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Asthma: Clinical History

by Jeremy Brown, PhD
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    00:00 because of the smoking on the background of asthma. So, asthma is the commonest chronic lung disease. In fact, it’s one of the commonest chronic diseases full stopped. A significant portion of the population have asthma about 5% in the U.K. And what this reflects is chronic inflammation and what we call is hyper-reactivity of the airways.

    00:19 The airways are twitchy. They will respond by bronchoconstriction tightening up to a variety of different end results and when they bronchoconstrict, that’s when you have airways obstruction and the patient will present with symptoms. Over decades, if somebody has poorly controlled asthma with this bronchoconstriction occurring frequently, they’ll end up with a degree of irreversible disease. So the bronchoconstriction of a treatment doesn’t fully reverse to normal bronchi diameters, but there is a degree of chronic airways obstruction present as well.

    00:52 Predisposing factors for asthma, well, a family history.

    00:57 Genetics, there are certain genes that I've mentioned as polymorphisms has been associated, ADAM33, for example. A history of atopy, eczema and/or hay fever in combination of nasal parts would suggest somebody’s more chance of getting asthma. Childhood infection, specifically, respiratory syncytial virus infection bronchiolitis is closely associated with developed asthma in later life. Other associations are prematurity, low birth weight, obesity, exposure to passive smoking especially as a child, active smoking in itself would stimulate an asthmatic type situation or make asthma more likely to develop, as does, inhaling recreational drugs.

    01:39 Crack cocaine is a very good stimulant for creating asthma in patients.

    01:44 The pathogenesis of asthma is complicated. It has probably no single pathology and it causes the end result of asthma. It’s largely a cell-mediated immune response, either Th2, allergic response to inhaled antigen such as pollen, house dust mite faeces, various moulds, animal hair, cat hair, for example, or a Th17 CD4 cell-mediated immunity which is independent of allergy. That will lead to airway information. In asthma, it could be eosinophilic which tends to be a Th2 dependent or a neutrophilic which tends to be a Th17 dependent.

    02:24 And that airways information tends to stimulate smooth muscle constriction as well, and there are quite a number of key mediators of that process, IL4, IL5, IL13, leukotrienes, etc. The end result of these airways information is bronchoconstriction. Tight bronchi, smaller bronchi should be impairing airflow on expiration.

    02:47 In addition, you get mucous hypersecretion with the mucous glands producing more mucous.

    02:55 And there will be swelling of the airway, airways oedema. And eventually, over time, you get airway remodelling with some fibrosis forming around the airways leading in to the irreversible components of asthma that may develop in patients over long periods of time that I described earlier. So, who gets asthma? Well, essentially, it could be anybody, all ages; children, young adults, middle-aged adults, and even the elderly.

    03:23 New asthma in the elderly perhaps is less common. But patients, when they have asthma, it lasts potentially for their lifetime. So there are many people who’ve had asthma for 20, 30 years who are now in their 80’s. It often starts in childhood, fades in later childhood, early adulthood, and then returns later in life. But there’s a second peak of diagnosis of asthma for the first time in people aged around 60. Women tend to be more affected than men, although that’s only a mild predominance.

    03:54 The history of asthma, again, is also very variable. The key is episodic symptoms.

    04:00 So, if you have mild disease, the symptoms would be cough, maybe there’s some wheeze.

    04:04 If it’s more severe disease, it will be cough, wheeze, and breathlessness with chest tightness, and a tension that you get pretty other phlegm production. The yellow phlegm production, as well, But the point about that is this episodic- bad periods, good periods, bad periods, good periods. When you examine the patient, they’re normally not actually having the bad period, and therefore, you don’t hear much in the way of abnormalities in their chest because there’s no ongoing airways obstruction. However, if they’re poorly controlled, you might hear a polyphonic wheeze throughout both lungs.

