COPD with Dr. Nina Maouelainin - Episode 87

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Hey everyone, welcome back to my podcast and I'm your physiology bit by bit.

This is your host, Dr. Steve Sullivan, coming to you from Bucks County, Pennsylvania,

where I've been teaching A&P since 2002.

I hope you're enjoying these latest episodes covering common conditions experienced by

the general public, and often seen in clinical situations.

These episodes are the perfect transition from the normal A&P I covered in the first

80 episodes, to the clinical application of A&P that shows mastery.

As always, I want to preface this episode by reminding listeners that this show is purely

educational and is never intended to be taken as medical advice.

And by no means, should you allow this show to be a substitute for seeing an appropriate

medical professional?

If you suspect you are not well, or if you have any of the signs or symptoms you hear

about in this episode, you should go to your local emergency room or contact your medical

doctor immediately.

Today, we're going to continue our coverage of diseases listed among the top ten

cause of death in the world, and today we're going to tackle number three, chronic obstructive

pulmonary disease, or COPD.

By the end of this episode, you should be able to explain why COPD patients feel like

they can't get air out, why they wheeze, why some turn bluish and swollen while others

look thin and exhausted, why oxygen can help, but isn't the whole story, and what clinicians

are really looking for on exams, labs, sparametry, imaging, etc.

And COPD is not one single disease.

It's a chronic progressive limitation of airflow that is not fully reversible, and it's

driven primarily by long-term exposure to inhaled irritants, especially cigarette smoke.

Three pathologic patterns dominate the story of COPD.

Pronchitis, bronchi-ectasis, and emphysema.

Chronic obstructive pulmonary disease is primarily treated by a pulmonologist, which means

lung specialist.

While the initial diagnosis often comes from one's primary care physician or family doctor,

a referral to a pulmonologist usually follows.

They manage the definitive diagnosis, medication, and advanced therapies like oxygen or rehabilitation.

Ultimately, a multidisciplinary team, including respiratory therapists, nurses, and dieticians

also support treatment.

And for that reason, I'm going to let my guest, Dr. Nina Malinin, CEO of Lung Health Services,

do the lion's share of the explaining.

Dr. Nina is an interventional pulmonologist who also did a fellowship in critical care.

She sees patients for all kinds of respiratory issues, but especially lung cancer and COPD.

Originally from Morocco and educated in France and the US, Dr. Malinin has a great story

behind what she does and why.

And she's awesome at explaining COPD.

So without wasting any more time, please welcome Dr. Nina Malinin to the show.

Okay, Dr. Nina Malinin from Lung Health Services, my first pulmonologist on the podcast.

Thank you so much for joining me.

It is a pleasure being here.

Thank you so much for having me.

First off, why don't you tell the listeners a little bit about yourself, maybe a little

bit about lung health services for which you are the president and CEO?

Why did you become a pulmonologist?

What did it take to become one?

And what basically do pulmonologists do?

Sure, absolutely.

Well, I've been all over the globe, I guess, except in Asia, but a quick background, originally

born and raised in Morocco.

My passion, whenever I was a very young girl, was to become a fighter pilot.

And obviously, as I developed myopia and I needed glasses, that went out the window.

Both my parents are physician.

I grew up in a hospital housing and really I was exposed to the dedication to make a difference

in people's life through my parents.

They are my role models and I've enjoyed watching their passion and their impact on so many

patients that pretty much set the tone from an early age.

A fast forward after finishing high school ended up going to France because I had a French

diploma and completed part of my medical school training in Normandy in France and then came

to the United States to subsidize and ended up starting all over again, learning English

in the mid-90s and the rest is history.

Why pulmonology specifically?

Well, that was an interesting journey because originally I wanted to do surgery, trauma,

critical care.

And again, life happened between pregnancy and time and requirement and at that time really

believe in that I had to make a choice and I've changed in from surgery to in trauma medicine

with the goal to do critical care.

You couldn't do critical care unless you did pulmonology.

And that's how I had to take pulmonology lectures and actually the anecdote during medical

school, whatever I attended in the second year, the first pulmonary lecture, I'm like,

who in the world would want to do pulmonology?

Look at this, the lungs and all these windpipes.

So it's amazing.

It's really funny how everything turned out to be when you're so sure you're not going

to do something.

I thought pediatrics or ophthalmology would be right up my alley, absolutely not.

So I started doing critical care mainly rotations in during my residency and pulmonology became

absolutely a fascinating topic because I was forced by life to face the drama from lung

carcinoma and really how it destroys people livelihood, whether they were smokers or

not.

My cousin in his mid 20s, my uncle, 50s and my aunt in her mid 70s, only two of them

were smokers, my cousin and my uncle.

And because of the stigma, they hit it.

And my aunt was absolutely out of the blue, non-smoker and I wanted to make a difference.

