you're laying flat, you're not
maximizing lung volumes. Okay. Anytime
you want to improve someone's breathing,
sit them up. Secondarily, uh if someone
does have gird and they're aspirating or
they're having post-nasal drip, they may
be having small degrees of aspiration
that will exacerbate when they're laying
flat. Okay. uh obviously those triggers
that seem to be show up especially with
changes in the weather or with exercise
it's correlated with some of those
activities in particular.
Okay. So how do we work these patients
up moving us towards the diagnosis of of
these patients which will then also put
us in the and how do we do a step-wise
approach to the management.
Okay. All right. The first being
obviously your vital signs physical
exam. The vital signs really what we are
looking at mainly. Yeah, if you think of
they're infected or something. Yes, of
course. But their respiratory rate and
then their O2 sats on room air that's
going to tell you a lot about what the
degree of obstruction. So if they're
hypoxic, you know you got a problem.
Okay? So that would be less than 90% on
room air typically. Labs, yes, you're
going to get a CBC, CMP, those kind of
basic things intermittently. But what
I'm really interested in on especially
in asthma is the eocinaphil count. Okay.
So you can get that with the CBC with a
differential or order a uh eocinophil
count itself blood level. Um because
again I'm trying to look for that
allergic type and the degree. Remember
it's one of the indicators of poor
outcomes and an increased risk of
exacerbation. So that's in part why it
matters. And it also matters if you are
going to initiate some of the drug
therapies that target
uh Ig antibodies and other things we
might also measure those okay because
this is some of the allergic patterns
that we see imaging if you're susp
suspicious of other causes and that's
usually a lower respiratory tract
infection in most cases. Pulmonary
function test spyometry those are kind
of the same thing. It's a blowing into a
closed circuit system that helps you to
assess the their total lung capacity,
their inspiratory reserve volumes, their
expiratory reserve volumes. It helps us
to calculate that
FEV1. Now these this is different than
peak flow
meters. This is done in a clinic
environment. The PFTS are spometry. It's
on a machine. But peak flow meters are
things that patients use at home to help
monitor and regulate their their asthma
before it gets out of hand. So that's
like a handheld device that you can blow
into and measure the peak flow to
correlate and it pick up on an
exacerbation that's evolving, especially
if they do get exposed to an allergen.
They can identify that and that's where
asthma action plans come in. Well,
that's feasible at home, but a pulmonary
function test is not always feasible at
home. So it's a correlation of the two.
But when you first have a diagnosis or
to get to the diagnosis, you need to do
this particular thing the spyometry or
or PFTS on these
patients. Um so keep in mind pulmonary
fun pulmonary uh peak sorry peak flow
monitors are things that they use at
home. The one thing else I wanted to say
I just remembered is that in COPD we use
pulmonary function tests and we use
spyometry also to assess for that
obstructive pattern the FEV1 FEC ratio
yes but we don't use peak flow meters in
COPD they don't correlate as well but
for asthma it definitely shows up and is
an important part of the overall
management of these patients.
So again this is helping us to assess
the peak expiratory flow and that helps
us to get that uh the FEV1s and look at
the um total lung capacity. It also
helps us to see how the patient's
disease is progressing over time. So the
procedure has a maximal inspiration
followed by a very rapid quick forceful
exhalation and then you try to continue
it. So you have these, you know, the
technician, if you've ever been in one
of these procedures, I mean, they're
like a coach screaming at the patient,
all right, take a deep breath in, hard,
deep breath, and then blow, blow, blow,
blow, blow. And they and you want them
to really give the full effort so that
you can generate these flow volume loop
curves that I'm going to show you here
in just a second. So they help us to
identify Feb1, FEC's, and those kind of
things. And that helps us to create
zones. And this is the same thing that
we use with a peak flow meter. Peak flow
meter. Okay, this is what we would use
at home and it helps us. But you you are
establishing the asthma action plan in
part on this. You can use the peak flow
meter to also establish the asthma
action plan. You just have to do it over
a period of two weeks and get their
personal best and they can't have any be
recently uh exacerbation all these
things. So, it's a very complicated
two-eek process to figure it out, but
you're generating a uh kind of like a
traffic light. You got the green,
yellow, and red. Okay, obviously red is
bad. If you pass through the
intersection at yellow, it's a little
scary. You got to be a little cautious
doing that. Generally, not advised.
