Pathophysiology of Asthma Disease

Description of Asthma pathology

Asthma is a severe socioeconomic and health challenge defined by the activity of the airways, which results in reversible airflow restriction, airways hyperresponsiveness (AHR) of the airways, and consequent inflammation. This ailment affects at least 300 million people worldwide, resulting in around 250,000 fatalities yearly (Coleman & Shaw, 2017). As inhaled corticosteroids have become the primary asthma treatment in the past few decades, asthma mortality has dropped. Meanwhile, urbanization has skyrocketed allergy-related conditions such as asthma in the past fifty years. When compared to other generations, children show relatively higher Asthma infection levels. The estimated patient population will most likely have grown by more than 100 million in the next three years.

Many Asthma cases start in children due to sensitized responses to common allergens like dust mites found in homes, bugs, pet dander, and pollens. The afore-mentioned allergens lead to T helper type 2 (Th2) cell growth, responsible for the formation and transmission of Th2 cytokines, which encompasses interleukins (ILs)-4, 5, 13 (Carpaij et al., 2019). Airway inflammatory response was found responsible for the pathophysiology of several illnesses in the basic and clinical investigations. For more than a century, asthmatics have known that chronic airway inflammation exists. According to Coleman and Shaw (2017), the release of powerful chemical mediators by pro-inflammatory cells causes inflammation. Airway remodeling, defined by the thickening of all sections of the conducting airways, occurs as a consequence of the chronic inflammatory process. It may have significant implications for the mechanisms of passageway constriction in asthma, leading to the severity extent of the condition.

Normal anatomy of the airways

Asthma attacks the airways/respiratory system, which comprises the organs of the breathing system that facilitate the flow of air for ventilation. They begin at the nares, extending to the buccal aperture and finally to the blind end of alveolar sacs. They are separated into many regions, each with its own set of organs and tissues that perform distinct duties (Hedenstierna & Borges, 2016). The airway is categorized into two sections: upper and lower airways, each with multiple subdivisions. The Upper Airway is separated into three sections, with each serving a specific role.

The mucosal membrane-lined part of the airways between the skull base and the esophagus is termed the pharynx. The part can be subdivided into three major parts: The Nasopharynx, sometimes referred to as the post-nasal gap, is a neuromuscular tube that connects the nares with the oropharynx. The back nasal cavity and the superior base of the skull are included in this section (Carpaij et al., 2019). The oro-pharynx forms the connection between the nasopharynx and the hypopharynx. The area constituting the palate-hyoid bone region, which is isolated from the oral cavity in the front via the tonsillar arch, is referred to as the palate-hyoid bone region. The hypopharynx is a portion of the pharynx under the hyoid bone that joins the oropharynx to the esophagus as well as the larynx.

The Lower Airway is made up of various components, each of which has a specific purpose. The trachea is a muscular tube lined with ciliated pseudostratified epithelia and supported by C-shaped bands of hyaline cartilage. The C rings’ vast open surface counters the esophagus, facilitating its expansion during swallowing (Hedenstierna & Borges, 2016). At the point of the sternal angle, the trachea subdivides and so finishes, superior to the heart. The bronchi, the trachea’s primary bifurcation, resemble the trachea in form but usually comprise full circular cartilage rings. The lung’s alveoli capacity ranges between 2 and 300 million and has an estimated entire surface area of about 140 square meters dedicated for gaseous exchange. They are supplied by twenty-three airways generations, each with an increased surface area, which is found to be 2.5 cm2 for the trachea and 70 cm2 for the 14th generation. This generation is one that joins the acinus to 8000 cm2 or rather 0.8m2 in the last generation (Carpaij et al., 2019). An increase in the area translates to a decrease in the speed of gas flow. The mean speed of the trachea’s gas during a normal breath is roughly 0.7 m/sec, yet it is no more than 0.001 mm/sec near the alveolar surface. This rate is comparably less than that of oxygen and carbon dioxide diffusion.

Notwithstanding an optimum expiratory effort, there is a remnant air volume in the lungs, which prevents collapse. The remnant volume of gas is referred to as residual volume (RV), ranging between 2 and 2.5 liters (Coleman & Shaw, 2017). Vital capacity (VC) is the greatest volume that can be inhaled and exhaled, and it is roughly 4–6 L. It is often lowered before a drop-in RV in restrictive lung disorders. What is less clear is whether or not VC is diminished in the obstructive lung condition. This arises from persistent ‘air trapping,’ which raises the residual volume at the price of VC.

Mechanism of Asthma Pathophysiology

The pathophysiology of asthma involves a variety of cell types. Mast cells can be found in abundance in the airways’ walls and alveoli, as well as in the airway lumen, where they can be retrieved by bronchial lavage. In allergen-provoked asthma, mast cell activation is the primary cause of acute bronchospasm. The mast cell surface and the immunoglobulin IgE connects through numerous binding sites (Hedenstierna & Borges, 2016). Cell activation is caused by the antigenic spanning of a small proportion of these neurotransmitters. They can also be activated by coagulation factors C3a, C4a, and C5a, in addition to substance P and many medications and chemical compounds.