I think now that I've been doing this for more than 20 years, it was exactly the right

choice and lung carcinoma has been my passion and that's how I created lung health services

and the word nationwide.

So I'm really excited about this journey.

That's amazing.

What a great service to provide.

I know that this episode is technically about chronic obstructive pulmonary disease,

but with lung cancer, lung cancer is so prevalent and you have a personal history with it.

And it is among cancers, I think it's the number one cancer.

Correct.

It's the number one cancer in men and women worldwide against all other cancer combines,

which is mind boggling.

And actually only, I think less than 7%, if not 5% of eligible people that should be

undergoing a screening for lung cancer are actually getting screened compared to 60, 70%

from mammography.

Right.

Right.

So we have so much work to do and it remains so this day to deadliest cancer.

Well, there's definitely going to be an episode specifically about lung cancer.

Looking forward to that.

So I might be reaching back out if you've got the time.

I did have an episode recently that was just in general, what is cancer?

And I was able to speak with a PhD who specializes in neuroscience and immunomontology.

So we had a really good discussion just on the general idea of neoplasia.

But now I want to get into chronic obstructive pulmonary disease if you don't mind because

that is also in the top five in terms of causes of death.

So just as a little bit of a side note, and most of the listeners know this by now, that

most of the normal anatomy and physiology that I cover in a typical two semester majors

level course, I've already covered in the podcast.

So we got to a point a few weeks ago where I decided that we're shifting gears to cover

specific diseases, illnesses, and conditions in each episode so that the students could

enter the clinical application phase of learning anatomy and physiology.

So that's where we are.

I decided to go with some of the big ones at first.

I did diabetes.

I did coronary artery disease.

We did cancer and now we're hitting COPD.

Awesome.

So that's why I chose to do this episode on COPD.

In clinical terms, would you be able to explain the underlying pathophysiology of COPD,

kind of like what is it, what is chronic obstructive pulmonary disease?

Absolutely.

So I always, and believe it or not, I always explain to the patients as well.

So they are able to understand the mechanisms.

I give a lot of analogies.

And then they hopefully would understand their symptoms better and would be able to express

how their symptoms are making them feel, and that helps me really diagnose them and

help them.

So in general, what I always say, the lung actual structure, the framework, as we all know,

spine in the back, sternum in the front ribs on the side.

That's the framework and the bony structure.

And there is a method to my madness.

So I start with that and I say, okay, your framework is sealed with muscles, right?

Intercostal muscles, neck muscles, back muscles, and diaphragm, which are dome shapes at

the bottom, are your main breathing muscles.

And inside this box, which is under pressure, because there's a pressure variation between

the inside of the chest and the outside, you have a tree that actually surrounds your

lung, your heart.

Upside down tree, main windpipe coming down to the right and to the left and it divide

like roots and tree branches all the way through.

And every single branch is hollow, leading to our VLI, which are the analogy that I give

to the patients usually, grapes, a clump of grapes that has no fruit in the middle and you

just have the sacs that inflate and deflates because it directly connects to these wind

pipes.

So when you take a step back, those wind pipes are lined up with muscles.

It's not just cartilage, it's a combination of cartilage and muscle.

That muscle can get brushburned and lead into an inflammatory component.

So when you look at it, even when you go down with a bronchoscope, you can actually recognize

who has COPD and who doesn't.

Why?

People that don't have COPD have a pretty good stiffness to their windpipe and airways.

People with COPD, because of the chronic inflammation, almost like a scaliness that

starts building like a callus, not scaling a sorry.

So the more you rub, the more you irritate, the more that muscle on the inside is actually

swollen.

We measure the lung capacity or force expire to re-volume for a reason.

First, someone is healthy, and you take a good, deep breath, force vital capacity.

I'm going to break in here for a second, because Dr. Melanin is going to be using some

terms I want to define for you in advance.

The first is forced vital capacity, or FVC.

This is the total volume of air that can be forcibly exhaled from the lungs after taking

the deepest breath possible.

There is also the forced expiratory volume 1 or FEV1.

This is the maximum amount of air a person can forcefully exhale in one second.

What really matters here is the FEV1 to FVC ratio.

So I'll explain that.

If FVC is the total amount of air you can exhale, the ratio is how much of that air you can

move in one second.

So basically, what percentage of your total ability to exhale can you do in one second?

Okay, back to Dr. Melanin.

You're able to hit 80% based on your height, your age, your sex, and your race of whatever

you're expected to breathe in.

Your muscle strength, your diaphragm is what pulls that air in.

So suppose now you're able to breathe in two or three liters of air.

When you ask these patients to blow out super fast, if the lining of these wind pipes

are stiff and not collapsible, they should be able to breathe in and breathe out 80%

of that amount of air within one second.

And that's really the determinant factor.

If the breathing and breathe out only 40 or 20, then your ratio really is not really close

to one because how do we define, do we define COPD?