Green zone is good. Keep going. So, that
has to do with the percent of the best
flow. Now, so you can get that from the
spyometry. You can also do it from the
peak flow. The whole goal here is to
create a plan. The patients know what to
do and can recognize this at home. And
obviously the peak flow meters are going
to be helpful at home. And this is where
we would then administer, you know,
certain treatments to them based on
their um compliance, adherence, you
know, all that kind of stuff. But the
pulmonary function test is showing this
flow volume loop curve. And so if you
look here, this is inspiration down
here and then the top is expiration. The
curve is actually
um done in a backwards manner. You
actually start right here and as they
take a deep inhalation it goes backwards
and then then they do a forceful very
abrupt expiration and that's what
generates the peak expiratory flow rate right
right
PF as they also blow that out it also
gives them the FEV1 in the first second
okay the amount of volume they can blow
out. Um, so this is a representation of
a normal curve, but at the end of
expiration, they're back here again.
Okay, this is an example of an
obstructive pattern. You can see that
it's not as
high. Okay, but so there's a loss of
volume. It collapses very
quickly. There's some obstruction. So
you see that thinning of that, right?
And then so their FEV1 is now
compromised. So you can see the
differences in the FEV1s here. They're
compromised. Another way of looking at
this is considering all the various
aspects of the volumes in our lung with normal
normal
physiology. So in the normal you know we
have our tidal volume that's just normal breathing.
breathing.
If I want to go above that, it's like
and I want to deep go above and beyond
this the normal breathing that I
consciously aware of. That is our
inspiratory reserve volume. If I blow
out more than what I would normally blow
out with a normal breath, that's my
expiratory reserve volume. And then
there's what's remaining. You will never
get out all of the volume of air in your
lungs. That's your
residual volume or the remaining volume
that stays and that's what gets trapped
and causes an obstructive airway
disease. Whereas restrictive it's less.
Um and so these give us our inspiratory
capacities, our functional residual
capacities, our vital capacity or the
total residual volumes that make us help
calculate the total lung capacity. Okay,
when you add them consider all of them.
So, this is a great visual to have wrap
your mind around what's going on when we
do a pulmonary function test, but even
physiologically what people are going
through because we need these we need
these capacities or these reserves to
help us to compensate for things that we're
we're
doing. So, this shows you a restrictive
airway disease pattern. Okay, the very
first one where you see the the residual
volume uh is less. You see the total
lung capacity is also less. Okay. And
then starts the obstructive patterns and
that's your asthma and COPD. And where
you see that's characteristic compared
to the normal patient is that the the
that reserve volume that residual that's
staying is being accumu is starting to
accumulate and it's the worst with COPD
especially emphyma and that's why they
develop those hyperinflated airways with
flattened diaphragms in COPD. But you
can see that residual volume is
increasing. The total lung capacity also
increasing but their expiratory reserve
capacity is being compromised. You see
how it's getting smaller compared. And
so that's because they collapse. They
obstruct their airway. So those things
should just make sense to you. Remember
we're about at high yield teaching you
why so that you don't have to memorize
things. It sort of just makes sense then
what's going on with the path of fizz
and the disease and if we understand
these cell types and the triggers and
things then it makes sense why we're
targeting the drug therapy the way that
we are. Okay. Now let's jump into our
diagnostic criteria which is for the
most part pretty
straightforward. So with asthma you have
a confirmed expiratory flow limitation.
Okay. Okay, so that
FEV1 is going to be compromised.
Okay, but you have a hyper respponsive
and they show a reversibility pattern
with bronco dilation. That's key.
Remember that was one of those
identifiers that makes COPD and asthma
different. There's that responsiveness
to the bronco dilator therapy that makes
it helpful. So you'll see things like
again if depending on how you what you
use you can use spyometry or pulmonary
function test which is the best it gets
the most accurate information quickly.
You can do expire you determines their
expiratory flow. You can also calculate
that by their peak flow meters and then
certainly their symptoms help to
quantify that. But what we want to do is
have objective indicators so that we can
create that asthma action plan that
allows the patient to know at this
point, you know, you're in your your
yellow zone or caution zone and you need
to probably pick things up or you're
going to find yourself uh you know, even
back in the clinic or in the hospital
having to be um admitted admitted to the
hospital. Now, what is a response to
bronco dilator? Well, they do a baseline
spyometry and then they do a post
expiratory flow rate after receiving the
albuterol. And so you would get the dose
and you you rememeasure it about 10 to
15 minutes later. Remember short acting
bronco diilators don't work immediately.
