Asthma pathophysiology | Respiratory system diseases | NCLEX-RN | Khan Academy

By Adem Lewis / in , , , , /

– Before we talk about
what asthma looks like, let’s take a look at a normal airway. So, we’ve taken a cross section of somewhere along the airway. Asthma is a small airway disease, so this is not the trachea
or the stuff in your throat, but in your chest. And one of the important players in the caliber of the
structure of the airway that I want to start with
is the smooth muscle layer. So, we’ll use red for muscle, and this layer controls the
diameter of the opening, diameter of the lumen. Of course, outside the muscle
there’s other things too. There’s connective tissue and cartilage, depending on where– If you’re high up enough on the airway. Those things are not really
as affected by asthma, so we’ll just leave it kind of like this. All right, so we’ve got our smooth muscle, which smooth muscle, remember, you can’t control consciously. It reacts to the environment, and usually it keeps our
airway nice and open like this. I’ll label that here, smooth muscle. Now, inside that we have
a layer of the mucosa. So, we call it the mucosal layer. Let me just label that, the mucosa. That basically coats the
inside opening of the airway, and within this layer it’s
very important that we have these glands that can
secrete mucus into the lungs. They’re there for lubricating the opening and keeping our lungs moist, enough so when there is inflammation, or there are foreign bodies
we have to get rid of, the mucus that they
secrete is important in clearing out the area. So when we cough, and
we cough up the phlegm, the phlegm comes from these glands that secrete the mucosa. So, they’re kind of everywhere
in the mucosal layer. And, of course, here we have the lumen. This is where the air
actually moves in and out. It is dry but nice and
lubricated by the mucus. So, this is a quick look
at what the normal lung, what the normal cross section
of the airway looks like. And now, let’s look at what happens when this person is having asthma. As you know, asthma comes in attacks, so most of the changes
happen during an attack. Depending on the severity, this person might get it more
often than the next patient. So, first we still have
our muscular layer, but now the lung is in spasm. The muscles are spasming,
which means it’s constricting, and the opening is going
to be much smaller. The connective tissue, like
the cartilage and other things, are still out there, so I’ll
still draw it like this, but the important thing
to focus on right now is the fact that the
muscular layer has thickened and is clamping down on this opening. In addition, the mucus layer, which is nice and round
here, that I’ve drawn, has swelled up in reaction
to the inflammation. So, instead of a nice
round opening like this, now we have this amorphous shape that further clamps down on the opening. So now look at what has
happened to our lumen. It’s much smaller, and
to make matters worse, don’t forget the glands. So, the glands are still
here, but this time they’re also reacting
to the immune response, and as a result, they’re
filling up with mucus, and they’re secreting it into the lumen that’s already narrow and blocked off. So, now we’ve got this
swirling mucus in here. That only makes matters worse. So, look at the difference
between air going through this nice big opening and the
air trying to get through this. So, between the constriction
and all the fluid in there, we’re going to have little bubbles. That’s why you hear the
popping and the wheezing when you listen to a person
having an asthma attack. The wheezing comes from the obstruction, both from mechanically narrowing this area and the extra fluid in there
from these glands going crazy. So, that’s how it happens, but why does this whole thing take place? What triggers asthma? Well, that is sort of the
million dollar question, because there’s so many
things in the environment. What I’m drawing here are,
it could be pollution. It could be smoke. It could be food or dander. Anything that this
particular person reacts to. These are the allergens in the air. And when they get into the body, our body has an immune response that reacts to anything that’s foreign. Some people react more than others. And we have these antibodies that kind of look like
a Y-shaped molecule. So these immune reaction tend to be IGE. That’s just the name of these antibodies. Now, the body has a tricky memory system. If it’s the first time that
it’s seeing these allergens, you might only get two IGEs, because they’re working
hard to make new ones, to recognize them, but
the third or fourth time, every time you get exposed, because the memory’s still there, it’s easier to make the IGE each time. It’s like fighting an enemy that you’ve already fought before. So, the IGE actually increases in number. So, the size of this IGE response is proportional to the size
of this immune response or to this allergic
response, I should say, because when the immune
response goes haywire, responding to something that’s foreign and trying to fight it off, that’s called an allergy. Okay, so we’ve got
these foreign allergens, whatever the trigger is, with these IGE. The job of the IGE is
to recognize and pick up these foreign particles. The IGE is in the same
family of antibodies that help us fight off infections, but in this case, it goes to search for a cell we call the mast cell. It’s spelled mast, like
the mast on a ship, and inside the mast cell, it’s just floating around our body, carrying little pockets of a
molecule we call histamine. And histamine is the main
player in any allergic reaction. If you remember, if
you’ve ever taken anything to fight off an allergy, there’s a class of drugs called
the antihistamines, right? So, histamine is just usually
walled off in the mast cell, not in our system, but the IGE antibodies
we just talked about, they are friends with the mast cells, and only when they’re carrying
a foreign body like this do they find the mast
cell and attach to it. So, every pair of IGE that
has picked up an allergen will go then look for a mast
cell to attach to it like this. This attachment right here kind
of wakes up the mast cells. So, all these little
pockets inside it open up. The histamine then flows out
of the mast cell like this and kind of floods into our
system, into our bloodstream, causing allergic reactions everywhere. This is why you sneeze,
and your eyes water. You can get hives. The whole cascade of
that allergic reaction is thanks to these little
histamine molecules, and in the lungs, if
this person has asthma, this is exactly what happens
as a result of the histamine. Let me just draw a few more
particles here to show you. And while we get this constriction, we get the mucosal swelling,
and we get the wheezing. So, asthma is really an immune
response going overboard, as all allergies are is a part
of our body’s natural response to a foreign body that then causes us harm by reacting too strongly and releasing things
that cause us discomfort. So, to sum up the
pathophysiology of asthma, remember first we’ve
got the muscular layer thickening and constricting. Then we’ve got the
mucosal layer swelling up, and third we have the glands
overproducing the mucus that then floods the
already constricted opening.

