COPD / Asthma

on

 

Chronic Obstructive Pulmonary Disease

Obstructive Disease
Bronchitis + emphysema

Concepts air trapping,

Dynamic Hyperinflation:

Pathophysiological Features of Airflow Obstruction in Chronic Obstructive Pulmonary Disease
Airflow obstruction in COPD is largely due to emphysema, characterized by disruption of the alveolar walls, along with inflammation of lung tissue, fibrosis, and mucus plugging in the distal airways (Panel A, normal distal airway surrounded by intact alveolar walls; Panel B, abnormal distal airway surrounded by disrupted alveolar walls). Alveolar attachments provide a radial tethering effect that is essential for keeping small airways patent in the normal lung. Airways narrow at smaller lung volumes because of decreased lung elasticity and weaker tethering effects. Consequently, maximal expiratory airflow decreases as the lung empties and ceases at 25 to 35% of total lung capacity. The remaining air is termed the residual volume. In patients with COPD who have emphysema, the disruption of alveolar attachments, coupled with distal airway disease, causes a substantial decrease in maximal expiratory airflow (Panel A, normal flow; Panel B, reduced flow). Residual volume may account for as much as 60 to 70% of predicted total lung capacity. Patients with COPD must breathe at larger lung volumes to optimize expiratory airflow, but this requires greater respiratory work because the lungs and chest wall become stiffer at larger volumes. These effects are accentuated with exercise. A normal respiratory system meets the increased ventilatory demands of exercise by increasing both tidal volume and respiratory rate, with little change in the final end-expiratory lung volume. In patients with COPD, the respiratory rate does increase in response to exercise, but with insufficient expiratory time, breaths become increasingly shallow and end-expiratory lung volume progressively enlarges (Panel A, normal response to exercise; Panel B, response with COPD). This phenomenon is called dynamic hyperinflation and is thought to be an important factor in the reduction of exercise capacity and the development of dyspnea.


RF: cigarette smoking

Chronic obstructive pulmonary disease (COPD) is characterized by persistent expiratory airflow limitation due to destruction of lung parenchyma and decrease in elastic recoil. COPD is associated with chronic airway and parenchymal inflammation, and the resultant airway obstruction leads to air trapping and hyperinflation. The decline in lung function in COPD is generally progressive.


Main Symptoms: 





 

Clinical question: How did GOLD revise its prior recommendations for the diagnosis and management of chronic obstructive pulmonary disease (COPD)?

Background: The World Health Organization and the National Institutes of Health convened the GOLD expert panel to make recommendations regarding the diagnosis and management of COPD. The 2023 GOLD report addressed prior concerns that the 2017 report lacked diagnostic utility in daily clinical practice. For example, an exacerbation was previously defined as an “acute worsening of respiratory symptoms that results in additional therapy,” and severity was defined after the fact based on what therapies were used, rather than objective measures that could guide initial treatments.

Study design: Systematic review guideline update (studies reviewed through 2022)

Setting: Inpatients and outpatients at risk for or with known or suspected COPD

Synopsis: For hospitalists, the most important updates include the following:

The GOLD assessment/treatment groups were pared down from four to three, notably with a focus on dual long-acting beta-agonist (LABA) and anti-muscarinic (LAMA) bronchodilators, rather than LABA or LAMA monotherapy, for those with significant symptoms or any hospitalization for a COPD exacerbation. An inhaled corticosteroid (ICS) should be added to LAMA+LABA (i.e., triple therapy) if elevated blood eosinophils (≥300 cells/microliter). This has been shown to be superior to LABA+ICS, though note recurrent cases of pneumonia may be an indication to stop ICS therapy.

They describe new criteria to grade the severity of exacerbations. A moderate exacerbation requires three or more of five criteria: dyspnea, tachypnea, tachycardia, resting oxygen saturation on blood gas testing <92% and/or showing a change >3%, or CRP ≥10 mg/L. A severe exacerbation is the same plus acidosis on arterial blood gas, typically with new or worsening hypercapnia.