We'd like them to, but they don't. Um it
will take 5 to 10 minutes for those to
kind of kick in. So we give them a full
10 to 15 minutes because it will last
longer than that. But by then, if it's
going to work, it's going to be showing
up within that 10 to 15 minutes. Now,
there's also some other diagnostic
criteria based for kids versus adults
and you can use spyometry or peak
pulmonary function test to guide you and
what is the change in expiratory flow
rate that we want to see. So, there are
some variability of air flows that are
outlined in this particular table. So
it's a lot on here. Uh I would not
necessarily try to memorize it but
rather just understand the basic
concept. So we just covered for example
the post or broncoilatory response. So a
positive broncoilator
response is an FEV1 change or increase
that improve by 12% usually that is
greater than 200 mls of volume. That
piece of information I would say is
probably the highest yield content on
that table. I would definitely memorize
that if I were you because that's the
most common. Now there are ex things
where we look at increased lung function
after four weeks on inhal corticosteroid
especially in those patients with
eosinaphils but you should see very
similar positive
responses. Okay. So the inhale that's
why we want them on that inhaled
cortical steroid and we don't want to be
using that because this is
preventative right where short acting
bronco yeah it improves their symptoms
but it's not getting to the root of the
problem which is the exacerbation to
begin with there are some other things
that you can do there's a bronco
bronchial challenge where they get methyloline
methyloline
um induced or manitol or some other
environmental exposure uh to see that
that's not as commonly done. Um but I
just wanted you to see there are
variations that help us to identify that
hyper respponsive component and who's
going to receive the benefit from most
of this drug
therapy. Okay. Now we're going to move
into the treatment aspect. So let's
first cover some of the goals and then
we'll move into a little bit of some of
the approaches to management and then
I'll walk you through based on the age
because it does differ. Okay, does
differ. Okay, so our goals are
straightforward long-term control. We
want very few to no asthma symptoms. We
don't want kids waking up at night. So
we want good sleep so that they feel
rested in the morning. And we want
basically unrestricted physical activity
even if they have exercise induced uh
bronco spasms. Long-term we want to
minimize those exacerbations. We
definitely don't want them coming into
the hospital. No major side effects from
the medicines. So one of the problems
with steroids is you're going to swallow
some of them. All right? About 12 maybe
sometimes 20% of what you inhale goes
into your stomach. you do systemically
absorb a little bit but remember chronic
steroids can have a a impact on growth.
Um now that doesn't mean we don't use
them. It just because also exas
exacerbations can impair growth but we
want to try to minimize that but also
even inhaled um steroids can cause oral
fingial thrush. And so you want to make
sure that after they inhale this you
rinse out their mouth and you spit it
out. Okay. But just keep in mind these
things do do happen and we want to
maintain good pulmonary function. So
especially if they get exposed to a
virus or bacteria, they aren't likely to
have an exacerbation and need to be in
hospital. So this is a management a
personalized management
process assess adjust and review. Okay.
And part of this was developed to remind
us as health care providers. I think you
know with us being busy and specialists
that sometimes we forget things. Tables
and summaries like this can be helpful
but we need to make sure that we don't
put blindfolds on and make assumptions.
So we need to make sure that we you know
don't have the wrong diagnosis.
We're controlling other comorbidities,
especially those that can be controlled
like gird, right? Weight management
issues that we talked about. Look at
their inhaler technique. I'll I'll be
talking about that here in just a little
bit because a dry powder inhaler is a
little bit different of a technique from
a meter dose or aerosolized inhaler,
which is different from a nebulized
inhaler. Okay?
And then you review and assess the goals
with the patient and the patient's
caregivers. Adjust again strategies for
treatment, modifiable risk factors. Make
sure that that a plan is working for
them, their asthma action plan. Do your
education and skills, really good
institutions and stuff. When a child
gets admitted for asthma, they they get
enrolled to programs. Those programs
have been very helpful at getting
families educated and help control these
symptoms long term. And then you want to
review obviously on a regular basis when
they're following up. How are they
doing? Have they required any admissions
or exacerbations? Are they having any
side effects? Any changes in their risk
factors? Maybe they moved um to a
different area. Okay, so all those things
things
matter. So what are our tools? Well, we
have a lot of them. And I know again
this is a a kind of a a busy table, but
it's it almost walks through some of
those early stage drugs and then our
options. And then the biologic agents
down at the bottom are really for our
more difficult patient populations to
control. So they're usually adjunctive
therapies added on later. Um uh and so
there that class has grown and evolved.