    04:34 So, the sort of pattern of disease that patients have tends to vary a lot between different patients. So some patients have very mild disease, no symptoms in large portions of the time, and then something will kick off the asthma and they’ll have symptoms for a period of few weeks then they’ll settle down again. Some patients have symptoms the whole time, and actually does disrupt their life quite a lot. They have occasional exacerbation as well. But it’s just generally a low-level disruption of their life by symptoms most days. And then you can get acute life-threatening attacks that occur and they bring the patient into the hospital. And some patients, after long periods of asthma, can develop chronic disability through the airflow obstruction with chronic breathlessness, as well as the intermittent episodes of disability due to deteriorating asthma control as well. So there are certain triggers that characteristically worsen the symptom of asthma. These tend to vary between patients. But generally speaking, asthma has a diurnal variation. So patients who are poorly controlled will have their cough more at night and on waking first thing in the morning when the asthma is worse than they do in the evening. Exercise characteristically induces asthma attacks in some patients.

    05:58 So they’ll start to do some exercise or develop a cough, chest tightness, unable to breath and have to stop their exercise. Exposure to dust, cigarette smoke, cold air also stimulates asthma symptoms. Certain drugs, beta blockers, and also nonsteroidals such as aspirin can precipitate asthma attacks. Asthma frequently, and in fact usually, may worsen people who have a viral upper respiratory tract infection. So a very classic history is that when my wife gets a cold, it lasts--she coughs for a few days but I cough for weeks.

    06:33 What’s actually happening there is if the patient has asthma, they get the cold from their wife, they cough for a few days, but then the asthma takes over and the cough that persists for weeks is not due to the viral infection. It’s because the viral infection has kicked off the asthma inflammation and made the asthma worse.

    06:51 And people can be very allergic to very specific allergens, and they often know this. So for example, they know that when they go to a friend’s house with a cat, their asthma will get worse, or there is a thunderstorm that releases quite a lot of moulds spores into the atmosphere, and that can precipitate asthma attacks, and patients get worse during the pollen season as well because of the allergy to pollen. And then certain patients will have occupational asthma. That is asthma set off by antigens that they inhale when they’re at work. And this commonly happens in people who work as cleaners, bakers, with animals, or paint sprayers, et cetera. And the last, a very, very important component to making asthma worse is psycho-social stress. When patients are stressed, they tend to have worse asthma. And this is a major driver for many patients conditions. So, we can characterize


    About the Lecture

    The lecture Asthma: Clinical History by Jeremy Brown, PhD is from the course Airway Diseases.


    Included Quiz Questions

    1. Haemoptysis
    2. Symptoms that get worse after an viral upper respiratory tract infection
    3. No history of childhood asthma
    4. Waking in the middle of the night due to cough
    1. Asthma
    2. COPD
    3. Tuberculosis
    4. Sarcidosis
    1. Being born as a large for gestational age baby
    2. Exposure to smoking
    3. Having history of eczema or hay fever
    4. Being obese
    5. Having family history of asthma
    1. ADAMTS 33 polymorphism
    2. ADAMTS 13 polymorphism
    3. ADAMTS 5 polymorphism
    4. ADAMTS 11 polymorphism
    5. ADAMTS 1 polymorphism
    1. RSV
    2. Measles
    3. Moraxella catarrhalis
    4. Streptococcous pneumonia
    5. Influenza virus
    1. Th 17 CD4 and Th 2 CD 4 lymphocytes
    2. Th 15 CD4 and Th 2 CD 4 lymphocytes
    3. Th 17 CD8 and Th 2 CD 8 lymphocytes
    4. Th 15 CD8 and Th 4 CD 8 lymphocytes
    5. Th 18 CD8 and Th 4 CD 4 lymphocytes
    1. IL -2
    2. IL-4
    3. IL-5
    4. IL-13
    5. Eotaxin
    1. Warm water bath
    2. NSAIDS
    3. Exercise
    4. Beta blockers
    5. Psychosocial stress

    Author of lecture Asthma: Clinical History

     Jeremy Brown, PhD

    Jeremy Brown, PhD


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