Respiratory - Asthma Midterm Notes PDF

4 1 RESPIRATORY – Asthma Asthma Asthma is a chronic inflammatory disorder of the airways that results in variable airflow obstruc5on, bronchial hyperresponsiveness, and airway remodeling. It is o=en reversibl...

4 1 RESPIRATORY – Asthma Asthma Asthma is a chronic inflammatory disorder of the airways that results in variable airflow obstruc5on, bronchial hyperresponsiveness, and airway remodeling. It is o=en reversible with treatment. 1. Most Likely Cause Cause: o Inhaled Allergens (Environmental Triggers): The most common trigger for asthma aAacks is exposure to allergens such as dust mites, pollen, pet dander, mold, and cockroach droppings. o Air Pollutants and Irritants: Exposure to air pollu5on, tobacco smoke, strong odors, and chemical irritants can trigger asthma. o GeneGc and Environmental InteracGons: Gene5c predisposi5on (family history of asthma or atopy) combined with environmental exposure increases the risk of developing asthma. o Respiratory InfecGons: Viral infecGons (like RSV and rhinovirus) in childhood can increase the risk of asthma development. 2. Pathophysiology The pathophysiology of asthma can be described in terms of immune responses, airway inflamma5on, and the physiological consequences of these processes. 1. SensiGzaGon and IniGal Immune Response: o Inhaled allergens are processed by anGgen-presenGng cells (APCs) (like dendri5c cells) in the airways. o APCs present allergens to naive T-helper cells (Th0), which differen5ate into Th2 cells that secrete cytokines such as IL-4, IL-5, and IL-13. o IL-4 s5mulates B cells to produce IgE anGbodies specific to the allergen. These IgE an5bodies bind to receptors on mast cells, making them sensi5zed to subsequent exposures. 2. Early Phase Response: o Upon re-exposure to the allergen, mast cells degranulate, releasing histamine, leukotrienes, and prostaglandins. o Histamine and leukotrienes cause bronchoconstricGon, vasodilaGon, and increased vascular permeability, resul5ng in mucus secreGon and airway swelling. o Bronchospasm (contrac5on of airway smooth muscle) occurs rapidly, causing wheezing, shortness of breath, and chest 5ghtness. 3. Late Phase Response (4-8 Hours AVer IniGal Exposure): o Recruitment of eosinophils, neutrophils, and basophils to the site of inflamma5on occurs, along with the release of addi5onal pro-inflammatory cytokines and cytotoxic mediators.  2 oThe resul5ng mucus hypersecreGon, airway swelling, and airway hyperresponsiveness worsen airflow obstruc5on, leading to prolonged symptoms. 4. Airway Remodeling (Chronic Changes) o If asthma is not controlled, chronic inflammaGon can result in structural changes in the airways. o Smooth muscle hypertrophy and goblet cell hyperplasia increase mucus produc5on, while deposi5on of extracellular matrix proteins (subepithelial fibrosis) s5ffens the airway wall. o This process makes the airways hyperresponsive to irritants, further perpetua5ng the cycle of asthma. 3. Disease Transmission Transmission: o Not transmissible. Asthma is a non-communicable chronic disease. o However, exposure to viral respiratory infecGons (like RSV) in childhood is a known risk factor for developing asthma later in life. 4. Risk Factors Risk factors for asthma can be categorized as modifiable and non-modifiable. Modifiable Risk Factors Allergen Exposure: Pollen, dust mites, animal dander, cockroach droppings, and mold can trigger asthma aAacks. Air PolluGon: Exposure to air pollutants like nitrogen dioxide, ozone, and par5culate maAer increases asthma risk. OccupaGonal Exposure: Exposure to chemical irritants and fumes in certain workplaces (like bakeries, paint shops, and farming) can increase asthma risk. Respiratory InfecGons: Viral infecGons in childhood (e.g., RSV, rhinovirus) are linked to asthma development. Smoking: AcGve and passive smoking during childhood is a risk factor for asthma development and exacerba5ons. Obesity: Obesity is a significant risk factor for asthma, possibly due to the influence of pro-inflammatory mediators from adipose 5ssue. Diet: Diets low in an5oxidants, omega-3 faAy acids, and fruits/vegetables have been linked to higher asthma risk. Non-Modifiable Risk Factors GeneGc Factors: Family history of asthma, eczema, and allergic rhiniGs increases asthma risk. Age: Childhood exposure to allergens and infec5ons can increase the risk of developing asthma. Sex: Males are at greater risk for asthma in childhood, while females have higher risk in adulthood. Ethnicity: Some studies show higher rates of asthma among First NaGons and Indigenous communiGes.  3 Summary Table Criteria Asthma Most Likely Inhaled allergens (dust mites, pollen, pet dander, mold), air pollu5on, viral Cause respiratory infec5ons, gene5c predisposi5on. Inhaled allergen → Th2 acGvaGon → IgE producGon → mast cell Pathophysiology degranulaGon → release of histamine and leukotrienes → bronchoconstricGon, mucus producGon, and airway swelling. Transmission Not transmissible. Asthma is a non-communicable chronic disease. Modifiable: Allergen exposure, air pollu5on, occupa5onal irritants, smoking, Risk Factors obesity, and respiratory infec5ons. Non-Modifiable: Family history, male sex (in childhood), female sex (in adulthood), age, and ethnicity. Clinical ManifestaGons Intermi]ent Symptoms: Wheezing, shortness of breath, chest 5ghtness, and cough that worsens at night, early morning, or a=er exposure to triggers. Airway ObstrucGon: Causes difficulty in exhaling, leading to air trapping in the alveoli, which can cause a prolonged expiratory phase and reduce lung capacity. HyperinflaGon of the Lungs: Results in dyspnea (shortness of breath) and accessory muscle use during breathing. Severe Asthma ExacerbaGons: May lead to respiratory acidosis due to carbon dioxide (CO2) retenGon, which can be life-threatening.