Asthma: Pathophysiology, Treatment and Education
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This case study analysis of a 6-year-old girl with allergic asthma discusses the pathophysiology, treatment and education of asthma. It covers the different types of asthma, treatment options and recommended education for parents and children. The paper also includes a discussion on the Australian context of asthma management.
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Introduction
The current paper is a case study analysis of a patient, Tegan Smith, a 6-year-old girl with
asthma. The case study will be analyzed in order to better understand the asthma disease process
and management. The pathophysiology of asthma and treatment in the Australian context will be
discussed. Lastly, the standard asthma education offered to parents and children will be analyzed
in the Australian context.
Type of asthma.
The asthma subtypes are due to the different presentations in different people and depend
on the pathogenesis, age, and occupation and include allergic asthma, non-allergic asthma, cough
variant asthma, occupational asthma, exercise-induced asthma, and nocturnal asthma (Mukherjee
& Zhang, 2011). Tegan Smith has presentation suggestive of allergic asthma. Her symptoms
suggest atopy, a range of conditions including eczema, allergic conjunctivitis, allergic
rhinosinusitis, and asthma (O'Connell, 2014). A symptom suggestive of allergic conjunctivitis is
watery eyes while nasal discharge is highly suggestive of allergic rhinosinusitis (Van Aalderen,
2012). There is a familial history of atopy. Atopy is defined as a genetic predisposition to allergy
and is hereditary (O'Connell, 2014). Tegan’s mother had a history of atopy including symptoms
of nasal polyposis that follows chronic rhinosinusitis, and allergy. Since atopy is hereditary,
Tegan could have inherited her allergic predisposition from her mother. Tegan and her family
moved to the highlands recently and this corresponded to the onset of symptoms. This could be
due to exposure to new allergens for example pollen supporting the idea that it is allergic asthma.
Allergic asthma has environmental triggers including animal dander, pollen and foods (Vernon,
Wiklund, Bell, Dale, & Chapman, 2012).
Introduction
The current paper is a case study analysis of a patient, Tegan Smith, a 6-year-old girl with
asthma. The case study will be analyzed in order to better understand the asthma disease process
and management. The pathophysiology of asthma and treatment in the Australian context will be
discussed. Lastly, the standard asthma education offered to parents and children will be analyzed
in the Australian context.
Type of asthma.
The asthma subtypes are due to the different presentations in different people and depend
on the pathogenesis, age, and occupation and include allergic asthma, non-allergic asthma, cough
variant asthma, occupational asthma, exercise-induced asthma, and nocturnal asthma (Mukherjee
& Zhang, 2011). Tegan Smith has presentation suggestive of allergic asthma. Her symptoms
suggest atopy, a range of conditions including eczema, allergic conjunctivitis, allergic
rhinosinusitis, and asthma (O'Connell, 2014). A symptom suggestive of allergic conjunctivitis is
watery eyes while nasal discharge is highly suggestive of allergic rhinosinusitis (Van Aalderen,
2012). There is a familial history of atopy. Atopy is defined as a genetic predisposition to allergy
and is hereditary (O'Connell, 2014). Tegan’s mother had a history of atopy including symptoms
of nasal polyposis that follows chronic rhinosinusitis, and allergy. Since atopy is hereditary,
Tegan could have inherited her allergic predisposition from her mother. Tegan and her family
moved to the highlands recently and this corresponded to the onset of symptoms. This could be
due to exposure to new allergens for example pollen supporting the idea that it is allergic asthma.
Allergic asthma has environmental triggers including animal dander, pollen and foods (Vernon,
Wiklund, Bell, Dale, & Chapman, 2012).
