Overview
Primary care facilities are likely to see cases of allergic rhinitis, as it is the fifth most common chronic disease in the United States (Honan, 2019). Allergic rhinitis impacts 9-42% of children in the U.S. (Rafiq, 2019). It’s onset typically occurs between the ages of 8-11 with 80% of cases being confirmed by the age of 20 (Rafiq, 2019). It is slightly more prevalent in females (15% of population) than males (14% of population) (Rafiq, 2019). There is a strong genetic component to this condition, as 80% of those diagnosed will have family members with allergic rhinitis as well (Rafiq, 2019). Numerous genes have been connected with this Type I hypersensitivity response (McCance & Heuther, 2019). Individuals with this genetic predisposition to develop an immune response are referred to as atopic (McCance & Heuther, 2019). Typically, the allergen or aggravating particle is inhaled. Allergens can be seasonal, such as allergies caused by pollen, or continuous (perennial), such as allergies caused by dust and indoor molds (Honan, 2019).
Figure 9. Allergen route of entry, allergen examples, and occurrence periods (Ento Key, 2016).
Physiology
Physiologically, the immune response is designed for protection so that the body remains functional (in a state of homeostasis) and cells stay productive (Justiz Vaillant, 2019). The immune system encompasses two responses (Justiz Vaillant, 2019). The first is an innate or non-specific response that reacts quickly to anything foreign (Justiz Vaillant, 2019). It can include various cells (phagocytes and natural killer cells), the skin, and fluids such as tears and saliva (Justiz Vaillant, 2019). The second response that targets specific pathogens is known as the adaptive response (Justiz Vaillant, 2019). It includes the production of immunoglobulins and cytokines (Justiz Vaillant, 2019). This response involves three imperative characteristics: specific pathogens being sought out and targeted, many responses being triggered simultaneously, and the recollection of the pathogen at a later time in order to carry out a response more quickly and with more strength (Justiz Vaillant, 2019).
According to normal physiology, particles in the air or environment (such as pollen or dust) will not cause the immune system to initiate an attack to destroy the foreign particles (Justiz Vaillant, 2019). The physiologic response is the absence of an immune system reaction (Ragiq, 2019). In other words, the body does not recognize the substance as harmful. There will be no mast cell degranulation or tissue disruption. According to normal physiology, individuals without allergic rhinitis are not sensitized to the perceptually harmful substances those with allergic rhinitis react against. However, it is possible for a person to develop an allergic response to something they were previously not allergic to if the body is exposed to a point in which antibodies are created and antigens react (McCance & Heuther, 2019). This threshold is unique for every individual (McCance & Heuther, 2019). Allergic rhinitis is an abnormal hypersensitivity response to harmless foreign substances.
Pathophysiology
The pathophysiological response of allergic rhinitis is characterized by an immune response to substances that the patient’s body determines to be foreign. The immune response and antigens of an individual with allergic rhinitis will mistake the substance, such as dust or pollen, as something the body needs to be alerted about and protected against (Bjermer, Westman, Holmstrom, & Wickman, 2019). The presentation of these antigens from outside of the body by dendritic cells causes the body to develop Immunoglobulin E (IgE) antibodies from converted T cells that can produce a Type I hypersensitivity reaction (McCance & Heuther, 2019; Min, 2010). This is an example of the innate immune response working with and triggering the adaptive immune response as specific immunoglobulins are produced. In this situation, mast cells respond to antigen-specific IgE antibodies (McCance & Heuther, 2019). This process can occur over time as an individual is reintroduced to the environmental substances, causing IgE synthesis to the point where the antigen will put the antibodies on high alert (McCance & Heuther, 2019). This will cause an individual to become sensitized, meaning that the next time an individual interacts with the allergen, the IgE antibodies will bind to mast cells with the use of crystalline fragment (Fc) receptors and begin an immune reaction (McCance & Heuther, 2019).