Hospital management remains similar to that recommended prior: short-acting beta-agonists (SABA), with or without short-acting muscarinic antagonists (SAMA), long-acting bronchodilators per above—ideally during exacerbations, prednisone 40 mg equivalents for five days, antibiotics (if sputum change) for five to seven days, and goal oxygen saturation on pulse oximetry 88 to 92%. Referral to pulmonary rehab after discharge remains controversial and of uncertain benefit. Five-year mortality after a COPD exacerbation requiring hospitalization is high, around 50%.

Bottom line: The GOLD 2023 report clarifies COPD diagnosis and exacerbation assessments, and chronic management of suspected or known COPD in hospitalized patients should rely on LABA+LAMA (with or without ICS) in addition to typical acute management with shorter-acting bronchodilators, oxygen, steroids, and antibiotics as indicated.



Scoring Systems:

  • COPD Assessment Test (CAT): measures COPD symptoms (e.g., cough and shortness of breath) on a 0–40 scale; a score of ≥10 indicates COPD symptoms that limit quality of life

Cough, Phlegm, Chest Tightness, Breathlessness, Activities, Confidence, Sleep, Energy

CPCBACSE


mmRC: dyspnea only w/ strenuous exercise, when hurrying or walking up a slight hills, walks slower than ppl of same age bc dyspnea has to stop fro

| / --- -- -
Strenuous, hill, slower than same age, 100 yads, can't leave house






Exacerbations ( E ) 
A / B
mMRC 0-1/ CAT < 10
mMRC > 2 CAT > 10


















Conan Liu

what are the new 2023 gold guidelines on
the management of COPD is albal still
our default rescue inhaler for the
management of asthma and as hospitalists
should we be starting patients with COPD
on things like chronic aiyin and reflu
COPD Treatment
last first thing to really notice what
we always have to look for is a
potential trigger and for asthma some
typical things you may hear are you know
exposure to cold can cause an asthma
flare or exercise you can get exercise
induced asthma and then of course you
know viral Uris is very common as well
in COPD very often it's going to be a
viral URI but there's actually a lot of
literature that states that up to 30% of
COPD exacerbations may be triggered by
pees and so this is obviously something
you do not want to miss you don't want
to just have somebody come in for a COPD
exacerbation treat them and never work
them up for a potential PE you know when
no other trigger is is found so in terms
of treatment it's fairly standard um so
Bronco dilators is really our first line
so we're going to start with dubs and
you can start off q1 hour Q2 hour for
the first several Doses and then
generally we start to space them out to
Q4 hours uh scheduled and then you
switch them to PRN we also are going to
start patients on prednizone and the
most common dose is going to be 40
milligrams and the duration is going to
be for 5 days now uh in the past they
used to treat patients for like 14 days

duonebs q4hours scheduled PRN
Prednisone 40mg x5 days
Oxygen 88 - 92%

Airways that have airtrapping will now have higher oxygen percent and giving oxygen will reverse hypoxic vasoconstriction

IV magnesium

ABCOM
Abx, Bronchodilators, corticosteroids, Oxygen, magnesium
abx 2 of 3 cough, sputum, dyspnea