It is literally a numerical entity that was defined by measuring the ratio of a forced

expiry volume in one second over a forced vital capacity.

In plain English, how much air you're breathing out super quickly in one second over how much

air you were able to breathe in.

And that ratio ought to be more than 70%.

If it's less than 70, then effectively the person has what we call chronic obstructive

pulmonary disease.

And that's the COPD part of it.

Collapsible airway that whenever a patient blow out, that muscle is so floppy that it's

collapsed on itself and does not allow you to really breathe out 80%.

We need to keep in mind that the umbrella of COPD has multiple entities.

You can have a patient with COPD that doesn't cough at all and has an overextended balloons

because they couldn't breathe out 80% so they were retaining the air.

That's emphysema.

Over time those balloons hold onto air, it stretched out and they lose that bounciness.

The other umbrella that is covered under COPD is chronic bronchitis, where patients have

so much mucus production that they are coughing chronically in addition to having a COPD

based on the numbers that I defined earlier.

And last but not least, you can have bronchiectasis, which is another entity that is added

in there and that is definitely much more recognized nowadays, which is an overproduction

of mucus because of remodeling of the airway, trapping mucus, causing chronic inflammation

and so forth.

And then you lose the ability to really clear out your airways completely.

So hopefully that summarizes what COPD looks like.

That was a really good summary.

So it sounds like for a long time, chronic bronchitis, emphysema, those are the two that people

were focusing on.

So bronchiectasis is something that is coming up and on the rise in terms of being diagnosed

and treated as a separate entity.

Correct.

Bronchiectasis is a new entity that is now finally recognized.

We even have an association of bronchiectasis that started in the UK.

Patients who are misdiagnosed or people really did not think that bronchiectasis existed

unless you have cystic fibrosis.

That you have heard the term cystic fibrosis, even if you are not sure what it is.

Cystic fibrosis or CF is a hereditary disease affecting primarily white children of European

descent.

Remember that the respiratory tract uses silia to move mucus up and out of the airway?

Well, they need a layer of saline or saltwater on the cell surface to keep the mucus from

getting too thick and sticky for that to be effective.

So the cells have these chloride pumps that pump chloride onto the cell surface and

then sodium ions follow.

What you get as a result is sodium chloride creating the necessary saline on that cell

surface.

Cystic fibrosis is the result of a genetic defect in which the cells still make the chloride

pumps, but they can't install them in the plasma membrane.

So there's an inadequate saline layer on the cell surface and the mucus is dehydrated

and overly sticky.

That thick mucus causes the respiratory tract to become congested and this often leads

to chronic infection and pulmonary collapse.

And it's not just the respiratory system, it also plugs the ducts of the pancreas and

prevents it from secreting digestive enzymes into the small intestine.

So digestion and nutrition are also compromised.

Unfortunately, the average life expectancy of people with cystic fibrosis is only about

44 years.

Okay.

Now we have this new entity that we call non cystic fibrosis bronchiactasis.

And when you look at the CAT scans, it's diagnosed on CAT scans.

You see that there is what we call bronchial cuff-in and mucus plug-in.

Literally, the airways that are supposed to be open are full of mucus and debris and

people when you hear them, they sound like a washing machine when they cough, and that

generally is a pretty good indication because that cough, even if they clear it, never goes

away.

And they can produce a good amount of mucus every day.

So and that goes under that same umbrella and the management, of course, is different

based on whether you have emphysema, bronchiactasis, or just plain COPD.

Okay.

So I want to focus on emphysema for a second.

Sure.

What is the anatomical changes that take place in the lungs that causes them to be overinflated

and difficult to exhale?

Sure.

So as I explained earlier, 80% of that air is supposed to be released within one second

every single time we take a breath.

People that have emphysema over time, every single time they were breathing in, they never

really completely emptied.

And I'm talking about one milliliter of air.

And over time, if you can imagine those little balloons and alveoli start to retain in

what we call residual volume.

If you go back into your physiology of the lungs, you can measure how much air there you're

breathing in, which is the FVC quickly on the spirometry, but truly the alveoli contain

a total lung capacity, which includes your residual volume at the end of each breath,

as well as your force vital capacity.

That residual volume is supposed to be minimal.

And when I teach, why do I say we need a minimal residual volume inside these balloons?

Why can't you just blow out all your air to the point where it collapses?

Well, think about it.

Earth they balloons.

Whenever we need to inflate them, you have to go over that point pressure to be able

to completely inflate with ease that balloon.

Imagine each alveoli collapses down at the end of each breath like that's birthday balloon.

We would have to struggle to get over that pressure point to actually reopen with each breath

16 times a minute, every single alveoli.

So we are well made in such a way that at the end of each breath, you don't collapse

your alveoli completely.

You always have a little bit of air, so the next breath is just as easily inflated.

And if you see my patient, lose that ability to have, if you want, an elastic recoil of

these balloons because they have been hyperinflated and stretched over time.

