Question

Ms. Teel brings in her 7-month-old infant for evaluation. She is afraid that the baby might have respiratory syncytial virus (RSV) because she seems to be coughing a lot, and Ms. Teel heard that RSV is a common condition for infants. A detailed patient history reveals that the infant has been coughing consistently for several months. It’s never seemed all that bad. Ms. Teel thought it was just a normal thing, but then she read about RSV. Closer evaluation indicates that the infant coughs mostly at night; and, in fact, most nights the baby coughs to some extent. Additionally, Ms. Teel confirms that the infant seems to cough more when she cries. Physical examination reveals an apparently healthy age- and weight-appropriate, 7-month-old infant with breath sounds that are clear to auscultation. The infant’s medical history is significant only for eczema that was actually quite bad a few months back. Otherwise, the only remarkable history is an allergic reaction to amoxicillin that she experienced 3 months ago when she had an ear infection.

What is the description of the disorder and underlying respiratory alteration associated with the type of cough in the scenario. Then, explain the pathophysiology of the respiratory alteration. Finally, explain how the two factors(genetics, gender, ethnicity, age, or behavior) you selected might impact the disorder.

Answer 1

The child is exhibiting the signs of asthma. Crying is one of the triggers of asthma in this child, chronic ear infections also indicate sensitivity towards the food or other allergic conditions, the child also had an allergy towards amoxicillin.

Pathophysiology: Asthma caused due to persistent subacute inflammation of the airways. The clinical features and physiology of the asthma are due to the interaction of the infiltrating and resident inflammatory cells, inflammatory mediators, and cytokines with the airway surface epithelium.

Due to the inhalation of the allergens or due to luminal stimuli, Inflammatory mediators (endothelin-1, PGE2, 15-HETE), Cytokines (GM-CSF, IL-8, RANTES) and growth factors (EGF, IGF-1, PDGF) are released. Endothelin-1 causes bronchoconstriction. PGE2, PGI2, 15-HETE results in vasodilation. Cytokines cause inflammation and growth factors cause fibrosis and smooth muscle hyperplasia.

Inflammatory response during the immediate phase asthma: Allergen stimulates mast cells and mononuclear cells -à Releases spasmogens such as prostaglandins, leukotrienes (LTC4, LTD4, and LTE4) and histamine. Also, chemokines and chemotaxis are released. Results in bronchospasm. The immediate phase symptoms can be effectively relieved by adrenergic beta-2 receptor agonists (salbutamol).

Inflammatory response during the late phase asthma: Chemotaxis and chemokines (from the immediate phase) cause infiltration of cytokine releasing Th2 cells, and monocytes. Eosinophils and other inflammatory cells are stimulated. They (particularly eosinophils trigger the release of leukotrienes, NO, and neuropeptides; these trigger airway inflammation. Eosinophils also trigger the release of EMBP (eosinophil major basic protein) and ECP (Eosinophil cationic protein); they cause epithelial damage and airway hyper-reactivity. The late phase effects lead to bronchospasm and cough. The late phase responses can be effectively relieved by glucocorticoids (prednisolone).

Both the immediate phase and late phase symptoms can be relieved by the mast cell stabilizers (cromoglicate and nedocromil sodium). All these changes lead to airway remodeling, bronchial hyperresponsiveness, and airway obstruction.

People with the family history of asthma are at increased risk of developing asthma, and the children experiencing sensitivity towards drugs, and other chemicals, those who are susceptible to frequent viral infections are also at increased risk of developing asthma.