A spike in inositol phosphate and increased intracellular ions serve as mast cell’s stimulus, making it extremely sensitive. Within half a minute of activation, degranulation begins, resulting in the production of a wide range of mediators (Hedenstierna & Borges, 2016). H1 transmitters in smooth muscles of the bronchi produce contraction, increasing microcirculation by acting on more H1 receptors, and increasing production of mucous by engaging with H2 receptors are all caused by histamine. Torn epithelial cells may cause desquamation and possibly activate neural reflexes, resulting in further bronchospasm if proteases in the granules, particularly striptease, are present.

It’s important to note that after mast cell upregulation, the synthesis of arachidonic acid derivatives begins. The principal cyclooxygenase pathway consequence is prostaglandin PGD2, a constrictor whose clinical significance is as yet unknown. Leukotriene (LT) C4 is produced via the lipoxygenase method, and two additional peptides, namely LTD4 and LTE4, are synthesized as a result (Hedenstierna & Borges, 2016). A variety of cytokines are produced by mast cells when they are triggered, some of that is already present in the granular. Chemotactic for both interleukin-5 as well as GM-CSF, Eosinophils secrete IgE that stimulates the production of mast cells, which in turn increases GM-CSF and interleukin-5 activity.

Eosinophils coexist with mast cells freely in the subcutaneous tissue, and they are assumed to be the primary cell responsible for asthma’s late-phase response. They produce potent bronchoconstrictor with a lengthy half-life, such as LTs B4 and C4. Inflammatory cells generate GM- CSF, which attracts them to the region. Mast and lymphocytes then activate it with IL-5, which they also create (Hedenstierna & Borges, 2016). In the regulation of eosinophil and mast cell stimulation, lymphocytes are pivotal. Mast cell degranulation requires the generation of antigen-specific IgE, which is produced by activated B-lymphocytes. T-‘helper’ lymphocytes control B-cells, and T-helper lymphocytes control B-cells. Th2 cells are essential pro-inflammatory cells in asthma, stimulating mast cells.

B-lymphocytes eosinophils enable individuals to promote bronchospasm and inflammation. No specificity is evident in Th2 cells’ responses, and their generation from naive T-cells as well as their activation and production of pro-inflammatory molecules depend on dendritic cell stimulation (Hedenstierna & Borges, 2016). The comparative activity of Th1 and Th2 cells, which oppose each other in their effects, was long believed to have a key responsibility for the onset and prevalence of asthmatic symptoms until now. IL-33 and IL-25 produced by destroyed epithelial cells activate the newly found fourth regulatory T-cell (ILC2).


Although there is no single procedure attributed to asthma prevention, there are several steps one may take to limit the disease’s severity. First, one should identify asthma triggers and devise ways to avoid them. Asthma can also result from allergens found in the air outside and irritants (Coleman & Shaw, 2017). One should research what causes or worsens their asthma and develop solutions to mitigate those triggers while monitoring their breathing. One may develop discerning tactics for the signs of an impending attack, which may include wheezing, difficulty breathing, and coughing.

Another preventive measure is the use of a peak flow meter to help in early diagnosis by monitoring the breathing patterns. Owing to the probability of an undetected decline in lung function, it is crucial to use a peak flow meter to note and evaluate the highest level of airflow. A peak flow meter shows a person’s ability to breathe out to their highest levels. A doctor can enlighten patients on monitoring their peak flow by themselves. Again, one should promptly detect and handle risks for effective treatment. Fast response minimizes the chances of having a severe attack, and one does not need as much medication to control their symptoms.


Effective treatment for asthma is aimed at maintaining normal lung functioning and taking the least amount of time to recover with minimum medication. Inhaled corticosteroids (ICS) are by far the most effective inflammatory-preventing medications available for the treatment and control of asthma over an extended time period, recommended for first therapy. ICS has been found helpful in lowering the probability of getting asthma attacks (Coleman & Shaw, 2017). Another significant treatment approach entails a combination of a long-acting bronchodilator and an inhaled IC. In most cases, short-acting lifesaving inhalers are used to treat breakthrough signs, forming the basic quality of practice.


In conclusion, bronchial asthma is a common worldwide disease characterized by the hindrance of reversible airflow, including non-specific AHR concerning airway inflammation. Airway inflammation contributes to asthmatic symptoms, mainly characterized by reversible passageway obstruction and ASM contraction, and is also attributed to airway remodeling. The alveolar sacs, nares, and the buccal cavity are the key parts of the airways. Asthma can be prevented by continually monitoring one’s breathing patterns and avoiding the conditions that trigger it. It can be treated through ICS and bronchodilators.


Carpaij, O., Burgess, J., Kerstjens, H., Nawijn, M., & van den Berge, M. (2019). A review on the pathophysiology of asthma remission. Pharmacology & Therapeutics, 201, 8-24. Web.

Coleman, S., & Shaw, O. (2017). Progress in the understanding of the pathology of allergic asthma and the potential of fruit proanthocyanidins as modulators of airway inflammation. Food & Function, 8(12), 4315-4324. Web.

Hedenstierna, G., & Borges, J. (2016). Normal physiology of the respiratory system. Oxford Medicine Online. Web.

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