And therefore, as the balloons keep stretching, every single time you actually take a breath,

they can breathe the hit a wall, but when the empty, they never empty completely.

When you look at that patient, they take up, if you ask them to take multiple breath

or be active, they are take a breath, empty, and then take the next breath before they

completely empty the previous one.

So their residual volume is really high, their elasticity is lost, the actual alveoli

are over inflated.

And when you look at it on cat scan, it Swiss cheese why instead of having a grayish look

and a smooth look on the lung images on the lung view, you see literally black dark spots

on the lungs that are pure air, that are pure air rather than having at the surface of

these alveoli, those nice blood flow and blood vessels that suck the oxygen in.

That's the last aspect of the emphysema is you end up losing the vascularization components

if you want, because when you look at the lung structure, you look at the mechanics of

inflating and deflating, but you also look at the ability to transport oxygen by having

the blood vessels on these alveoli, so every single time you take a deep breath, oxygen

goes through the wall of the alveoli and is picked up by the pulmonary vasculature.

And the emphysema section tends not to have a good vasculature.

So not only are you losing the elasticity, so it's harder to exhale, correct?

You are also, and trapping carbon dioxide, you are also having a hard time oxygenating

the blood the way the alveolar capillaries are supposed to do it because you're losing

all the surface area that you used to have as these alveolar membranes degenerate.

So effectively you're creating what we call dead space.

So oxygen goes in there, but you're just wasting that amount of oxygen in an area where

you can't pick up that O2.

And that's why we talk about the anatomical dead space in my class, and we've talked about

in fact, I'll let the listeners know if you want to review spirometry episodes 51 and 52,

you go back, you can review spirometry, you'll be reminded what vital capacity is,

what residual volume is, and all that stuff.

Sometimes I give the same analogy you do about blowing up a balloon that's not even started,

but then also I usually ask my students if they've ever had the wind knocked out of them.

You know, if they've ever had like one of those where all of a sudden you're gasping for air,

it feels like the blow that you took forced out too much residual volume,

correct?

Now you're having to replace it to get it all in there.

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So I feel like with something like emphysema,

the trapping of the carbon dioxide is a real problem,

because we can get into respiratory acidosis situations

when we're not expelling the off carbon dioxide.

Yeah.

So what, I mean, I kind of, this is a loaded question,

I kind of know the answer.

That's okay.

What is causing this emphysema for most people?

So multiple theories.

You can actually, the easiest one to treat is a genetic cause.

So if you have an alpha-entry-tripsin deficiency,

an enzyme that impact not only the lung but also the liver,

very simple.

If the level is low and the testin is free,

it's a swab that you actually swab patients for in the office.

You send it in, the company usually tests it

and they look at their genetic material

and see if they have the actual gene.

And if they have the gene, you test the amount of alpha-entry-tripsin

and if it's very low, you can just get an infusion once a month.

Easy enough.

Now that does not reverse the emphysema that you had,

but it definitely can halt the progression.

What causes the actual emphysema to develop multiple level?

If you think about how I explained the COPD earlier,

and suppose, and again,

COPD can have an overlap with asthma,

not to make things more complicated.

But whenever you have chronic inflammation

of that lining, specifically in the small airways,

you end up trapping air effectively because of lack of expiratory methods, if you want.

So your windpipe is open.

You breathe in because it's an active process

where the diaphragm sucks the air in.

But breathing out is a passive process.

It's just literally because of the pressure change that you have.

So you let go and it's not like we breathe out actively.

So what happens is you breathe in

these patients that have small teeny tiny inflammation

at the level of the small windpipe.

You breathe in.

And then when you try to breathe out because it's not active,

you breathe out just a little bit.

And you end up having a residual volume increase in slowly.

And that causes over time a destruction of the alveolar wall

because of overextension of certain areas

that shouldn't have been overextended.

So that's definitely one of the causes

whenever COPD is not well controlled and is becoming chronic

or asthma is not well controlled,

lead into COPD and ultimately lead in

to an overinflation and elastically called destruction

and that becomes a vicious cycle

and progressive dyspanias actually developed.

Okay.

So what role does cigarette smoking play?

So cigarette smoking, hot steamy air going in with bunch of chemicals

definitely whenever.

And that's always why I say the line of your windpipe

is almost like the lining of your actual nose

because it's all respiratory.

So when people tend to have a sinus problem

or they say you know what it was in my head

and now it moved to my chest,

it's all a single lining.

And that lining is extremely sensitive.

So think about it like when you smell pepper

or you inhale pepper or you inhale something toxic,

you just feel the burning.

Same thing is happening inside your lung.

It's not because you don't actively feel it

that it's not happening.

So the actual cigarette and chemicals and heat

tend to destroy the surface of the actual windpipes

and bronchi.

