Asthma - signs and symptoms, pathophysiology

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armando has to do gun biology and medicine videos please make sure to subscribe join the Forman group for the latest videos please visit Facebook Armando Superman in this video we're gonna talk about asthma so here I am drawing a human and his respiratory tract asthma is defined as a chronic inflammation disorder of Airways asthma can be divided as either a topic or non a topic a topic asthma is is extrinsic asthma meaning it is triggered by environment and and and this type of asthma is the most common atopic aspera involves inflammation mediated by systemic IgE production non atopic asthma on the other hand is an intrinsic asthma and this is far less common non-atomic asthma therefore refers to inflammation and constriction of the Airways that is not caused by exposure to an allergen the information is mediated by local IgE production so now let us look at a cross-section of a normal lung the bronchioles of a normal lung so here we have the mucous layer and we have pseudostratified endo endothelial cells we have the lamina propria and we have the smooth muscles surrounding all this so that was normal and if we were to look at an asthmatic bronchial the lumen here the inside is much narrower but before we focus on the asthmatic bronchial and stuff like that let us look at a normal history normal histological layers of a of a bronchial so here we have the mucus and on this layer we have this pseudo stratified columnar epithelial cells below this we have the basement membrane within the epithelial layer we also can find goblet cells which are responsible for secreting mucus into the lumen below the columnar cells we have the lamina propria which contain many cells including ma of macrophages and mast cells marcelles are responsible for secreting histamine below the lamina propria or surrounding the lamina propria we have two smooth muscles now if we were to compare the normal bronchial layer here to an asthmatic bronchial layer we can see many differences firstly we can see that there is an increase in mucous production so there is an increase as well in goblet cells also with this there is an increase in cinah fills in the mucus and tissue here we have the certified pseudostratified columnar epithelial cells and below it the basement membrane thickens lamina propria within the lamina propria we see an increase in mass cell numbers and so we get an increase in histamine release we also have an increase in other cell types including neutrophils during in during and during inflammation as well as T helper cells we also can find that there's smooth muscle cell hypertrophy so smooth muscle cells increase in size and this is due to the constriction now because of all these changes there are three characteristics of asthma the triad these are airflow obstruction bronchial hyper responsiveness cuz of histamine release and inflammation due to the increase in neutrophils and other immune cells to the area symptoms of asthma include shortness of breath therefore wheeze chest tightness and dry irritating cough so now that we have identified some changes that occurs during in an asthmatic bronchiole let us look at the pathophysiology so let's look at some players in the first in the pathophysiology of asthma so we have a main one IgE antibodies now IgE antibodies are important because they can bind to receptors on mast cells forming a mast cell IgE complex the mast cell IG complex will recognize Allinger are allergens and essentially begin releasing heaps of histamine other important players in the pathophysiology of asthma include is Cinna fills dendritic cells as well as t-helper cells now there are two types of T helper cells main overall types there's T helper 1 and there's T helper 2 now tearful one is normally found in the lungs so in normal lungs T helper 1 are normally found however there is an imbalance like in in asthma because in asthma T helper 2 cells which are not normally found in the lungs are up-regulated in in asthma so we have more T helper 2 cells in in the lungs of asthmatics T helper 1 you see normally promotes inflammation by increasing cell mediated immunity however T helper 2 cells promotes inflammation by increasing the humoral immune immunity so promoting antibody production so I hope you can see how this correlates anyway let's look at let's let's put all these cells together and try to create a diagram looking at the pathogenesis of asthma and we're specifically focusing on a topic asthma so here we have the columnar pseudostratified columnar epithelial cells with goblet cells which secrete mucus on top and here we have the lumen below the column the pseudo serif pseudostratified columnar epithelial cells we have the lamina propria where we have Mar cells and dendritic cells macrophages and okay so in asthma okay let's just say an asthmatic inhales an allergen and this allergen will trigger a reaction so few things can happen one thing is that the allergen will be will be engulfed by dendritic cells and activates the dendritic cells also the columnar epithelial cells will recognize this and secrete a substance called Sime external lymphocytes if I'm external lymphocytes will condition activated dendritic cells to produce chemokines to attract specifically T helper to cells the activated dendritic cell itself will activate the T helper cells to differentiate into T number two and also will secrete chemokines to attract the T helper two to the area to the bronchioles or the lungs so the activated T helper to cells does several things firstly the T helper to stroll is to promote the humoral immunity so it will stimulate plasma cells through interleukin 13 and interleukin 4 and this will promote IgE production by the plasma cells IgE will obviously help Bo by none to muscles to create the IgE muscle complex th T helper to itself through interleukin 9 will stimulate or promote Marcel Marceau activity another important function T helper to cells do is that it will base stimulate a cinephile production from the bone marrows through interleukin 5 so angel Lucan 5 will it will stimulate a cinephile production so you get morris inner fills and with Morris inner fills there's a chemo there's a chemotactic basically thing occurring which will attract the a Sinha fills to the area to the lungs and so we have increase in a cinephile amounts in the lungs so the inhaled allergen will will bind onto IgE muscle complex and this will cause the Marcelle to release a few things mainly histamine prostaglandins and leukotrienes all this specifically histamine will will will stimulate smooth muscles in the airways to cause constriction so we get bronchoconstriction also during this whole process and endothelial cell will will release stem cell actors that will essentially I'll maintain the mast cells to the area and so you can imagine that if there is this IgE being produced this essentially this memory being produced whenever the same type of allergen is inhaled it will trigger this whole process of histamine release and bronchoconstriction and you get you know more sinha phil so you get this whole process still occurring and occurring so i hope you enjoyed this video on asthma and the pathophysiology of asthma hopefully made sense thank you
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Channel: Armando Hasudungan
Views: 729,395
Rating: 4.9286971 out of 5
Keywords: Asthma (Disease Or Medical Condition), Pathophysiology Of Asthma, Health (Industry), obstructive pulmonary disease, restrictive pulmonary, pathogenesis, respiration, respiratory disease, treatment, signs and symptoms, atopic, types of asthma, immune system, Medicine (Field Of Study), biology, Pathology (Medical Specialty), hypersensitivity, Allergy (Disease Or Medical Condition)
Id: NNfx27io8-k
Channel Id: undefined
Length: 10min 29sec (629 seconds)
Published: Mon Dec 01 2014
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