A lot of them are parentally
administered. They're biologic agents.
They're monoconal antibodies. So that's
down here at the bottom. Um, and I'll
come back to that in just a minute. But
let's talk about the historically
available drug classes. We have our
short acting broncoilators and those are
specifically uh our beta agonist in
particular. Um, those can be albuterol,
lavalerol. You could even use uh
epotroprium although that's not common
in if you had nothing else that's what
you would use. That's more common in
COPD. So that's a short acting
muscerinic antagonist uh epotroprium.
It's not listed on this table uh because
I wanted to make sure that that's not
the thing you should be trying to use in this
this
case. Uh short acting betagnus work just
a little bit better in in asthmatics. uh
inhaled corticosteroids with a short
acting um beta agonist. So you have
budesinide which is a a steroid followed
with combined with aluterol. There's
long acting broncoilators foroterol
probably being the more common one in
this group. Salmetrol has been around
for a long time. Valantrol
uh has also been around for a little
while, but for Motorall is better in
some respects because of its pharmacco
kinetic and dynamic profile that allows
for earlier onset of action and still be
long acting. So that's very helpful for
even acute symptoms in some patients or
exercise induced bronco constriction.
And then we have inhaled
corticosteroids, which we're not going
to dive into all the pharmarmacology and
drug class review here. If you need
that, you need to go look that stuff up.
The assumption is that you know some of
those basic things. But they come in
low, medium, and high dose formulations.
Basically, just the amount that you're
getting and how you administer it. Uh so
fluticazone's been around for a long
time. A metazone, boudesinide, pomacore,
it's been around for a long time. also
comes as a nebulizer option. So those
things make it convenient for patients.
Obviously long acting betaagonist
combined with the nail cortical steroids
can improve compliance adherence. So we
have some combination therapies that you
know are have evolved over the years and
there are some lung acting anti-muscular
antagonists that are also used in
asthma. Again, these tend to be a little
bit more commonly used in COPD, but
remember there's an
overlap overlap. So that sometimes is
needed for patients. This is not
typically first line therapy. It's
typically a second or third line option,
but they are already on an inhaled
steroid in this case. Okay. And then of
course our biologic agents that you can
see there that we have interlucan
antagonist or uh drugs that would modify
those. Again, they're all monoconal
antibodies. So you have to administer
them parentally via subq injection or
IV. Um you know omalusmab has been
around for a while. This is the one
that's a uh a binds to IG antibodies. So
that's when you need the levels because
that's how you dose it in part. Um and
then we have um tesalus
um down here another subcutaneous again
monoconal antibbody. So all of these
targets uh some of those immunologically
mediated responses that show up more
severe disease. So they're not first
line, second line, they're really that
third and fourth, you know, or some
reason that you can't use some of these
things up
above. All right. So all patients with
asthma should have access to reliever
medication. The problem is is that we
don't want to only prescribe that to the
patient. you should not be doing that.
That means that they're you're missing
the opportunity to start those um
treatments that are going to help
prevent and that would be your inhaled corticosteroids.
corticosteroids.
So if you are going to use reliever
medications, you'll see probably the the
combination of an inhaled corticosteroid
with formoterol uh as needed. So yeah
like wow these are in patients with very
minimal risks very minimal side effect
uh symptoms. Um but these are preferred
for most patients. Remember quick onset
of action and it has also the
preventative medicine in there. Okay. So
you don't see on here listed the short
acting beta agonist like albuterol or lev
lev
albuterol. That doesn't mean you never
give it to them. So keep in mind
guidelines like I said before are
guides. They're not
absolutes. Every patient is different.
But as the majority of our thinking and
the approach to management, you really
want these patients to be even in a PRM
basis inhaled corticosteroid. And if you
are going to be using reliever
medicines, then you need to make sure
they're on one.
Okay. Uh and then you kind of go step up
and down, you know.
um you know as you go through the
disease and I and I'll work I'll work
through that here in just a second. Now
which has been like I said been around
for a long time has a slower onset of
action so it's not as helpful um you
know and volanterol is more commonly
used in um you know more preventative
situations rather than acute especially
if they're symptomatic.