28 thoughts on “Asthma pathophysiology | Respiratory system diseases | NCLEX-RN | Khan Academy

  1. Where do the mast cells go and what exactly does the histamine do? Lil' confused here, but a great video nonetheless!

  2. Really wonderful informative video. Another resource I also found useful for pediatric asthma
    is Knewreck Asthma Eradicator Guide – it should be on google if you need it

  3. Mate I have been a paramedic for 15 years and this is the simplest way I have ever seen Asthma described, Thanks

  4. Thanks for this, i am a 3rd year pharmacy student with exams coming up in a few weeks, this really helped, im going to look at your other videos too.

  5. What about exercise? A doctor told me that I have exercise induced asthma and I shouldn't overwork myself, and when I do, I have huge coughing fits

  6. 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..

  7. Could someone explain to me why blacks are affected MORE by Asthma than other races? I was just curious about this but there isn't much information.

  8. African Americans: Most diseases affects A.M mainly due to their social economy status and/or educational level the person. This is also true with their diet intake. Looking at this factors, this population would be more pron by diseases like this. @Pavati Sharma

  9. Goblet cells secreting mucous AND increased capillary permeability causing build up of mucous? I cannot find academic info on this. All sources say that the mucous comes from the goblet cells, but my patho book states that it can also be from a change to capillary permeability. If someone can clarify this so I can get on with my life that would be great.

  10. Your parents smoking 2 to 4 packs of cigarettes daily in your youth damages your lungs, pollution ans all the lethal chemicals in food and cleaners.

  11. This is the best and easiest to understand explanation on the pathophysiology of asthma I have found. Thanks so much!

  12. Let me add something from Dr Charles Robert Richet – Nobel Lecture – December 11, 1913

    "……. by 1902 we were able to state three main factors which are the corner-stone of the history of anaphylaxis:
    (1) a subject that had a previous injection is far more sensitive than a new subject;
    (2) that the symptoms characteristic of the second injection, namely
    swift and total depression of the nervous system, do not in any way
    resemble the symptoms characterizing the first injection;
    (3) a three or four week period must elapse before the anaphylactic state results. This is the period of incubation.

    Once these first factors in anaphylaxis were well grounded, the field
    opened right up, thanks to the skilled and fruitful research of many

    In 1903 Arthus, in Lausanne, showed that a first intravenous injection
    of serum on a rabbit causes anaphylaxis, i.e. three weeks after the
    first injection the rabbit is hypersensitive to the second injection.
    The phenomenon of anaphylaxis was becoming of general application.
    Instead of applying only to toxins and toxalbumins, it held good for all
    proteins, whether toxic at the first injection or not.

    Two years later Rosenau and Anderson, two American physiologists,
    demonstrated in a noteworthy piece of work that the phenomenon of
    anaphylaxis occurs after every injection of serum, even when the
    injection is minute, for example of 0.00001 ml which is an infinitely
    small amount but nevertheless sufficient to anaphylactize an animal.
    They quoted examples of anaphylaxis from all organic liquids: milk,
    serum, egg, muscle extract. They specified the reaction and clearly
    showed that of all the subjects, the guinea-pig appeared the most
    sensitive in anaphylactic terms."

    Now look up Wikipedia's List of vaccine ingredients @t

    You should notice that the excipient contains a great number of proteins like egg, milk, gelatine ………

    Now think about what happens when you have leaky gut or dysbiosis, IBS, etc


  13. Great video. I have uploaded an animated video discussing all the causes, symptoms, pathogenesis and RECENT treatment approach and new modalities to treat severe and uncontrolled asthma.
    Just take a look and do let me know how's it.


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