Azithromycin 500mg x3 days or 250mg x5 days

COPD
LAMA -> LABA -> ICS

Asthma the opposite way

<2x a week
<2x a month nocturnal symptoms





or even a month with steroids but there
was actually this really important Tri
trial called the reduce trial which
compared 5 days versus 14 days of
prazone and found that uh a 5-day course
was non inferior to the prolonged
courses another common pimp question
that attendings may ask you is is there
any benefit to IV solumedrol or IV
methyl prisone in The Upfront treatment
of COPD and uh definitely if the patient
is unable to tolerate oral intake that's
something we're going to consider or if
it's a very very severe COPD
exacerbation but in general the evidence
has not shown any advantage to using IV
steroids compared to oral steroids and
then afterwards you're going to give
them oxygen as needed uh for a goal set
of 88 to 92% the reason we only target a
goal of 88 to 92% is also a very common
question and you may have been told that
this is because high levels of oxygen
will reduce the respiratory drive in
patients with COPD but this is actually
not the primary reason for uh avoiding
High oxygen in these patients it's
actually due to a reversal of hypoxic
pulmonary vasil constriction so imagine
Hypoxic pulmonary vasal constriction
you have the patient's lungs right here
and there are areas of the lungs that
are having significant air trapping and
very poor air movement so let's say all
of this is kind of knocked out what your
uh pulmonary vessels are actually going
to do is they are actually going to
start increasing the blood flow to the
areas with better oxygenation and then
these places with worse oxygenation
they're going to start vasoconstricting
so they'll start narrowing these vessels
down like this now what you do when you
give them really high oxygen let's say
um the patient is suddenly sing 100%
what happens is this area now has
adequate oxygenation but it still hasn't
reversed the air trapping that's been
going on here so all of a sudden the uh
you know pulmonary vessels going up here
are going to start dilating because it's
like oh we have good oxygen here now so
this is going to dilate and the problem
is there's actually still no gas
exchange going on here because of the
air trapping and that subsequently
you're going to start vasoconstricting
these ones that were actually getting
good oxygen before so that's the whole
concept of not giving them too much too
much oxygen because you would
potentially reverse the hypoxemic
pulmonary vasal constriction the next
treatment to consider in both asthma and
COPD is actually IV magnesium and then
regarding antibiotics how do you make
that determination on whether a patient
should be started on aiyin or not
obviously a ziyin not not only to treat
you know atypical pneumonias and things
like that but also because it's not to
have its own anti-inflammatory effect as
well so what you should determine is if
they have increased sputum increased
cough or increased dmia if you meet two
out of three of these then you can start
aiyin 500 mg for 3 days or you can do
the basic approach to the management of
an acute exacerbation of asthma or COPD
Maintenance therapy
now let's talk about maintenance and I
really had a great um attending once
tell me a very easy way to remember the
escalation of treatment that and the way
that it differs between asthma and COPD
so what you have is a whole host of
different inhalers and so we're going to
start with IC or inhaled cortico
steroids and then we're going to
progress to a long acting beta Agonist
like formoterol or salmeterol and then
we're going to progress to a long acting
muscarinic antagonist so this is a
progression of inhalers for uh the
treatment of asthma so if you're
thinking asthma then this is the
direction that you would be going for
COPD it's actually the exact opposite uh
and so for COPD we're going to go this
way we're going to start with the long
acting muscarinic antagonist add the
long acting beta Agonist and then add
the IC on top of that so how do you know
when to escalate therapy uh in a patient
with asthma so what you really want to
pay attention to is the rule of twos and
the rule of twos is that you want your
patients to be using their rescue
inhaler less than two times a week and
they should be having less than two
times a month of nocturnal symptoms if
your patient is using the rescue inhaler
more frequently than that or having
nocturnal symptoms more than twice a
month then the patient should be um
stepped up in terms of their therapy
let's talk about the rescue inhaler now
so all of these patients should actually
be on a rescue inhaler so they've got
these maintenance inhalers on the right
side which they take every day um no
matter what to just kind of keep the
inflammation at Bay but if they're
starting to feel a flare up then they're
going to use their rescue inhaler and so
previously our rescue inhaler of choice
was a short acting beta Agonist uh also
known as albuterol however if you
Rescue inhaler
actually look at the updated 2019 Gina
recommendations or the global Initiative
for the treatment of asthma you can
actually see that the preferred reliever
is now as needed lowd do IC Plus for
motorol so it's IC plus aaba uh which is
very interesting and you can see the
other reliever option is a short acting
beta Agonist such as albuterol but the
preferred reliever again is now an IC
plus lava combination so therefore
change your Association of Albuterol
being the rescue inhaler for uh asthma
to being that of an IC Plus for motorol
or ICS plus lava for COPD however it is
still typically going to be a short
acting beta Agonist and then finally one
Mortality benefit
last thing I wanted to mention for
asthma is that there's a few adjunctive
therapies uh for example if somebody has
allergies you may want to consider
something like 