Okay, so we know that short acting beta
agonists and bronco dilators are known
to especially on a regular basis
increase the risk of exacerbations.
That's a take-home point core concept
and if used alone this increases the
asthma related complications and need
for health care resources which is again
why we don't want them on that by itself.
itself.
Okay. Now all patients are different.
Not everybody can afford everything that
we want to
do. So you may have to compromise in
certain areas because that's all that
you can do.
Okay. Now what you see here are a series
of tables that are basically summarizing
the approach to management and kind of
in a step-wise approach based on the
guidelines. In this particular uh table,
this is referring to patients who are
adults or adolescents. Okay? So the
majority, you know, people you there was
pediatrics and we break it down to 6 to
11 and those who are less than six years
of age 0 to
five. Again, when you look at the
patients with very little symptoms, you
see lowd dose inhaled steroid for
motorall being the preferred. I didn't
say it's the only, it's the preferred.
if you can do it and they can afford it
and they can get it as needed, even as
needed. Step one, step two. Okay, so
these patients have very little symptoms
throughout the week. When you start to
get to symptoms greater than four to
five days per week or they're waking up
due to the symptoms more than one night,
then these are the patients that you
want to um consider smart therapy which
is down defined down here for you.
Single inhaler maintenance and reliever medicine.
medicine.
So now this is where we're going to be
using it on a regular basis and we want
it to be combined so that we make it
easy for compliance
adherence purposes.
Okay. Now you'll see um most of these
recommendations are coming from the GINA
guidelines, okay, which is the kind of
the global initiative for asthma
management. But there the United States
also has the NABP and they've been
around for many years and decades.
There's a lot of overlap. Um again the
goal here is the big picture. Okay.
Sometimes people get buried in the
minutia and legalism of a chart or a
table or a statement and they don't have
the full context. So that's kind of why
I'm we're we've tried our best to
combine them as the the the intended
meaning of the guidelines in the
literature recognizing that every set of
guidelines is influenced by the people
who got write them and that varies from
time to time. Um as you get to step four
where these patients are having daily
symptoms waking up more than one night
okay either one then these patients need
to be on medium dose. Okay. So, you see
that the dose of that steroid is now
changing. Again, you have to look that
stuff up. If you don't know what I'm
talking about, you have to know that
there comes in multiple formulations and
you have to choose and there's, you
know, different doses for each of the
inhaled steroids as to what constitutes
low, medium, and highdose steroids. And
again using smart
um you know kind of approach where we
use a single inhaler maintenance and
reliever therapy as much as
possible when you see again you mention
I you you heard me mention the addition
of long acting muscerinic antagonist
that's your teatroprium in particular
um those agents are added on towards the
end right these patients are more severe
symptoms and despite being on some of
these other um treatments, they're not
getting response. But you're also
considering even higher dose
incorticosteroids to get it under
control. Even considering oral
corticosteroids in some patients, but
these are usually patients with a very
low peak expiratory flow of less than
60% compared to the norm. This is also
where you see the biologics being added
on. So remember it was towards the end
or more severe cases where we would use
them. So you should not ever see
biologics being used monotherapy first
line. That's a wrong answer on any kind
of board exam or test for sure and it's
also very wrong in the clinical practice
of the management of this disease. The
next table here is again children 6 to
11. You see again the very similar
stepwise you see the very similar uh
abbreviations and again you'll see the
use of a lowd doc corticosteroids when
taken with a short acting beta aagonist
or bronco dilator and then we see here
daily and step two which is a little bit
different than the adults right we want
to make sure we get them their airway
the kids airways are really small so we
want to definitely be a little bit more
aggressive where we are having them on
inhaled corticosteroids preferentially
but the short acting beta aagonist is a PRN.
PRN.
Okay. And then as you progress, you just
basically see the addition of more
medications and the escalation of the
dose of that inhaled corticostero from
low to medium dose and then you
eventually get to high. And consider um
obviously um biologic therapy a little
bit sooner, especially referral to a
pediatric asthma specialist because we
do not want these patients getting out
of control. One is the risk of death is
much greater. Secondarily, they they're
missing school, they get behind,
physical activity, a lot of things
negative can uh begin to happen.
happen.
Now, this is uh in children 0 to 5 years
of age. Um there's not as many steps.