Body tries to heal it,

sends troops and inflammatory cells

and bunch of immune responsive cells

to try to fix whatever was injured.

The remodeling happened.

The windpipe tends to thicken.

And that is one of the main reason why eventually

you will develop emphysema

because you cause a COPD picture

from the cigarette smoking.

So one lead to the next.

So sometimes you have just pure emphysema

because your body is able to actually fix the windpipe

but little too late.

Another time you might develop emphysema

while remaining with a chronic bronchitis

or a COPD picture.

According to the American Long Association,

about 75 to 80% of all emphysema cases

in the United States

are directly attributed to cigarette smoke.

With 25% of those being non-smokers

who have had long-term exposure

to secondhand cigarette smoke.

This means that if you live with a smoker

who smokes indoors,

you are also at risk of developing emphysema over time.

If you work somewhere that allows smoking, you're at risk.

So other than spirometry,

what else goes into diagnosing COPD?

Other than spirometry.

So remember, COPD entered the umbrella

of chronic bronchitis, COPD and emphysema

and we can even add asthma to it

if it's not well controlled.

The way to diagnose it other than spirometry

and there's a difference between spirometry

and full PFTs for pulmonary function tests

which will give you the total lung capacity

and the DLCO is cascans.

So the CT chest is paramount in being able

and you should be ordering it.

I'm going to have to plug this one in.

You should be ordering a low-dose CT

as a screening for all patients that smoke

anyways or have smokes within the past 15 years.

Age 50 to 70 years old.

So that cap scan is very typical

and you can see the emphysema very clearly

in the lung section obviously.

And if the emphysema is there,

then your determination is spot on usually.

It's pathognamonic.

So how long can this go undiagnosed

and how much damage can take place during that time?

So that's the unfortunate part.

As we get older, people tend to think

that being short of breath is normal.

They tend to think that a cough,

oh, it's just my normal cough because I'm getting older.

I mean, by all means,

the main cause of emphysema

is cigarette smoking either active or second hand

because that chronic inflammatory change,

the process of releasing if you want the enzymes

that break down the tissue,

the damage to the alveolar wall,

the loss of a lung elasticity,

all those are not going to happen

from a day to the next so you wake up

and you can't do anything.

It slowly creeps up on you.

And what I tend to tell patients

and community education,

in my community education session,

I tend to say make sure

to keep track of an activity

that you do every day,

whether it's going to the mailbox,

whether it's gardening,

carrying the groceries,

and noticing how close you park now

to the actual door of the supermarket

versus when you used to.

And all of those little activities

tend to hint to a development of a lung condition.

So it's very easy to completely ignore it and miss it.

And that's one of the main reason why people

are extremely surprised to find out

that in fact they have COPD

because it's like, I don't understand.

Until, because unconsciously,

they just adjust

you don't park that far.

You don't go get the mail as often.

You don't carry your groceries all together at one point.

You just carry one at a time.

So I always urge everyone,

please, when you ask patients,

or even yourself,

if you want to pay attention,

make sure that you are true to yourself.

Do not fake yourself if you develop a dry cause.

If you notice that it takes you a little longer

to go up the steps from the basements

to the first floor,

carrying the laundry.

There might be something more to it

than just,

oh, I'm getting older.

Does that?

And you don't want to admit it.

There's such a stigma about

developing lung diseases,

specifically if you are a smoker.

But there's also this fear

that you're going to become a burden

onto other family members and caregivers

if you admit that there is an issue.

At some point,

I diagnose patients with COPD and emphysema

and they refuse to wear oxygen

because they're too ashamed,

even though it fixes the problem

of being short of breath.

So I think we can do better

as a society,

as a medical community,

to make these patients feel at ease

and accept that it's no different

than diabetes and hypertension.

Right, that's good to know.

I mean, you don't want people

shamed into not being treated.

Correct.

Yeah.

So people get bronchitis,

like people have infections,

they get bronchitis,

they take antibiotics, it goes away.

What is the difference between that

and chronic bronchitis?

Okay, so chronic bronchitis is

a bronchitis that does not resolve.

That's the best way

of actually explaining it.

But a cough generally,

whenever a cough occurs,

you want it to get to improve

if you want within a couple of weeks,

four weeks, six weeks.

Generally, when it goes above eight weeks,

we're starting to get in trouble

and we call it a chronic cough.

Acronic bronchitis is a production

of mucopyral and sputum chronically.

And the reason why that happened

is because, as I explained earlier,

some of them actually end up

developing into bronchiactasis.

So primarily,

the airway is affected

rather than the alveoli.

And structurally, when you look at it,

you pretty much have

an inflammation,

similarly, of the bronchial walls.

But that thickening of the walls

is combined with an enlargement

of the mucus glands.

And you start having an overproduction

of mucus.

So when you look at the biopsies

or if you look at the slides

of the mucus glands

surrounding the airways

of somebody with chronic bronchitis,

you can see these big, huge glands

that are overproducing mucusin.