Allergies: Montelukase ( singulair ) 
Mont lucast or singular
and also if they have an elevated
IG uh this would probably be done by the
pulmonologist but they may qualify for
something called uh omalizumab now let's
move back to COPD so uh one of the
common things that we actually ask in
COPD is what are treatments that
actually have mortality benefit you know
does being on all of these inhalers
provide mortality benefit or are there
only a few uh treatments that actually
have been proven to have mortality
benefit and so the things that are shown
to have mortal it benefit is going to be
number one it's going to be smoking
sensation number two is going to be
oxygen therapy for patients who have
persistent hypoxemia uh sing less than
lung volume reduction surgery which can
be done surgically or the Interventional
pulmonologists actually have a technique
called Endo endobronchial valve
placement which basically in these
surgeries they are collapsing the most
diseased parts of the lung so that it
kind of allows the healthier lung to
expand more and be able to participate
more in gas exchange 

Mortality benefit in COPD 
- Smoking cessation
- oxygenation
- Lung volume reduction
- Pulmonary Rehab
- BODE 5-6 lung transplant referral

and so that's how
that's been shown to uh improve
mortality in patients with COPD other
things that you really should consider
um basically every patient with COPD uh
would benefit from pulmonary rehab which
has been shown to improve six-minute
walk time and quality of life metrics
and then also if they have a really
elevated uh what we call a bode score so
very very severe um COPD uh then we
would consider something like referring
them to a lung transplant center but I
want you to remember these are the three
things that really have been shown to
have mortality benefit smoking sensation
oxygen and lung volume reduction surgery
all of these other uh treatments
inhalers and everything like that
improves the quality of life but does
not have an actual mortality benefit so
Pathophysiology
now that we've talked about the
treatment and the maintenance of copia
and Asthma why don't we actually talk
briefly about the pathophysiology and
then also uh diet diagnosis and how you
actually make a official diagnosis so
the pathopysiology is very interesting
um and I would say that for asthma you
know what you really can think of is
you've got your Airway and then you've
got your uh alvioli with all these
little tiny Alvar sacks here and in
asthma what you get is hypertrophy or

asthma, hypertrophy of airway smooth muscle, hyperreactivity, 
Asthma airway smooth muscle inflammation relieves obstruction positive bronchodilator response



inflammation of the airway smooth muscle
right so this is all going to start
getting inflamed whether it's due to an
IR irritant or some other um kind of hyp
sensitivity of the airway smooth muscle
and that's going to lead to Airway
obstruction so again all of these are
leading to Airway obstruction the key
thing with asthma is that this Airway
obstruction responds to Bronco dilators
so uh when you give them a Bronco
dilator you're going to reduce that
Airway smooth muscle inflammation and
that's going to relieve the obstruction
so they do have a positive Bronco dilat
response on the other hand when you have
COPD you you've got again your Airway
here and you've got your alveolar Sachs
and you've got the alvioli here um but
what happens is you know COPD is
typically associated with you know
long-term exposure to toxins like
cigarette smoking being the major one
and this leads to elastin breakdown uh
and basically what happens is all of
your uh air sacks become really loose
and floppy and so you know imagine uh
you know Dr satar said it the best in
pathoma but imagine these over here in
the asthma patient or the normal lung
are kind of like tight balloons and so
when you want to get rid of that um you
know air from them it's a balloon right


air in them, dilated air sacs, grocery bag, air in it. Air ends up functionally getting trapped. Destruction of cartilage int he airways and can lead to airway collapse. Collapse fo the airways when there is too much pressure. Unlike smooth muscle inflammation not responsive to bronchodilators


it's got a lot of tension and it's going
to just let that air uh go out of the
body but when you have uh really dilated
um air sacks that are just floppy it's
basically like a grocery bag and if you
let go of a grocery bag you know there's
still a bunch of air in it it doesn't
push the air out or anything so all this
air just ends up functionally becoming
trapped uh not only that but you also
get a destruction of the cartilage in
your Airways and so this can lead to
Airway collapse so now all of a sudden
you're getting collapse of the Airways
uh whenever there's like too much
pressure and that unlike the smooth
muscle inflammation of uh asthma is not
responsive to Bronco dilators so no
Bronco dilator

collapse in airways, unlike smooth muscle inflammation in asthma is not responsive to bronchodilators