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Pathophysiology of allergic asthma
Asthma is a chronic airway disease characterized by hyperresponsiveness to various
stimuli leading to bronchoconstriction, airway remodeling and symptoms of wheezing and cough
that are related to various environmental triggers (Kumar, Abbas & Aster, 2015). After exposure
to an allergen, the body mounts a Th2 mediated immune response with production of IgE
antibodies (Just et al, 2014). On re-exposure to the same allergens, there is crosslinking of the
antibodies that bind to the surface of mast cells leading to mast cell degranulation with release of
inflammatory mediators and histamine (Kim, Kim, Jeon, & Kim, 2011). This is a common
pathway in most type 1 hypersensitivity reactions of which asthma is one. (Kumar, Abbas &
Aster, 2015). There are two phases of reaction, an early phase, and a late phase. Mast cell
degranulation and release of cytokine drive the early phase with mucosal hyperstimulation
leading to excess mucus production, vessel dilatation and the direct effect of mediators on vagal
receptors causes bronchoconstriction (Kim, Kim, Jeon, & Kim, 2013). The late phase occurs due
to the recruitment of T lymphocytes, neutrophils and eosinophils that will mediate acute and
chronic inflammation (Bogaert et al, 2011). Inflammation in the wall of the respiratory tree leads
to smooth muscle hypertrophy and deposition of collagen with gland hypertrophy. This is termed
airway remodeling (Kumar, Abbas & Aster, 2015). This underlying pathology will present
clinically as wheezing due to blockage of the airflow and cough due to the hyperresponsiveness
of the airway with excess mucus production (Van Aalderen, 2012).
Treatment
The treatment of asthma involves the use of medications in a systematic stepwise manner
with clear regard for the severity of Asthma and symptomatology (Queensland Health, 2015).
The category of asthma according to the symptoms is assessed so medication can be given in a
Pathophysiology of allergic asthma
Asthma is a chronic airway disease characterized by hyperresponsiveness to various
stimuli leading to bronchoconstriction, airway remodeling and symptoms of wheezing and cough
that are related to various environmental triggers (Kumar, Abbas & Aster, 2015). After exposure
to an allergen, the body mounts a Th2 mediated immune response with production of IgE
antibodies (Just et al, 2014). On re-exposure to the same allergens, there is crosslinking of the
antibodies that bind to the surface of mast cells leading to mast cell degranulation with release of
inflammatory mediators and histamine (Kim, Kim, Jeon, & Kim, 2011). This is a common
pathway in most type 1 hypersensitivity reactions of which asthma is one. (Kumar, Abbas &
Aster, 2015). There are two phases of reaction, an early phase, and a late phase. Mast cell
degranulation and release of cytokine drive the early phase with mucosal hyperstimulation
leading to excess mucus production, vessel dilatation and the direct effect of mediators on vagal
receptors causes bronchoconstriction (Kim, Kim, Jeon, & Kim, 2013). The late phase occurs due
to the recruitment of T lymphocytes, neutrophils and eosinophils that will mediate acute and
chronic inflammation (Bogaert et al, 2011). Inflammation in the wall of the respiratory tree leads
to smooth muscle hypertrophy and deposition of collagen with gland hypertrophy. This is termed
airway remodeling (Kumar, Abbas & Aster, 2015). This underlying pathology will present
clinically as wheezing due to blockage of the airflow and cough due to the hyperresponsiveness
of the airway with excess mucus production (Van Aalderen, 2012).
Treatment
The treatment of asthma involves the use of medications in a systematic stepwise manner
with clear regard for the severity of Asthma and symptomatology (Queensland Health, 2015).
The category of asthma according to the symptoms is assessed so medication can be given in a
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stepwise manner (National Asthma Control Council of Australia, 2018). In Tegan’s case, this is
her initial diagnosis and no prior records of asthma control are available. The initial treatment
requires the prescription of a reliever that is taken in case of a flare up and a controller that is
taken daily as a preventive measure (National Asthma Control Council of Australia, 2018).
Recommended relievers include salbutamol 2 -4 puffs (100 mcg per puff) using a pressurized
metered dose inhaler or terbutaline for children over 6 years, 1-2 puffs (500 mcg per puff) via a
breath- actuated powder inhaler (National Asthma Control Council of Australia, 2018). Using
controllers depends on the level of asthma severity. The levels include infrequent intermittent
asthma, frequent intermittent asthma, and frequent severe asthma. In infrequent intermittent
asthma, a controller is not needed and treatment of flare-ups is recommended. Frequent to severe
asthma, however, controllers are needed. They include an inhaled corticosteroid, Montelukast,
and sodium cromoglycate (National Asthma Control Council of Australia, 2018). Treatment
follows the stepwise manner, either step up or step down. This is done by regular assessment and
if the asthma is well controlled with no flare-ups then the dose of controllers can be gradually
reduced to a therapeutic level (step-down). Also, if the Asthma flares-up despite the prescribed
medication then it can be slowly increased to the required level (step-up) (National Asthma
Control Council of Australia, 2018).
