Asthma Explained Clearly: Asthma Symptoms and Diagnosis
22
August

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , /


welcome to another MedCram lecture
we’re going to talk about asthma and specifically the causes the
pathophysiology diagnosis and treatment of this very common disease I want to
kind of show you what’s going on at the bronchial level you remember if you look
at our pulmonary function test discussion we looked at a flow volume
loop and what happens when you blow out air very quickly your your forced
expiratory volume or flow rate goes up very quickly and then comes down and
then you take a inhalation in and thus obstruction that occurs in asthma and in
COPD occurs in this area here which is the small Airways and as that
obstruction gets worse you see a decrement in the flow rates especially
later on in blowing out and the point here I want to make is that these are
the small Airways so this is where asthma is occurring it’s obstruction of
these small Airways not the large ones but the small ones and as such I want to
diagram what it is that’s going on so you’ve got the airway and this is a very
simplified version of what it is that’s going on you’ve got this lumen of the
airway that’s here and as you may know it is lined with smooth muscle when that
smooth muscle contracts this lumen gets smaller okay so there’s two major things
that are occurring in an asthma or obstruction of these small Airways is
you’ve got some sort of an inflammatory process for whatever reason that’s going
on here this inflammation stimulates certain cascades that occur and it
causes smooth muscle constriction and as a result the inflammation causes the
lumen to get smaller and smaller and smaller until finally there’s wheezing
there’s obstruction and the primary problem is that you can’t get air out of
these small Airways and that is why in an asthma attack you will see that this
flow volume loop comes down and the flow rates in these small
Airways is almost non-existent that’s when you run into asthma attacks
now the severity of this contraction is going to give you the severity of the
asthma attack and how we affect this and what the pathophysiology is of this is
going to determine how this is treated so let’s talk about that a little bit
once again I want to emphasize that in asthma what we have is reversible airway
inflammation that is opposed to irreversible which we would see in COPD
where there’s really this airway inflammation has occurred and this
constriction has occurred in COPD it’s kind of irreversible in asthma we can
actually reverse it back to almost completely normal this inflammation and
constriction can sometimes be mediated by IgE so sometimes you will see
elevated IgE levels and that fits into the pathophysiology and the treatment
what is IgE it’s an immunoglobulin specifically it’s an immunoglobulin E
and that’s important because immunoglobulin E affects a cascade that
releases histamine which causes swelling which is going to make the area in that
Bronco even smaller IgE uses the basophils and mast cells you these release histamine there are ways
of preventing these cells from releasing histamine and that is sodium chromo
gleich 8 you’ll see for instance medications like Chrome illan sodium
criminal Glock 8 is used to stabilize these mast cells and basophils and
prevent histamine so sometimes we actually use that in the treatment of
asthma ok so again I want to review the bottom line here is is that we’ve got a
situation where you have inflammation which causes constriction of the smooth
muscles in the bronchioles so let’s talk a little bit about this smooth muscle
then okay we’ve got nerves that affect this smooth muscle two types of nerves
specifically and they have receptors the first one I want to talk about is the
beta receptor okay so you have a nerve that comes down and it releases compound
which hits this beta receptor and this causes relaxation and there’s another
receptor which is the muscarinic receptor and that causes constriction and so in
both asthma and COPD as it turns out we want this muscle to be relaxed that’s
the goal we want relaxation and so what we’re going to actually end up doing is
activating this receptor and blocking this receptor and so what you see is
pharmacologically we’re going to be using anti muscarinic s’ and we’re going
to be using beta agonists that’s how we get to the treatment now the other thing
that we’re going to see pharmacologically and we’ll talk about
this is inflammation inflammation is going to cause constriction because of
inflammation so what we’re also going to use is an T
in flama tories so what I’ve just shown you here are the three cornerstones of
asthma treatment some of them are going to be used first because they’re much
more effective than others and you could probably guess which one is going to be
most effective because inflammation is starting everything off the
anti-inflammatories are gonna be number one the beta agonists are going to be
number two and the anti muscular Nick’s are going to be number three okay so
we’ll get into the pharmacology of that let’s talk about the pathophysiology
about perhaps clinically where this inflammation may be coming from so
asthma there’s there are lungs things that can trigger problems in our
Airways based on a number of things first of all because of the stuff that
we breathe in so that’s a trigger the air that we breathe
what else could trigger a spot what else could be causing it well there’s a tube
that sits right next to the trachea which goes down to the stomach called
the esophagus and sometimes stuff in the stomach can reflux up and irritate the
airway that continues up so another thing that can cause this is
gastroesophageal reflux disease that can sometimes cause symptoms of asthma now
if we go up here we have the nasal passageway sometimes you can have
allergies that drip down and cause irritation in there and that so that
post nasal drip can cause asthmatic symptoms and so when I ever I see a
patient with asthma and whenever you see a patient with a sore you’re asked about
on a test you should think about these things as causing asthma so what we call
coughing it’s asthma post nasal drip and gastroesophageal reflux disease some of
the other things that can contribute to all of these think about down feather
pillows pets in the bedroom these are places that you spend a good
six seven eight hours a day and could affect some of the treatment symptoms so
these are some of the things that by getting rid of we might improve asthma
there’s also environmental things and things from work for instance from your
occupation there’s something called isocyanates or cotton dust wood dust solvents all of these things can by
breathing the men set off asthma exacerbations there’s one other thing
that I should make you aware that they might ask you on a test they love to ask
things that are uncommon in asthma that could be very unique or make you think
of something and there’s something called samplers triad where you see
number one aspirin sensitivity number two asthma and number three nasal polyps now when these people take aspirin or
any type of NSAID what can happen is that these medications inhibit
cyclooxygenase and as a result they’re going to have increasing compounds that
are going to set off asthma exacerbations the key here is that
within hours of taking aspirin they’re going to start to feel flushed and
they’re going to go into an asthma exacerbation these patients who are
typically sensitive to aspirin or NSAID products are also going to have nasal
polyps the key here is that they need to stop using aspirin and NSAID products
and find an alternative these patients by the way and we’ll talk about
treatment also respond very well to leukotriene receptor antagonists and
we’ll talk about those so just remember samplers try it in your
patients without I’m asking that they’ve had a history of
aspirin sensitivity or if you’ve noticed that their symptoms have gotten worse
after taking aspirin or NSAIDs and then ask them about a history of sinus
problems maybe even sinus surgery or nasal polyps okay will join us for part
two where we talk about the diagnosis and the treatment of asthma you