Diagnosis
response so now let's talk about
diagnosis and this of course is going to
rely predominantly on your pfts so first
we're going to talk about asthma and
then we're going to talk about COPD so
with asthma it's really quite simple and
basically what I said earlier we're
looking for signs of obstruction with a
Bronco dilator response so how do we
actually determine if there's a Bronco
dilator response so basically you do the
pfts before giving them a Bronco dilator


Asthma bronchodilator response
FEV1 > 12%
Tv 200
methacholine challenge

COPD FEV1/ FVC < 0.70
formal diagnosis

Gold1 < 80%
2 50-80%
3 30 - 50%
4 <30%

GOLD
A
B high MMRC LAMA + LABA
E many exacerbations

Group A Bronchodilator mMRC 0-1, CAT < 10
Bronchodilator 
LAMA, LABA, ICS, blood eosinophils > 300







then you give the that Albuterol and
then you repeat the pfts and what you're
looking for is an increase in their fe1
greater than 12% or an increase in their
tidal volume by greater than 200 the
other thing you should know is you know
what if a patient's not in an acute
asthma exacerbation how can you actually
induce them to get kind of this
obstructive picture so you can actually
run this test uh well that's when we
would run something called a methine
challenge which is basically giving them
a very uh irrit a very strong irritant
to induce an axma exacerbation and then
you'll get the PFT measurements and then
you'll give them the Bronco dilator to
check for Bronco dilator response COPD
on the other hand is really going to be
defined by looking at the F1 over FEC
ratio of Greater of less than
COPD you really want to make sure that
they have actual documented pfts showing
this ratio because uh there's a lot of
times people are just given the label of
COPD but they don't actually have a
formal diagnosis and then after that we
have various levels of gold staging so
first of all we've got 1 2 3 and four
and these are based on your fev1 so for
a gold stage one your fev 1 is less than
is going to be 30 to 50% and then gold 4
is going to be less than 30% in addition
to this classification however we also
have the gold a through e staging so it
goes from a b and e so this is a little
confusing because it actually used to be
a b c d and what it helped us do was
determine what inhaler regimen uh
patient should be on uh but recently in
the 2023 gold guidelines this was
updated to being a b and e and really
how it goes is this so uh you've got
gold e up here and you have a and b so A
and B you know these are people with uh
low scores on the mm RC or low cat
scores these are basically measures of
their quality of life uh and then this
would be high
mmrc or High cat
scores and then here would be no
exacerbations or
hospitalizations and this would be
basically many exacerbations they Define
it as two plus
exacerbations or um uh be ever being
hospitalized for COPD exacerbation okay
so that's how you determine if the
patient is gold stage a b or e okay and
here I've just brought in a image from
the gold guidelines so you can see that
group a should be started on a Bronco
dilator and remember you know our first
line is really going to be that long
acting muscarinic contagonist Group B
will qualify for Lama plus laba and then
group E will qualify for Lama plus laba
and if their blood eosinophils are
greater than 300 you should start an
inhaled corticosteroid this is another
Risk



Strong support for initiating Inhaled Corticosteroid Treatments
- History of hospitalization for exacerbations of COPD
- > 2 moderate exacerbations of COPD
- Eosinophils > 300
- Hx of asthma
Consider use
- Moderate exacerbation of COPD per year
- Eosinophils 100 - 300
Against
- repeat pna
- Eosinophils < 100
- mycobacterial infection



image from the gold guidelines and I
want you to know that starting an
inhaled uh corticosteroid is not without
risks so patients who have blood
eosinophils greater than 300 are the
most likely to benefit from starting
inhal corticosteroid and then if they've
ever been hospitalized for COPD or had
multiple exacerbations now you can
consider the use if their eosinophils
are 100 to 300 however they recommend
strongly against use if patients have
repeated pneumonia if they have blood
eosinophils less than 100 or history of
microbacterial infection the reason is
because inhaled corticosteroids are
associated with increased pneumonia
events so it's not without risk as I
mentioned and if their blood eosinophils
are less than 100 they're probably not
going to benefit from starting inhaled
corticosteroids lastly I also want to

