we're going to talk about asthma so here i am a human and his respiratory tract asthma is defined as a chronic inflammation sort of airways asthma can be divided as either a topic or non a topic a topic asthma is is extrinsic asthma meaning is triggered by environment by the environment and and and this type of asthma is the most common a topic
aspen involves inflammation mediated by systemic IG production non a topic a spell on the other hand is an intrinsic asthma and this is far less common non-atomic asthma therefore refers to inflammation and construction of the airways that is not caused by exposure to an allergen the information is mediated by local AG production so let us look at a cross section of a normal on the bronchioles of a normal lung so here we have the mucus layer and we have pseudostratified into endothelial cells we have the lamina propria and we have the smooth muscles surrounding all this so that was normal and if we will we were to look at an an asthmatic bronchiole the lumen here the inside is much narrower but before we focus on the ass matic bronchiole and stuff like that let us look at a normal history the normal histological layers of a of a bronchial so here we have the mucus and on this layer we have the pseudostratified 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 columnist cells we have the lamina propria which contain many cells including my of macrophages and muscles muscles are responsible for secreting histamine below the lamina propria are surrounding the lamina propria we have the smooth muscles now if we were to compare the normal bronchial layer here to an asthmatic bronchiole layer we can see many differences firstly we can see that there is an increase in mucus production so there is an increase as well in goblet cells also with this there is an increase in sinaa fills in the mucus and tissue here we have the suta fides pseudostratified columnar epithelial cells and below it the
basement membrane thickens lamina propria within the lamina propria we see an increase in Marcel numbers and so we get an increase in histamine release we also have an increase in other cell types including neutrophils during in during in 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 construction now because of all these changes there are three characteristics of ass mama the triad these are airflow obstruction bronchial hyperresponsiveness because of histamine release and inflammation due to the increas in neutrophils and other immune cells to the area symptoms of asthma
include shortness of breath therefore we chest tightness and dry irritating cough so now that we have identified some changes there that occurs during in an in an asthmatic bronchiole let us look at the pathophysiology so let's look at some players in the first and the pathophysiology of assam so we have a main one ige antibodies now ige antibodies are important because they can bind to receptors on mast cells forming a Marcel ige complex the masks lig complex will recognize Allinger our allergens and essentially begin releasing heaps of histamine other important players in the pathophysiology of assam include is sin of Phil's dendritic cells as well as T helper cells now there are two types of T helper cells main / all types there's to help of one and there's T helper - now two people one is normally found in the lungs so in normal lungs t helper 1 are normally found however there is an imbalance late in in asthma because in
asthma t helper to cells which are not normally found in the lungs are regulated in an asthma so we have more t helper to cells in in the lungs of asthmatics the upper one you see normally promotes inflammation by increasing cell-mediated immunity however t helper to cells promotes inflammation by increasing the humoral immune in 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 a spur so here we have the Columbus pseudostratified columnar epithelial cells with goblet cells which secrete
mucus on top and here we have to lumen below the columbiana the to serve pseudostratified columnar epithelial cells we have the lamina propria where we have mast cells and dendritic cells macrophages and ok so in a swell ok let's just say in a somatic inhales and 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 activate the dendritic cells also the Columbia epithelial cells will recognize this and secrete a substance called thymic stromal lymphocytes family normal 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 two hopper to and also will secrete chemokines to attract the t helper to to the area to the bronchioles or the lungs so the activated t helper to cells just does several things firstly the t helper tues role 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 i ge will obviously help more by not to mast cells to create the IgE muscle complex t have T helper to itself through interleukin nine will stimulate or promote Marcel our master
activity another important function to the opportu CIL's do is that it will base stimulate a cynical production from the bone marrows through interleukin five so interleukin five will it will stimulate his sinful production so you get more snow fills and with more Center Phil's there's a chemo there's a chemotactic basically a thing occurring which will attract the center Phil's to the area to the lungs and so we have increased in a sinful amounts in the lungs so the inhaled allergen are will bind onto ige Marcel complex and this will cause the marcel to release a few things mainly
histamine prostaglandins and local trains all this specifically histamine will will will stimulate smooth muscles in the airways - cause constriction so we get bronchoconstriction also during this whole process the and endothelial cell wall will release stem cell factors that will essentially are maintained the mast cells to the area and so you can imagine that if there is this I GE being produced this essentially this memory being produced so I hope you enjoy this blog on accident and the pathophysiology of a small hopefully makes sense thank you
Please Support by Upvoting, Following & Sharing. Because I'm Your Best Friend Always