It's step one through four. The
diagnosis, especially very early on, is
very difficult to make because they're
get especially around that six-month
window when they their antibodies are
gone from what the mom was able to
provide. Those are falling off and
what's happening is they're now
developing their own active immunity and
a lot of things can cause airway
problems. So, it makes it a little bit
difficult. But um you can see here that
short acting uh bronco dilators and
consideration of a short course of daily
inhaled cortical steroid if there's
respiratory tract
infections and then it's step two. Okay.
Um especially again they're still
working it out trying to get the because
you can't do pulmonary function test on
a three-month-old. It's not very easy to
do that because they can't participate
and follow instructions. So you're
looking at a lot of their patterns of their
their
symptoms and the frequency of followup
is starting to drive a little bit of
that. Okay? Making sure you rule out
other diagnoses as well. But you see
here that the low
dose of unheld steroids, we don't see it
escalating up as high because member
steroids do have that risk of
suppressing growth, but so does
uncontrolled asthma. So just these are
unfortunately some of the things that
you have to you have to memorize
um a little bit closer and look at them
especially if when you're treating those
special patient
populations. All right. Now we're going
to kind of dive into a few clinical
pearls of knowledge uh that you know
take this one step further uh that are
just worth you know kind of knowing. So
the first is don't forget your vaccines.
Okay, prevention is key and that's
influenza, it's COVID as appropriate,
RSV depending on the age uh pneumonia uh
and that would be remember pediatric as
the conjugate vaccine that's your prevar
and then the polysaccharide vaccine or
pneumax depending on the age of the of
the patient uh and then also against
pertasus. So at minimum those should be
done on a very regular basis. Okay, look
at how they're using their reliever
medicines. They remember they should not
be on that generally by itself, but you
want to assess that. And there are some
tools that are out here that we've
listed here that can help you to assess
some of their overall asthma control,
but part of it's also based on their
peak flow meter, okay, that can help
guide you a little bit. So, at home, the
peak flow meter helps us to gauge the
peak expiratory flow rate. that helps us
to keep up with and catch the early
progression of the disease. And then
intermittently you want to do spyometry
to make sure that their pulmonary
function and those lung volumes that we
talked about earlier are still their
personal best, still achieving their
their benchmarks and they're not getting
worse. And then you know don't forget to
consider monitoring of eosinaphils if
they have allergic asthma. If you're
moving to the biologics and you consider
things like omalooab or something like
that then you need to monitor the IG
levels. Now devices and
education. So we have dry we have the
pressurized or aerosolized meterd dose
inhalers and then we have dry powder
inhalers and then we have nebulizers.
The inhalation technique that is
utilized in these is different. Even the
timing of how we do things. So
pressurized meterd dose inhalers up here
require a slow deep continuous
inhalation. the inspiratory pressures or
v you that you flow rates that you need
to generate with a meter dose inhaler is
is less than with a dry powder inhaler
because you got to get the dry powder
out of the device and into your lungs.
Whereas the pressurized device,
something is propelling it
out. Okay, propelling it out. So you if
you if you suck in too hard too fast
with the propellant pushing it out, you
could just deposit it all in the back of
your oral fairings and it never gets
down into the lungs. And so there
there's a very important coordination
between the triggering of the device and
the inhalation. And so that's where the
use of spacers, it can be really huge
because it avoids that timing problem
which most people have in using the dry
powder inhalers. You're ready to do it
when you're ready to do it, but you got
to generate a more forceful inspiratory
flow rate to get the medicine out of the
device and down into the lungs. In
either direction, this is aerosolized
almost at some level. so fine of a
powder or aerosolize that if you
immediately blow out what you just
inhaled in, you're going to blow out the
medicine with it. And that's why we want
people to take a deep breath in and hold
it if you can for 10 seconds. That
allows the drugs to deposit on the
tissue and start to exert their effect
and then you blow out and try to get rid
of the rest of that.
Nebulizers, you know, their biggest
problem is you can't carry that thing
around. I mean, where you going to plug
it in, right? Um, so it's it's not the
end all beall and when you look at all
the evidence when you use an inhaler
with a spacer with a proper technique
many times you're getting exposed to
less drug and you get greater degree of
efficacy as compared to a nebulizer.
Well, everybody wants a nebulizer
because it's cheap. It's easy. You just
put the thing on their face and move on
with life. Well, but remember this drug
is spewing into their eyes. It's not
necessarily even going down their lungs.
