Asthma and Restrictive Lung Disease PDF

Asthma & Restrictive Lung Disease Miranda LaCroix, MSPAS, PA-C Augsburg University Fall 2022  Objectives - Summarize the etiology, pathophysiology, clinical features, how diagnosis is established, and treatment for the conditions listed below...

Asthma & Restrictive Lung Disease Miranda LaCroix, MSPAS, PA-C Augsburg University Fall 2022  Objectives - Summarize the etiology, pathophysiology, clinical features, how diagnosis is established, and treatment for the conditions listed below: Asthma (adult & pediatric) Interstitial lung disease Idiopathic pulmonary fibrosis Sarcoidosis Occupational pulmonary diseases Hypersensitivity Medication induced lung disease Radiation lung injury - Assess a personalized asthma management plan and recognize how this tool is utilized in the management and treatment of a patient presenting with asthma. - Compare and contrast the pharmacological and non-pharmacological approach to managing acute asthma exacerbations differentiating between mild, moderate, and severe.  Obstructive & Restrictive Lung Disease Asthma  “ "Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread, but variable, airflow obstruction within the lung that is often reversible either spontaneously or with treatment.” o Global Initiative of Asthma (GINA) 2022  Asthma epidemiology Prevalence: 25.1 million (7.8%) of population in 2019 Mortality: 10.7 deaths per million (3,524 deaths) in 2019 Racial Discrepancies in Asthma  Asthma Risk factors Overall Risk Factors Childhood - Maternal age < 30 years - Males (until puberty) - Prenatal exposure to maternal - Atopy smoking - Allergen Exposure - Prematurity Air Pollution Exposure - Family history of asthma - Obesity - 2.6x more likely to have - Early Puberty asthma if have 1 asthmatic parent Adolescent/Adult - 5.2x more more likely to have - Obesity asthma if have 2 asthmatic - Tobacco Smoke (Exposure) parents - Occupational Exposures - Atopy / Rhinitis  Asthma Pathophysiology Atopic Asthma – genetic predisposition to develop specific immunoglobulin E (IgE) antibodies directed against common environmental allergens Intrinsic abnormalities in: Airway smooth muscle function Airway remodeling in response to injury or inflammation Interactions between epithelial and mesenchymal cells Airway Inflammation Mast cell activation Initial antigen exposure à elaboration of allergen specific IgE antibodies related to overexpression of Th2 type T cells à IgE antibodies bind to high-affinity receptors on mast cells (and basophils) à subsequent allergen exposure cross links with IgE antibodies on mast cell surface à rapid degeneration and mediator release (early phase reaction)  Early and Late Phase Reactions Early Phase Reactions Late Phase Reactions Allergen inhalation by a sensitized individual à Recurrence of bronchoconstriction several hours bronchoconstriction within several minutes later Correlates with the release of mast cell mediators Characterized by recruitment of inflammatory and during the immediate hypersensitivity reaction immune cells, particularly the eosinophil, Cell mediators (histamine, prostaglandin D2, and basophil, neutrophil, and helper, memory T-cells cysteinyl leukotrienes) contract airway smooth to sites of allergen exposure. muscle (ASM) directly, and may also stimulate The mediators released by these cells also cause reflex neural pathways ASM contraction that is largely reversible by beta- agonist administration  Eosinophils The most characteristic cell that accumulates in asthma and allergic inflammation. While the presence of eosinophils is often related to disease severity, some patients with asthma do not have eosinophilic infiltration of the airways Activated eosinophils produce lipid mediators, such as: Leukotrienes and platelet activating factor: mediate smooth muscle contraction Toxic granule products: can damage airway epithelium and nerves Cytokines and interleukins: involved in airway remodeling and fibrosis  Asthma Triggers Air Pollution Allergens Cigarette Smoke Exercise Viral Illness Estrogen/hormones Medications Childhood Asthma - Most common chronic disease in childhood in resource-rich countries - Approximately 7.5% of US children had asthma in 2018 - Increasing prevalence in poor children, Southern US - Highest prevalence in Puerto Rican and non- Hispanic Black American children - Boys > Girls until puberty - Approximately 80% of children with asthma develop symptoms before 5 years old  Childhood Asthma - Most common symptoms: coughing, wheezing, breathlessness, chest pressure or tightness, chest pain - Cough (nocturnal, seasonal, secondary to exposure) - Wheeze - Seasonal symptoms (especially with atopy) - Exercise induced bronchospasm - Occurs in up to 90% of children with asthma  Adult asthma - New diagnosis as adult (>20 years), Persistent/Recurrent since childhood - New diagnosis as adult ~ ½ of adults with asthma - More commonly non-immune - Remission rate lower - Blurring of asthma vs COPD in those with history of smoking and new diagnosis at older age  Classic asthma presentation - Episodic Wheeze (high-pitched whistling - Factors that Lesson Probability of sound, usually upon exhalation) Asthma - Lack of improvement following - Episodic Cough (often worse at night) anti-asthmatic medications - Episodic Shortness of breath or difficulty - Onset of symptoms >50 yrs breathing - Concomitant symptoms such as - Episodic Chest tightness chest pain, lightheadedness, syncope, or palpitations - Characteristic triggers - History of cigarette smoking  Physical exam findings - Wheezing (may not be present - Acute Exacerbation between episodes or mild - Tachypnea, tachycardia, prolonged expiratory exacerbations phase - Rhinitis, nasal polyps - Expiratory (and inspiratory) wheezing - Tripoding or hunched shoulders - Dyspnea on exertion - Accessory muscle use (see picture) - Pulsus paradoxus (inspiratory decrease in systolic arterial pressure) - Diaphoresis - Mental status changes (EMERGENCY) - No breath sounds (EMERGENCY)  Physical exam findings – no/mild acute exacerbation - VS: 120/76, HR 72, RR 14, SpO2: 96%, and Temp 98.6 F - General: Alert and oriented x 3. NAD - Neck: No cervical lymphadenopathy. - HENT: Normocephalic and atraumatic. No erythema or exudates in the pharynx, TM are clear and translucent. No nasal discharge. - CV: RRR with no murmurs, rubs, or gallops. - Pulm: No accessory muscles use. Mild expiratory wheezes are noted on auscultation on posterior and anterior lung fields. No prolonged expiratory phase. - Skin: No rashes or bruising.  Physical exam findings – Moderate/Severe acute exacerbation - VS: 110/66, HR 136, RR 32, SpO2: 89%, and Temp 98.6 F - General: Alert and oriented x 3. Acutely ill-appearing, in moderate respiratory distress. - Neck: No cervical lymphadenopathy. Trachea midline. Negative JVD. - HENT: Normocephalic and atraumatic. No erythema or exudates in the pharynx, No nasal discharge. - CV: Tachycardia with no murmurs, rubs, or gallops. - Pulm: Tachypnea. Intercostal and suprasternal accessory muscles use. Significant expiratory and inspiratory wheezes are noted on auscultation on posterior and anterior lung fields with prolonged expiratory phase. Tripod positioning. Speaking in 1-2 words sentences. - Skin: No rashes or bruising. Pulmonary Function testing and the Diagnosis of asthma  Interpreting Spirometry Step 1: Determine if FEV1/FVC is Low ( 30-40 status, worsening hypercapnia, SpO2