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Asthma: Treatment

by Carlo Raj, MD
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    00:01 Now, the asthma treatment therapy. We’ll go from what’s known as relatively mild to severe. First and foremost you always take history and with the history you’re looking for.. What’s the most common type of asthma? Extrinsic. Go step by step. Exposure to the external world and that’s called atopy, right? Atopy. So, maybe your patient needs to then remove himself or herself from that environment. That’s your first step of management if that’s the case. Next, short-acting bronchodilator. So what does that do? Albuterol as needed, puff whenever they’re having an attack or bronchospasm. And so therefore, relieves that obstruction. Next, what about inhaled steroids, ICS, corticosteroids low to mid. Remember, inhaled corticosteroids is it going to do what? It’s going to then help you with some of that bronchoconstriction perhaps, and whenever you deal with your corticosteroids you tell me what enzyme is it knocking out? Is it LOX? Is it COX? Or is it phospholipase A2? Good, it’s phospholipase A2. You’ve knocked out the leukotriene and prostaglandin pathway, haven’t you. And by knocking out some of that leukotriene pathways especially C4,D4,E4, then you may then avoid bronchoconstriction. Are you clear about that pharmacology? Management is important.

    01:35 Continue. Long-acting beta agonist, leukotriene modifier. Give me some. Well, what if you knock out the LOX? Zileuton. What if you knock out the receptors for leukotrienes? -kast. Montelukast, Zafirlukast, things you’ve looked at, is that clear? Which leukotrienes are you trying to avoid in asthma, in bronchospasms? C4,D4,E4. About theophylline. Theophylline will help you, well this goes back to biochemistry, you should be liking this. This beta 2 that’s a receptor on the bronchial smooth muscle, what does it work through? What second messenger from biochemistry? Good, GS. What’s GS mean to you? A-A-A-A-A… what does that… what do I mean A-A-A? Well, that’s your adenylyl cyclase, that’s your ATP to cyclic AMP. That means protein kinase A. What does that mean? I am knocking out my myosin light chain kinase because I phosphorylated. Remember all this? If you don’t then this would be a good time to go back and take a look at your biochemistry with smooth muscle mechanics. So, if you knock out the myosin light chain kinase, guess what happens to the bronchi? Relaxation. So, what do you think theophylline might do? Theophylline, well how do cyclic AMP break down? Phosphodiesterase. What if you inhibit some of that phosphodiesterase? Voila! You knock out the phosphodiestrase, your cyclic can’t be forevermore. Isn’t that what you want with Beta2? Yes you do.

    03:09 Now, I’ll tell you right now the two major approaches for smooth muscle relaxation especially for the bronchi. Either Beta2 you look for that mechanism in pharmacology and biochem and you take a look at NO, nitric oxide please. Those are two that you want to pay attention to.

    03:26 Let’s continue, you have anti IgE therapy, alright so with IgE therapy you’re thinking about well some of those drugs that inhibit what? Your breakdown of your mast cell. So anything that then inhibits the degranulation of your mast cell is always important. Hence you’re looking at things like this, anti IgE therapy.

    03:48 Alright now in terms of severity we’re just going to move from top to bottom which is just the severity in the beginning will be quite minimal and then as you go through your severity and it gets worse then obviously as far as management, things become a little bit more complicated. Prevention in all. So how do you educate your patient? Important. If you can avoid giving medication to your patient that is your answer. So therefore, educate your patient. “Oh, hey doc, my child is having coughs episodically”…“Oh, okay”… “And well, I can hear kind of wheezes and such”… “Okay”…”and he goes and plays, he plays in this particular park and every time he comes back after he plays, oh, he doesn’t seem so well.” Okay, so, you want to try and figure out as to what was the child exposed to in that park that makes him feel like this? Prevention.

    04:43 Now after this, mild intermittent, Mild persistent, moderate persistent and severe. Remember we start getting to severe and such and even at night if there’s coughs, not a good sign, you need to make sure that you’re intervened ASAP.

    04:58 Let’s talk about that acute flare, so during the acute flare in your head you should be thinking about that loop spirometry which we saw a scalloped portion. Here, when you have an acute flare what are you trying to do? Immediately try to bronchodilate.

    05:15 Nebulizer. So, what does that mean? That means that you have a gas mask. I call it as such.

    05:22 Which is then attached to a machine which is then exerting or expressing what? Albuterol.

    05:28 Ipratropium, keep in mind there are two ways you can approach this, right? Either you could stimulate the Beta2 receptors. I just walked you through that in great detail, or you could block your parasympathetic. Two methods, albuterol much more so.