And so functionally,

it leads to a productive cough chronically.

And all you need

is having some airflow obstruction.

Bacteria starts sitting in there.

They love that petri dish.

And you start having exacerbations,

which is infections over and over again.

Antibiotic, prednisone,

they feel better,

they come off the antibiotic,

they get infected again,

and it goes on,

and that cycle doesn't stop.

So ultimately,

the airways become narrow

because of the thickening of the airway

and the overcrowding of the glands.

And finally,

you end up having clogged airways

with secretions.

And that officially would put you

as becoming a chronic bronchitis patient.

In lame language,

we call it the Smoker's cough.

Now, if you thought the number

of emphysema cases

linked to smoking was high,

get this.

According to the US Department

of Health and Human Services,

90% of patients who present

with chronic bronchitis

are smokers.

90%.

That means that about 85%

of total COPD cases

in the US

can be linked to smoking.

It's astonishing.

These are diseases

that have been virtually

invented by the tobacco industry.

Now, I've never been a smoker.

I don't vape.

But I cannot imagine why anyone would

even consider it,

knowing what we've known for so long.

I want to clarify and see

if I've been correct about this.

But years ago when I was in school,

we learned

that the chemicals

in the cigarette smoke

paralyze the silia

in the bronchioles

and the bronchi.

And that is part of the reason

why the mucus

starts accumulating

because you lose that

bronco-musillary escalator

situation

that

might most my listeners know

about because they're A&P students.

So is that the case?

So we still believe that

there are chemicals

within the actual airway

that causes

if you want a paralysis

of the

the silia.

Specifically,

the formaldehyde

or the acralin

or the hydrogen cyanide.

All those are absolutely

able to either limit

that beaten or slow it down.

But the toxicity,

most of the time,

helps that motion.

Some cigarettes have actually ammonia

and others have phenol

and oxidants that definitely impair.

But genetically speaking,

there's nothing that is translated

to the inner aspect

if you want of that silia

or if it starts to get regenerated.

And all that definitely

is impactful.

And with that limitation of movement,

your mucus is actually clogged

and bacteria is trapped.

So yes,

overall, it is true.

Did you hear that?

For maldehyde.

Hydrogen cyanide.

Ammonia.

These are poisons.

And people are voluntarily inhaling them.

Stop it.

Just stop it.

Although now people say,

well, you know what?

If I do the vaping,

it's much better.

I don't have as many chemicals.

Wrong.

Definitely.

Anything you inhale,

it's not that's not belong there.

So pollution is a big issue.

So some people that don't smoke

turn out to have chronic bronchitis

because of the work that they do

or where they live

and more importantly,

what type of cook in

they end up having inside their kitchen.

And I always tell people,

make sure you have a clear,

I don't know how many people really

clean that vents

where they cook.

Right.

I mean, if you take it off,

the amount of grease

and the amount of particles,

if it's trapped there,

I can guarantee you are breathing it in.

The other thing that people tend not to think about

is the vent most of the time,

just to recycle.

It does not take it out.

So that's important

to actually have a true vent

that takes everything out.

And if you don't have it in the house,

make sure you have an air filter

that is specific to kitchens.

So it traps that type of particles.

So hopefully that answers the questions.

That's good to know.

That is definitely good to know.

So with COPD being different diseases,

how does that affect the treatments?

Yes.

So the treatments should target the clinical picture.

Once we diagnose COPD,

we use to measure COPD based on gold 1, 2, 3, and 4.

Gold criteria, which are published every year,

are published to help the clinician treat their patients.

Before we used to say,

do the spirometry measure the FEV1

and determine if they are stage 1, 2, 3, or 4?

And based on that stage,

we will give you

X amount of inhaler.

Inhaler for this level,

inhaler for this level,

a triple inhaler for this level.

Fast forward today,

when I presented the gold of 2026,

2025, sorry,

which is for 2026,

we added a very significant aspect

to the therapy.

It's not as simple as determining

the FEV1 with a patient.

It's actually encompasses a full social,

clinical, and if you want,

environmental intervention.

The most important one is

the clinical, like I stated,

the clinical picture of the patients.

Has the patient have an exacerbation?

Have they had more than two per year

and have they been hospitalized?

If they have,

you need to be very aggressive about initiating

an inhaler that includes

a long-acting,

mascarinic agonist,

and a long-acting beta agonist.

That's category E.

The other categories are

category A and B,

which is based on

their MMRC and CAT scores,

which are the dyspnea scale,

and you can find them on the MD calc,

you can Google them.

So when the patient comes in,

you ask them specific questions

to see how dyspnea and how short of breath they are.

If they have no symptoms,

even if their gold is four,

or the FEV-1 is like 23%.

If they have no symptoms and they're able to move around,

you do not need to give them technically an inhaler.