87 thoughts on “Asthma Explained Clearly: Asthma Symptoms and Diagnosis

  1. Great lecture on聽 Asthma, but the propaganda commercial about the Keystone pipeline is terrible, and makes people think it is a good thing. sorry not true.聽 Please watch your commercials.

  2. Loved the med cram videos. 聽Very helpful. 聽I couldn't understand how to read a pulmonary function test by reading a book but the videos made it much more understandable!

  3. There is no sympathetic innervation per se of airway smooth muscle as your diagram suggests, interestingly though beta2 receptors are conserved!

  4. I have asthma it's not fun taken a bunch of meds or going to the hospital a lot I hope they find a cure soon馃槉

  5. there are virtually no sympathetic nerves going to the airways. The beta receptors are stimulated by circulating adrenaline

  6. am arabic studant nurse and i have a littel problem with your writing i wish to be careful with your writting i will try to understanding your writting … there is alot of information that i dont know it .. thanke you for the great vedio 馃檪

  7. I have had asthma all my life and it has gotten worse over the years. The last time I went to a doctor for an asthma attack was when I was eight. I am now twelve and when I even lay in bed I always have to take in really deep breaths. It has gotten to a point where I have had asthma attacks just from laying on my bed watching YouTube. I hope everyone reading this will have a greater appreciation for being able to breath with no problems, because it's awful having to get used to not being able to breath

  8. With Christmas being the season of goodwill, please dig deep to support the great work Asthma UK do
    http://uk.virginmoneygiving.com/fundraiser-web/fundraiser/showFundraiserProfilePage.action?userUrl=John_Drew_April2016

  9. For anyone who has asthma I feel bad for I used to have it but it just went away as quickly as it came..which to this day I don't understand..

  10. I use to get asthma bad but around 16 I started to outgrow it and now im 21 I haven't used my inhaler in about 4 years

  11. Thank you so much for this! I have a chemistry project on a disease/medicine, and I chose asthma as my focus disease. This really helped me in understanding the cell-level mechanics of asthma 馃檹

  12. based upon hygiene theory we still believe that diseases which are immune mediated like asthma is more common in developed world when compared to developing world where people are dying more of infectious diseases..

  13. Fighting adult asthma. Babies had but allergies run tampet in the family. In all these years no doctor has explained this so I could understand. Thank you.