Asthma management education.
According to the National Asthma Control Council of Australia, (2018), the
recommended education for parents and children involves information on asthma and its
management strategies. The parents should be told about the pathology associated with it
including information that is a chronic condition, with its causes and treatment options available.
The medications are introduced as relievers that treat acute attacks and preventers that are taken
stepwise manner (National Asthma Control Council of Australia, 2018). In Tegan’s case, this is
her initial diagnosis and no prior records of asthma control are available. The initial treatment
requires the prescription of a reliever that is taken in case of a flare up and a controller that is
taken daily as a preventive measure (National Asthma Control Council of Australia, 2018).
Recommended relievers include salbutamol 2 -4 puffs (100 mcg per puff) using a pressurized
metered dose inhaler or terbutaline for children over 6 years, 1-2 puffs (500 mcg per puff) via a
breath- actuated powder inhaler (National Asthma Control Council of Australia, 2018). Using
controllers depends on the level of asthma severity. The levels include infrequent intermittent
asthma, frequent intermittent asthma, and frequent severe asthma. In infrequent intermittent
asthma, a controller is not needed and treatment of flare-ups is recommended. Frequent to severe
asthma, however, controllers are needed. They include an inhaled corticosteroid, Montelukast,
and sodium cromoglycate (National Asthma Control Council of Australia, 2018). Treatment
follows the stepwise manner, either step up or step down. This is done by regular assessment and
if the asthma is well controlled with no flare-ups then the dose of controllers can be gradually
reduced to a therapeutic level (step-down). Also, if the Asthma flares-up despite the prescribed
medication then it can be slowly increased to the required level (step-up) (National Asthma
Control Council of Australia, 2018).
Asthma management education.
According to the National Asthma Control Council of Australia, (2018), the
recommended education for parents and children involves information on asthma and its
management strategies. The parents should be told about the pathology associated with it
including information that is a chronic condition, with its causes and treatment options available.
The medications are introduced as relievers that treat acute attacks and preventers that are taken
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ASTHMA 5
regularly to prevent attacks. The adverse effects of medications are explained including the
inhaled corticosteroids that have the worst side effects. Asthma management devices and how to
use them is explained. They include inhalers, spacers, and puffers. The cleaning and care of these
devices is also demonstrated and to assess if the information has been retained, the parents and
children have to demonstrate what was taught. Finally, the educators should help the asthma
patient and parents come up with a written action plan that contains treatment goals, medication
used, dosages and clear guidelines on what to do in different clinical situations. (National
Asthma Control Council of Australia, 2018).
Conclusion
In conclusion, Tegan has allergic asthma due to his symptoms and family history of
atopy. Allergic asthma is a chronic airway disease characterized by hyperresponsiveness to
various stimuli leading to bronchoconstriction, airway remodeling and symptoms of wheezing
and cough that are related to various environmental triggers. The treatment options for asthma
include reliever medication and preventer medication and avoidance of trigger allergens. Asthma
discharge education to help in self-management of this lifelong condition is given to parents and
children.
regularly to prevent attacks. The adverse effects of medications are explained including the
inhaled corticosteroids that have the worst side effects. Asthma management devices and how to
use them is explained. They include inhalers, spacers, and puffers. The cleaning and care of these
devices is also demonstrated and to assess if the information has been retained, the parents and
children have to demonstrate what was taught. Finally, the educators should help the asthma
patient and parents come up with a written action plan that contains treatment goals, medication
used, dosages and clear guidelines on what to do in different clinical situations. (National
Asthma Control Council of Australia, 2018).
Conclusion
In conclusion, Tegan has allergic asthma due to his symptoms and family history of
atopy. Allergic asthma is a chronic airway disease characterized by hyperresponsiveness to
various stimuli leading to bronchoconstriction, airway remodeling and symptoms of wheezing
and cough that are related to various environmental triggers. The treatment options for asthma
include reliever medication and preventer medication and avoidance of trigger allergens. Asthma
discharge education to help in self-management of this lifelong condition is given to parents and
children.