If they are symptomatic,

you can give them something.

But the combination of clinical picture

and actual number from spirometry

have to be combined

to ensure that you treat them using an inhaler.

Now, if they're not coughing

and they're just short of breath,

inhalers can help

to open up the airways.

But also,

pulmonary rehabilitation

which tends not to be emphasized in the therapies.

Pulmonary rehab,

which is going to the gym

and learning how to breathe is paramount.

Why?

If you go back to what I explained earlier,

people in emphysema trap

and when they start breathing fast,

they stack their air

and they cannot have any more incentive

or ability to suck more air in

because they're literally full.

They need to learn to breathe

differently than a normal person.

Rather than having a long

inspiratory effort

and a short

expiratory effort,

emphysema patients ought to have

an inverse IE ratio,

long expiratory effort,

short inspiratory efforts.

So whenever they're walking,

they should be

breathing three times out

and breathing in one,

specifically when they're active

to allow themselves

to not trap as much air.

That's pulmonary rehabilitation aspect

is important to teach these patients

to actually adhere to

and there are tons of programs

thankfully nowadays

online where pulmonary rehab

is approved online.

Now, those are the patients

that have emphysema

that are not producing

any mucoprolant secretions.

On the other aspects,

you have people

that are producing tons of mucus,

chronic bronchitis,

bronchiacusis.

You can give them all the inhalers

you want.

If their airways are clogged

with mucus,

that inhaler ain't going to be

completely inflated.

That's why I tell them.

You have to empty the pipe.

How do you do that

by being aggressive

with expectation methods?

Literally the same way

you tell a cystic fibrosis patient

to use inhalation therapy

via a nebulizer

with hypertonic saline.

You do the same thing

with these people

that are producing mucus.

You give them saline

nebulizers.

You can give them mucolytics

that can actually inhale

and help them liquefy that mucus

so it's not too sticky

and they just go into

have to learn how to do

the huff cuff.

It's a method that they can

learn online

to help their diaphragm

and their abdomen

to force the actual

mucus to be expected.

More importantly,

you need to make sure

that you culture that mucus

if it's infected

to know what you need

to treat them with.

You cannot be given

them antibiotic

regularly around the clock

every three weeks

because ultimately

it's going to backfire.

You're going to develop

resistance and you're going

to have nasty bugs.

Some of these patients

because of chronic inflammation

and recurrent exacerbations

we tend to put them on

Zythromax chronically

28 days on 28 days

off.

Zythromax is an

antibiotic commonly used

to treat lung infections.

You probably heard the term

Z-pack.

That's not a 28 day version

but the Z and Z-pack

stands for Zythromax.

And last but not least

if the end up having

complicated infections

they might need what we

call inhaled

antibiotic that are available

now on the market

specifically if the end

of growing a specific entity

that we call

mycobacterium avium

which is really what I call

the bug that grows in the

shower heads and in the soil.

So if you love gardening

and you don't clean up

your shower heads

heads up and you're like

taking hot showers

chances are

if you have bronchiectasis

you might be prone

to develop in

the mycobacteria infection.

Well thank you for all

that information.

That was that was a ton.

There's so much

that goes into this.

And Doug

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So I guess the big

a million dollar question is

what is the most important thing

people can do to prevent

getting COPD?

So that is a million dollar question.

So first and foremost,

not smoke.

Or if you smoke,

please stop smoking.

And I know it's a lot easier said than done.

And asking for help,

joining smoke and cessation classes

are paramount.

You might think,

I've done it.

I've been there not working.

You know what?

Every single time you go in

and now they have them online

and you don't even have to have

your face showing.

Just listen to the tricks

and tools that they give you

to be able to actually

at least decrease the amount of

cigarettes or vape that you're doing.

It is important.

Smoke and cessation should be

part of everyday life

whenever you are a smoker.

It is an addiction.

It takes time.

And I always say,

you won't be able to stop a bad habit

until you develop a good habit

to actually help you stop.

So just saying I'm going to quit

might not help.

So stop in the cigarette

and the inhalation injury.

That's number one.

Number two,

making sure you are

environmentally aware.

Within your homes,

how much chemicals are you inhaling daily?

Are you a freak of cleaning

by in all these chemicals

that you spray around the house

to make sure your floor is

spanked clean?

If you do that,

do you have a good ventilation?

How much of these chemicals

are you inhaling?

Maybe in your job,

whether you are a dental

hygienists,

whether you are working in construction?

You are involved

with high environmental factors

that can cause lung injury

and can cause you to develop

in long-term COPD.

Last but not least,

how many products do you have

in your bathrooms?

Do you love using your dry shampoo?

Do you love having this makeup

with the powder?

Are you using the actual spray tan

that we use?

Anything that's aerosolized

and benzene-based

isn't no-no.