    05:44 What else? Oral or IV steroids? IV steroids. What’s my problem? Acute flare. Oxygen if hypoxia is present. Antibiotics if there is infection keep that in mind as well. Often times with these flares there is going to be some type of upper respiratory tract infection that is involved. Acute flare, well the magnesium just keep that in mind. Magnesium is a big deal for your medicine though, okay? Remember with magnesium two major things, number one seizures if it’s hypomagnesemia, also if it’s hypomagnesemia you’re thinking about long QT syndrome. So those are major things you want to think about when dealing with magnesium. Close monitoring, make sure chronic treatment are being used correctly.

    06:28 By chronic we’re talking about well is the patient on the right bronchodilator? Is it a Beta2 agonist? Is it a leukotriene inhibitor of the right type or maybe it’s even a type of corticosteroids. So those are things you want to keep in mind.

    06:43 Now, what I wish to bring to your attention that you will be asked, is if there is an acute flare especially when you have a child that has an asthma attack, not only is this child breathing really quick and the diaphragm obviously is being used but then the accessory muscles of breathing are also being used, do you remember this conversation? So, look for this and don’t forget. If you find a patient come in and they’re breathing, the sternocleidomastoid is working and the intercostal muscles are working, this is a child who, at some point, those muscles are going to fatigue and tire. And the child starts quieting down and maybe it’s an intern who didn’t know any better and feels as though that he or she has treated the child and the child is quieting down, thinks that he or she is managing the child properly. But why is the child quieting down? The muscles are getting tired, the child’s not breathing anymore. What’s your next step of management? Intubate. Break a few teeth rather than have your child die on the table. Is that clear? That is a big deal. So, what are you going to measure? You tell me, use common sense. What are you going to measure in the blood? This will tell you that the child’s acute flare is actually getting worse? The pH, of course. Because if the child’s muscles are tiring and the child’s not breathing, what’s the child retaining? Carbon dioxide, good. What will happen to your pH? Decreased. Welcome to respiratory acidosis and that is no joke.


    About the Lecture

    The lecture Asthma: Treatment by Carlo Raj, MD is from the course Obstructive Lung Disease.


    Included Quiz Questions

    1. Short-acting bronchodilator
    2. Inhaled steroid
    3. Leukotriene modifier
    4. Theophylline
    5. Anti-IgE
    1. IgE therapy
    2. Leukotriene modifier
    3. Theophylline
    4. High dose ICS
    5. Long-acting beta agonist
    1. Severe asthma
    2. Mild persistent
    3. Mild intermittent
    4. For avoidance of a trigger
    5. Moderate persistent
    1. Avoiding the triggers
    2. IgE therapy
    3. Systemic steroids
    4. Theophylline
    5. Long-acting beta agonist
    1. Reduces airway obstruction by decreasing edema and inflammation
    2. Helps prevent further attacks of asthma
    3. Helps reduce the effect of allergens by subduing the allergens
    4. Potentiates other drugs in treatment of asthma
    5. Helps in increasing sensitivity of other drugs
    1. Phospholipase A2
    2. Cyclooxygenase
    3. Lipooxygenase
    4. Prostaglandin
    5. Papain
    1. Smooth muscles of bronchial tree
    2. Mucus-producing cells
    3. Skeletal muscles used for respiration
    4. Breaking down the viscid mucus
    5. Interstitial space to decrease edema
    1. ...Albuterol
    2. ...Methacholine
    3. ...NSAIDS's
    4. ...Leukotriene agonists C4, D4, E4
    5. ...Allergens
    1. Theophylline phosphorylates the myosin phosphate kinase causing bronchodilation
    2. Theophylline methylates the myosin phosphate kinase causing bronchodilation
    3. Theophyllin phosphorylates the Actin phosphate kinase causing bronchodilation
    4. Theophylline sulphates the myosin phosphate kinase causing bronchodilation
    5. Theophylline nitrates the myosin phosphate kinase causing bronchodilation

    Author of lecture Asthma: Treatment

     Carlo Raj, MD

    Carlo Raj, MD


    Customer reviews

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    Very good
    By Pablo V A. on 18. May 2018 for Asthma: Treatment

    You guys have to read the articles and study some things before getting to Dr Carlos videos. He is very fast and dont explain certain terms because you have to know this stuff before watching the video.

     
    Right to the point!
    By Gualberta v. on 23. March 2018 for Asthma: Treatment

    Right to the point, just like we are asked on the exam :) Nice!

     
    Explanation is not coherent.
    By Nicole G. on 30. January 2018 for Asthma: Treatment

    Explanation is not coherent, does not use full sentences, connections between concepts are not logical. Does not articulate.