ASTHMA 6
References
Bogaert, P., Naessens, T., Koker, S. D., Hennuy, B., Hacha, J., Smet, M., . . . Grooten, J. (2011).
Inflammatory signatures for eosinophilic vs. neutrophilic allergic pulmonary
inflammation reveal critical regulatory checkpoints. American Journal of Physiology-
Lung Cellular and Molecular Physiology, 300(5), L679-L690.
Just, J., Saint-Pierre, P., Gouvis-Echraghi, R., Laoudi, Y., Roufai, L., Momas, I., & Annesi
Maesano, I. (2014). Childhood Allergic Asthma Is Not a Single Phenotype. The Journal
of Pediatrics, 164(4), 815-820.
Kim, Y. M., Kim, Y. S., Jeon, S. G., & Kim, Y. K. (2013). Immunopathogenesis of Allergic
Asthma: More Than the Th2 Hypothesis. Allergy Asthma Immunol Res, 5(4), 189-196.
Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease.
(Ninth edition.). Philadelphia, PA: Elsevier/Saunders
Mukherjee, A. B., & Zhang, Z. (2011). Allergic Asthma: Influence of Genetic and
Environmental Factors. Journal of Biological Chemistry, 286(38), 32883-32889.
National Asthma Control Council of Australia. (2018). Australian asthma handbook. Melbourne,
Australia: National Asthma Council Australia
O'Connell, E. J. (2014). The burden of atopy and asthma in children. Allergy, 59(s78), 7-11.
Queensland Health, (2015). Chronic Conditions Manual: Prevention and Management of
Chronic Conditions in Australia. (1st Ed.). The Rural and Remote Clinical Support Unit,
Torres.
Van Aalderen, W. M. (2012). Childhood Asthma: Diagnosis and Treatment. Scientifica, 2012, 18
References
Bogaert, P., Naessens, T., Koker, S. D., Hennuy, B., Hacha, J., Smet, M., . . . Grooten, J. (2011).
Inflammatory signatures for eosinophilic vs. neutrophilic allergic pulmonary
inflammation reveal critical regulatory checkpoints. American Journal of Physiology-
Lung Cellular and Molecular Physiology, 300(5), L679-L690.
Just, J., Saint-Pierre, P., Gouvis-Echraghi, R., Laoudi, Y., Roufai, L., Momas, I., & Annesi
Maesano, I. (2014). Childhood Allergic Asthma Is Not a Single Phenotype. The Journal
of Pediatrics, 164(4), 815-820.
Kim, Y. M., Kim, Y. S., Jeon, S. G., & Kim, Y. K. (2013). Immunopathogenesis of Allergic
Asthma: More Than the Th2 Hypothesis. Allergy Asthma Immunol Res, 5(4), 189-196.
Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease.
(Ninth edition.). Philadelphia, PA: Elsevier/Saunders
Mukherjee, A. B., & Zhang, Z. (2011). Allergic Asthma: Influence of Genetic and
Environmental Factors. Journal of Biological Chemistry, 286(38), 32883-32889.
National Asthma Control Council of Australia. (2018). Australian asthma handbook. Melbourne,
Australia: National Asthma Council Australia
O'Connell, E. J. (2014). The burden of atopy and asthma in children. Allergy, 59(s78), 7-11.
Queensland Health, (2015). Chronic Conditions Manual: Prevention and Management of
Chronic Conditions in Australia. (1st Ed.). The Rural and Remote Clinical Support Unit,
Torres.
Van Aalderen, W. M. (2012). Childhood Asthma: Diagnosis and Treatment. Scientifica, 2012, 18
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Vernon, M. K., Wiklund, I., Bell, J. A., Dale, P., & Chapman, K. R. (2012). What Do We Know
about Asthma Triggers? A Review of the Literature. Journal of Asthma, 49(10), 991-998.
Vernon, M. K., Wiklund, I., Bell, J. A., Dale, P., & Chapman, K. R. (2012). What Do We Know
about Asthma Triggers? A Review of the Literature. Journal of Asthma, 49(10), 991-998.
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