And actually,

as an FYI,

over the past two or three years,

if not five years,

we have noted a significant increase

in lung carcinoma

in non-smoking middle-aged women.

And we're trying to get to the bottom

of why are these women

developing these lung cancers?

We don't know for sure,

but environmental

more than genetics is probably plainable.

In Asia,

they have added

in a questionnaire for the patient

a cooking index.

Because when you deep fry,

when you use specific coal

or specific products to cook your meal,

specifically women tend to inhale

most of those products.

And that is believed

to be one of the causes

why patient developed,

not only lung carcinoma,

but also COPD.

That's interesting.

Yeah.

We heard a lot of the stuff

a few years ago about the gas stoves.

Correct.

Using natural gas stoves,

putting fumes into the air

that we're inhaling.

So, yes.

And that definitely makes

sure you always clean up

your gas stoves' sensors.

Because if your flame is not fully blue

and you have the tip of it

at different color,

you're not burning all that benzene.

And it's getting in there.

And I know benzene's

Oh, that's a hole.

And it's a nasty one.

Yes.

Yeah, my son,

who is a chemistry major

and his name is Ben,

when he turned 18,

he got his first tattoo.

And his first tattoo

was a benzene ring.

Oh, my God.

Stay away.

Perfect.

Yeah.

So, well,

Dr. Melanon,

thank you so much for joining me

and shedding so much light

on this really,

really important condition.

It is a top 10,

which is what I tell my students all the time.

I am going to make sure

that I put a little side note in

and have people go and review.

Muscarinic receptors,

because I heard you throw those in there a little bit.

I'm not sure they're going to remember that off top of their heads.

You may remember back in episode 27,

I covered the autonomic nervous system.

In that episode,

we talked about receptors

for the un neurotransmitter acetylcholine.

We call those colonurgic receptors.

Muscarinic receptors

and nicotinic receptors

are subtypes of colonurgic receptors.

So, these are basically receptors

for the neurotransmitter acetylcholine,

and each receptor

is responsible for some different actions.

You can review episode 27

if you're very curious about

what muscarinic and nicotinic receptors are.

The last thing could you tell?

Listen, there's one more thing

that you might want to share

or where they can find you.

Again, we talked about your website earlier.

Is there anywhere else, maybe on social media?

So, I did do a chat talk

and that actually addresses the phenomenon

that I call the fast food of health care.

The fast food of health care

is our urgent centers.

Urgent centers were originally developed

to help with acute issues.

If you have elaceration,

if you have a break of bone,

they tend to fix it.

Now, unfortunately,

convenience can be deadly.

So, people with cough,

COPD, chronic dyspnea

tend not to be able to come in

and find primary care physicians.

Unfortunately, because the weight

is so long,

six months sometimes.

So, I would like,

if you have a chance,

you can listen to my TED Talk.

And I am definitely reachable.

I am on social media,

as well, links to my lung health services website.

You can find actually my Instagram

and my Facebook on there.

And the last but not least,

women in interventional pulmonology

is a nonprofit organization

that I have founded

and is now international.

And we have educational webinars

that are for free

that tends to give you

an overview of where we are with lung carcinoma

and what we can do to make a difference.

So, definitely check that one out as well.

And of course, lunghealthservices.com

gives you an idea of where to find me,

where to contact me.

Happy to help, happy to teach.

Always reachable and approachable.

Do not hesitate.

And hopefully you learn something.

And if anything, please make sure

that people get screened for lung cancer.

We would love and appreciate everybody's help

to make sure we battle this deadly disease.

Well, I hope they're all doing that.

I will put links to all of those things in the show notes

that people can easily find those for you.

Thank you so much once again.

This was really, really beneficial.

Thank you.

Thank you for having me.

It was a pleasure.

Okay, I cannot thank Dr. Nina Mellon

and enough for coming on the show

and sharing her expertise with us.

I will post Dr. Nina's website, TED Talk,

social media,

the Women in Interventional Pulmonology Group.

I'll post all of those links to the show notes

so you can find her if you want to learn more

about the amazing work that Dr. Nina does.

Chronic obstructive pulmonary disease

or COPD is the number three cause of death in the U.S.

In fact, it is what my father passed away

from back in 2021.

He was a smoker for most of his life

and had emphysema by the time he was in his mid-60s.

Modern medicine extended his life until he was 77,

which is great, but most of it was spent

requiring supplemental oxygen wherever he went

and even the smallest amount of physical activity

was very difficult for him.

When I talk about the horrors of smoking,

I often hear people say,

well, you have to go somehow.

Let me tell you something.

This isn't how you want to go.

It takes you slowly, uncomfortably,

and needing a lot of care and medical intervention.

So if you take one thing from this episode,

please don't smoke or vape.

Nothing good can come from that.

Okay, having said my piece on that,

I sure hope this podcast is helping you get your beer

better in A and B.

Good luck.

Be well.

I'll talk to you next time.

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