BACE Trial Former smokers give azithromycin

Folumilast FEV1 < 50% and chronic bronchitis



Initiation
talk about the initiation of the
medications roflumilast and aiyin so
rast is like a phosphodiesterase
inhibitor and ziyin is obviously an
antibiotic and we've actually been
getting much better evidence for
initiating these Therapies in patients
who have been hospitalized for COPD so
as hospitalists that begs the question
should we be responsible for starting
these medications in you know frequent
COPD exacerbation um patients and I
would argue that the answer is yes so if
a patient is coming in for an
exacerbation you really really should
strongly consider do they qualify for
the medication roflumilast and the
criter would include an fev one of less
than 50% and chronic bronchitis subtype
or do they qualify for chronic aiyin
which is usually dosed like 250
milligrams Monday Wednesday Friday or
something like that and this would be
highly considered in patients who former
smokers for the zithro uh this was
actually based on the base trial which
showed a 20% reduction in COPD
exacerbations and the main side effects
were some mild nausea QT prolonging and
some uh mild hearing loss which was only
detected on sensory neur sensory neural
testing and not ever reported by the
patients and then also there was
reversal of the hearing loss after they
um after they stopped the zi that was a
Learning Points
lot of information to throw it you guys
but I actually got a couple more
learning points that I wanted to uh you
know discuss with you guys so um should
every single patient with COPD be tested
for Alpha 1 anti-in deficiency the
answer to that is actually yes per the
you see with COPD and has not been
tested before you should actually test
them for it and then secondly a very
common boards question for you know our
medical students taking step two or
interns taking step three a patient an
asthmatic who's coming in uh diffusely
Wheezy they're having like a little bit
of respiratory alkalosis because they're
breathing so fast uh their pco2 is kind
of low and then all of a sudden you you
know start treatment and patient uh is
starting to uh actually their pco2 is
starting to normalize so pco2 is going
back up it's up to 40 patient is no
longer wheezing um and so you're like
great uh the patient is not wheezing
anymore their pco2 is going back to
normal uh what is the next best step in
management that's how the board question
is going to ask it and the answer to
that is actually going to be intubate so
you should intubate this patient uh and
they're going to give you in the
question that the patient you know
they're not wheezing anymore but they
still look pretty bad and they're like
out of it they're like tired things like
that uh and the reason is because this
patient is starting to retain CO2 the
fact that the CO2 is normalizing is
actually a sign that they're tiring out
the lack of wheezing is actually because
the patient is now having such poor air
movement that they can't even generate
the sound of wheezing so that's why
they're not wheezing anymore and so both
of these signs together along with the
fact that the patient doesn't look
improved they look somal land the answer
to this question is that the patient
should be intubated very very common
board's question and I can almost
guarantee that you're going to get it on
one of your board exams I hope you guys
enjoyed this video thanks again for
watching and I'll see you in the next
one



everyone with COPD not tested before should be tested for alpha 1 antitrypsin disease
asthmatic coming in diffusely wheezy respiratory alkalosis PCO2 low start treatment and patient starts PCO2 starts to normalize. PCO2 goes back up to 40, patient no longer wheezing. Great. Patient not wheezing anymore. PCO2 goes back to normal. What is the best next step in management INTUBATE

patient retaining, generate such little air they are retaining and not making the sound of wheezing


Asthma Exacerbation


https://www.youtube.com/watch?v=IKwaivntkSI

https://www.medscape.org/viewarticle/929313_sidebar1


Q&A Based on Teaching Points from the Discussion

Q1: What are the key characteristics of asthma?

  • A: Asthma is a chronic and heterogeneous disease of the airways characterized by airway obstruction, inflammation, bronchial hyper-responsiveness, and recurring symptoms like wheezing, chest tightness, coughing, and shortness of breath.

Q2: How prevalent is asthma in the United States?