  14. I have a question for you. If asthma, true asthma is defined as a disease process of the lower airway, what is it then when its the MAIN airway that is the problem? Somewhere below my vocal cords and above the bronchial bifurcation is where my problem begins. It seems to spread from there. As long as I can get air through to my lungs my sats stay up, until of course I physiologically peter out, then I crash going into respiratory failure and have in fact arrested. I've been dealing with all this for 16 yrs (since Feb 2000) I've been hospitalized well over 30 times, have been intubated MULTIPLE times (I've actually lost count now) and have almost died 3 times. One in particular. I'm on O2 around the clock (6L at rest & 8-10L on exertion) I technically have NO diagnosis and they can't figure out why I need the oxygen, let alone so much. And to say that they've tried to figure it out, well, that would a gross misrepresentation. I think they want to know whats going on worse they I do! I'm to the point that I really don't care what it is anymore, because I'm not sure that it matters. I mean, if you can't fix it or make it better, than why does it matter what its called. I really just want to be treated palliatively and kept comfortable and have as high a quality of life as can be had. I still have a LOT I;d like to do before I leave, and I don't plan on going ANYWHERE for quite some time. There have been SO MANY doctors that have tried to figure it out. I keep telling them that as long as I can get any air into my lungs the gas exchange will happen, but once that main airway shuts down, it won't matter anymore how well my gas exchange works! Just so you know, COPD has been ruled out, as has vocal chord dysfunction (on multiple occasions) as well as many other things. The only thing that is known for sure is that all though my PFT's come back pretty normal, there is clearly a reactive spasm to air born particulates that presents like asthma, I'm especially sensitive to those particulates if I'm anywhere below my baseline. And all though it may take 3-5 times longer to respond to the typical emergent asthma treatment protocol, and even though you MAY (uhm, probably) will have to intubate me, and after treatment has begun, I will get a lot worse, almost a guarantee, but IF YOU WILL CONTINUE with the basic emergent asthma protocol treatment, I WILL eventually respond! I just got out of the hospital last week. Again. I've NEVER decompensated so far so fast as did the day it hit. And I again ended up in respiratory failure and intubated, when they first tried to titrate me down to breathing on my own to prepare me for extubating, my body was NOT happy about it and responded as such. So, I stayed right where I was. I was in the MICU for 5 days before being transferred to the regular floor where I had a flair up the next day. Things weren't handled well, and as a result I was left without treatment. No one really did anything wrong, I just kinda fell through policy loopholes, which we're working correcting. But all though at 6L of O2 of the whole time of the flair up my sats stayed up above 93% (my body compensates REALLY well, or at least it tries to) I was having so much trouble breathing and oxygenating my body that my wonderful normal BP of 90/60 skyrocketed to 206/77! Frankly, I feel very fortunate not to have had a stroke. They of course administered the appropriate medication and brought it back down, but even that wouldn't have happened had I not gone unresponsive and they not called the rapid response team.

    Apologies for the length. Please understand, I'm not asking for even a possible diagnosis from you. I'm just asking that if true asthma involves our lower airways as you describe, what is it when it all begins above the lungs in the main airway? I'm just curious. I expect no miracles. Well, not from man anyway . . . 馃槈 I'd REALLY appreciate some info if you could Oh, by the way, I suppose I should mention that before getting so sick, I to worked in healthcare. So I actually do have some medical education. All that means is that I usually understand things far better than the average lay person does. I was certainly NOT a doctor! I only mention it so that what ever you do come back with, it won't require a lot of explanation. I'll understand what you're saying. Thank you so kindly for your time!

  15. Zthank you very much! I dint know I shouldn't take aspirin and it can trigger asthma attacks! I recently had a issue and I think it's because I took the aspirin on a daily basis. So I'm happy that I found it out. Again thankyou

  16. if smooth muscles are constricting, shouldn't they be opening up the lumen more? I thought the muscles would be relaxing therefore taking up more room from the lumen –> hindering airflow

  17. From a Nursing student in a Pathophysiology class currently, thank you!
    This was broken down into a very easy to understand way.

  18. Dr. Seheult, B2 receptors in bronchioles smooth muscles are not innervated by the sympathetic nervous system, these receptors are stimulated by circulating NEPI, unlike the muscarinic receptors which are indeed innervated by the parasympathetic branch.

  19. MMS cured my COPD went from going to the er every 30 days to o2 levels of 94 in 5 days no other meds shoveled snow for 5 mins

  20. I actually have post pertussis cough variant asthma. I don't smoke and I can't really be around where it is without some form of perfect ventilation to get it out of the air I'm breathing. Other than perfect ventilation I just can't be around it at all. Before pertussis though, I never had asthma, no history whatsoever until after pertussis

  21. Is it difficulties breathing in or out? I have weezing only breathing in. And breathing through my nose is easier than breathing through my mouth.

  22. I have excess mucous, and must cough every 2-3 hours, day and night. I haven't slept much since August. It's now October.

    I'm on my 2nd batch of mucinex, which I try not to take more than 1-2 times daily.

    Coffee helps. I'd previously quit caffeine, but now I'm back.

    I'm quitting dairy, fried foods, added salt, bread, corn, peanuts, and limiting eggs.

    I've never had this in my 53 years.
    What inhaler is appropriate/safe to buy off-the-shelf at Rite Aid or Ralphs??? I've never used one.

    Thanks to anyone who can tell me in your response.

  23. I have asthma caused by foreign airborne asbestos particles that we're introduced into my lungs while I worked in construction at my old job.

  24. A whole foods plant based diet . Organic has helped my asthma tremendously. Also check I to eating foods high in magnisiium and potassium and vit c. This is the only thing that has ever helped my asthma and I've had my fair share of prednisone and hospital stays.

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