This process occurs in two parts:
Initial Phase/Immediate Responses: The initial phase can be expected within 5-30 minutes of contact with the allergen (McCance & Heuther, 2019). The activation of mast cells will cause them to degranulate or release substances (McCance & Heuther, 2019). This will slowly release leukotrienes to call upon and accumulate leukocytes (white blood cells) and prostaglandins, which will encourage vascular permeability and allow the leukocytes to enter the site more easily (McCance & Heuther, 2019; Min, 2010). This slow release allows the inflammatory response to be extended and chemical manifestations to be prolonged (McCance & Heuther, 2019). Additionally, histamine, which is “the most potent mediator” (McCance & Heuther, 2019, p. 256), is released. Histamine will then bind to H1 receptors (McCance & Heuther, 2019), which will ignite many processes. Impacts will be seen within facial features and among the upper respiratory tract (McCance & Heuther, 2019). The airways may experience bronchial contraction, leading to constriction (McCance & Heuther, 2019). The vascular system may become more permeable, making it easier for fluids to flow into the interstitial space, leading to edema (swelling) (McCance & Heuther, 2019). There will also be an increase in blood flow to the impacted location (McCance & Heuther, 2019). The initial phase will induce nasal and ocular symptoms. More specifically, ocular edema (puffy eyes) and rhinorrhea (runny nose) occurs due to the release of fluid into the interstitial space once the vascular system is more permeable (Bjermer, et al., 2019; McCance & Heuther, 2019; Min, 2010). Redness will appear in the impacted areas, specifically the eyes, as blood flow increases (Honan, 2019; Min, 2010). Additionally, sneezing will take place as the mucous membranes become irritated by the allergens along with itching from the histamine (Honan, 2019; Min, 2010). The previously described mechanisms also cause the patient to present with symptoms of conjunctivitis and rhinitis as the eyes and nose experience the immune response (Honan, 2019; Min, 2010). These symptoms, specifically inflammation and nasal congestion from the clear drainage, can have a significant impact on an individual’s quality of sleep (Bjermer, et al., 2019). B.B.’s clinical presentation is consistent with the described symptoms. The diagnosis of allergic rhinitis can be confirmed with a lab test to determine the amount of IgE found within the blood stream, as there will be increased levels in an individual with a Type 1 hypersensitivity reaction (McCance & Heuther, 2019). Further details about diagnostic testing are provided in the Differential Diagnoses section of this case study.
Late Phase/Late Responses: When the allergen exposure is removed from the presence of the individual, the late phase will occur between 2-8 hours later (McCance & Heuther, 2019). As the leukotrienes and prostaglandins begin to take full effect, the immune response continues. Over time, proteases are released which will begin breaking down proteins and initiating the process of tissue remodeling (Kale, Agrawal, & Arona, 2016). Additionally, eosinophil chemotaxis from the initial phase will cause more white blood cells to enter the tissues and aid in the remodeling of epithelial tissue (McCance & Heuther, 2019; Min, 2010). More specifically, eosinophils can contribute to the thickening of tissue membranes, resulting in stiffness as they prevent leukocytes from evacuating the inflamed location (Foley, Prefontaine, & Hamid, 2007; McCance & Heuther, 2019). Angiogenesis (the formation of new blood vessels) will occur due to monocytes and basophils (Crivellato, Travan, & Ribatti, 2010; Ogle, Segar, Sridhar, & Botchwey, 2016), as well as an increase in mucus cell size or hypertrophy (Amin, 2015). These changes assist in the priming of the immune response in the event that the body comes into contact with the allergen in the future, allowing for a faster and more intense response (Bjermer, et al., 2019). Overall, in this phase, the edema is worsened and nasal congestion continues. Continued edema and nasal congestion lead to sinuses that are sensitive to the touch as the pressure increases (Bjermer, et al., 2019). These conditions set in as the immune response is prolonged (Bjermer, et al., 2019). B.B. has experienced some of these symptoms as well, such as the continued nasal congestion and the sensitive sinus cavities.
Figure 10. Cellular level pathophysiology (Patel, 2015).
The allergic reaction can utilize a negative-feedback loop (McCance & Heuther, 2019). In this process, the previously released histamine can interact with H2 receptors on the mast cell and terminate further degranulation of histamine (McCance & Heuther, 2019). However, this process is not efficient if the allergen is reintroduced, as more inflammatory mediators will be activated (McCance & Heuther, 2019). The duration of symptoms from allergic rhinitis can result in atopic individuals becoming lethargic and irritable (Bjermer, et al., 2019). Individuals with chronic allergy symptoms report negative impacts of their quality of life and daily activities (Bjermer, et al., 2019). Individuals will likely experience chronic symptoms until the allergen is reduced/removed or if the patient receives treatment to manage the hypersensitivity reaction.