They still have to participate with deep
inhilations and exhalations. Deep
inhilations and exhalations to get that
drug distributed. Many times they are
exposed to a higher concentration of drug
drug
overall. Okay, kind of wraps up all the
clinical knowledge piece. Now let's move
to some practice test questions. Okay,
so question number one, which cell type
is most commonly associated with the
pathophysiology of asthma? And again I
would put that in the context of why is
it different than
COPD. Okay. So you have basophils,
eocinophils, you have macrofasages and
then neutrfils. Again the most common
predominant recruitment of cell line is the
the
eocinophil. Remember this is more
commonly associated also with the
allergic type which is the most common.
Neutrfils do show up with non-allergic.
So, you might have said, "Well, you
didn't clarify." But if you have two
answers on a test and and they're both
technically right in
scenarios, then you always go with the
one that is absolutely the for sure or
most accurate or more common. And that
would be the better answer is this
eosinaphils. Um, and I know that
frustrates sometimes people, but that is
the reality. You have to do that at
times on your exams and especially board
exams. So you got to get used to
thinking that way and dealing with the
information that way. And remember as
you read questions, don't make up new
information. Only utilize and assume
what you have been given. Which of the
following patient specific factors would
indicate an increased risk of poor
outcome or risk of asthma exacerbation?
daily use of an inhaled
corticosteroid. No, that would actually
that would actually help us. So that's
not going to increase the risk, right?
We kind of want that with blood tests
showing low eocinaphil counts. Again, we
that's what we want, right? High
eosinophil counts are a problem.
Weighing ideal body weight, well, no,
that's what we want. Remember, obesity
is a problem. So that I mean, even if
you don't even know what the last one
says, I mean, if processed by
elimination, that's the answer. A daily
use of a short acting beta agonist
without a doubt is the best answer and
is the only right answer here. All those
other ones are the opposite. Those are
all the things that would reduce the
risk and also risk of asthma
exacerbation. Okay, last question. You
have a 21-year-old male with asthma.
Symptoms occurring less than three times
per week. Lung function is mildly
reduced. Peak expiratory flow. Uh, which
of the following treatments would be
preferred? Okay.
Preferred. Albuterol MDI as needed for
motorol DPI as needed. Inhaled
cortosteroid for motorol as needed.
uh dupaloma uh subcutaneous remember
that's a biologic agent
um that's remember for that's way down
at towards the end right after multiple
remember this is a first time treatment
so inhaled corticosteroid with promoter
as needed all right hopefully some of
those practice questions help you to
apply the core concepts we talked about
and get just used to thinking that way
there's obviously a hundred other
questions we could ask but hopefully you
found it helpful
Okay, now we're going to wrap things up
and let's just jump into our
summary. So, asthma is a chronic
obstructive airway disease that is
influenced in its control by exposures
to antigens, but it's classically
described in a hyper respponsive airway
disease. That means it is got bronco
spasms. It results in wheezing, but it
also re gets relieved with bronco
dilators over uh especially when used
appropriately. They commonly present
with chest tightness, wheezing, cough.
Many times they have symptoms at night
when they're laying flat. That's very
classic. They have decreased peak
expiratory flows in particular FEV1 and
decreased uh flow rates. And again we
can we can identify this at home uh
using peak flow meters. Okay. Whereas
pulmonary function test spyometry is
more you know comprehensive but done in
the clinic. And then treatment we take a step-wise
step-wise
approach and it's largely influenced by
their symptoms um in particular and it's
influenced also by the age of the
patient. So consider smart technology
where we use those single agent
therapies especially that can improve
adherence and compliance and make sure
that we really give attention to those
inhaled cortical steroids and explain
that to the patient their caregivers so
that we're treating things appropriately
and not putting a band-aid over a
situation by using intermittent uh short
acting reliever medications as some way
of controlling the disease. Okay guys,
that's chronic asthma and hopefully you
found it to be helpful as an overview.
Click on any text or timestamp to jump to that moment in the video
Share:
Most transcripts ready in under 5 seconds
One-Click Copy125+ LanguagesSearch ContentJump to Timestamps
Paste YouTube URL
Enter any YouTube video link to get the full transcript
Transcript Extraction Form
Most transcripts ready in under 5 seconds
Get Our Chrome Extension
Get transcripts instantly without leaving YouTube. Install our Chrome extension for one-click access to any video's transcript directly on the watch page.