  • A: Approximately 20 million adults and over 6 million children in the U.S. suffer from asthma. Of these, up to 10% of adults experience severe asthma, requiring high-dose inhaled corticosteroids (ICS) and other controllers.

Q3: How is severe asthma defined according to the American Thoracic Society (ATS) and European Respiratory Society (ERS)?

  • A: Severe asthma requires treatment with high-dose ICS plus a second controller, such as a long-acting beta-agonist (LABA) or leukotriene receptor antagonist (LTRA), or the use of chronic oral corticosteroids (OCS) to maintain disease control.

Q4: What role does a team-based approach play in asthma management?

  • A: A team-based approach is crucial for managing asthma, particularly severe cases. It involves various healthcare professionals, such as physicians, nurses, and pharmacists, collaborating to assess and treat patients, optimize inhaler technique, and ensure adherence to treatment plans.

Q5: What non-asthma conditions should be ruled out when assessing uncontrolled asthma?

  • A: Conditions like rhinitis, gastroesophageal reflux disease (GERD), sleep apnea, depression, and obesity can contribute to uncontrolled asthma. It is important to assess these to provide appropriate treatment.

Q6: What is the role of inhaler technique in asthma management?

  • A: Correct inhaler technique is crucial for effective asthma control. Even long-term users can use their inhalers incorrectly, leading to poor medication delivery. Pharmacists and clinicians should regularly review and correct patients' inhaler techniques.

Q7: How do biomarkers help in determining asthma phenotype?

  • A: Biomarkers such as blood eosinophil levels, fractional exhaled nitric oxide (FeNO), and serum IgE levels help distinguish between type 2 and non-type 2 asthma. For instance, type 2 asthma is associated with elevated eosinophils and FeNO, guiding the selection of biologic therapies.

Q8: What are the primary biologic therapies available for type 2 asthma?

  • A: Five biologic therapies approved by the FDA target type 2 asthma: omalizumab (anti-IgE), mepolizumab and reslizumab (anti-IL-5), benralizumab (IL-5 receptor blocker), and dupilumab (IL-4/IL-13 blocker). These therapies reduce exacerbations and may lower the need for corticosteroids.

Q9: How long should biologic treatments be continued for asthma management?

  • A: Biologics often show quick improvements, but patients typically need to continue treatment for at least 3 to 6 months before determining its full effectiveness. Long-term continuation is often necessary as asthma symptoms tend to return if biologics are stopped.

Q10: How should healthcare professionals discuss the safety and expectations of biologic treatments with patients?

  • A: It's essential to set realistic expectations for biologic treatments and discuss potential side effects, such as injection site pain. Patients should understand that these medications control but do not cure asthma, and they should not stop treatment without consulting their provider.

Q11: What factors should guide the decision between home and clinic-based administration of biologics?

  • A: Patient comfort and confidence in self-administration play a significant role. Some patients may prefer clinic-based administration initially, transitioning to home dosing as they become more comfortable with the treatment.

Q12: What comorbidities may influence the choice of biologic therapy in asthma patients?

  • A: Comorbid conditions like atopic dermatitis, chronic rhinosinusitis, and nasal polyposis may affect the choice of biologic therapy, as some medications, like dupilumab and omalizumab, also treat these conditions.

Q13: How can healthcare professionals ensure good outcomes for asthma patients on biologic therapy?

  • A: Continuous education, regular follow-ups, and shared decision-making are key. Patients need to be fully informed about the importance of adherence to their biologic therapy and the consequences of stopping treatment prematurely.

Q14: How do pharmacists contribute to asthma management, particularly for patients on biologic therapies?

  • A: Pharmacists play a vital role in monitoring for adverse effects, ensuring medication adherence, and educating patients about proper use of their asthma medications. They also assist with vaccination requirements and potential drug interactions with biologics.

Q15: What are the final considerations for a team-based approach to asthma management?

  • A: The success of asthma management hinges on collaboration between healthcare professionals and patients. This team approach ensures that treatment plans are tailored to individual needs, optimizing patient outcomes through shared decision-making and clear communication.




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