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 (adult...

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. Obstructiv e& Restrictive Lung Disease Asthm a  “ "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 Discrepancies in Asthma Asthma Risk factors Overall Risk Factors Childhood ‐ Maternal age < 30 years ‐ Males (until puberty) ‐ Prenatal exposure to ‐ Atopy maternal 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 ‐ Obesity to have asthma if have ‐ Tobacco Smoke (Exposure) 2 asthmatic 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  elaboration of allergen specific IgE antibodies related to overexpression of Th2 type T cells  IgE antibodies bind to high-affinity receptors on mast cells (and basophils)  subsequent allergen exposure cross links with IgE antibodies on mast cell surface  rapid degeneration and mediator release (early  Early and Late Phase Reactions Early Phase Late Phase Reactions Reactions Allergen inhalation by a sensitized Recurrence of bronchoconstriction individual  bronchoconstriction several hours later within several minutes Characterized by recruitment of Correlates with the release of mast cell inflammatory and immune cells, mediators during the immediate particularly the eosinophil, basophil, hypersensitivity reaction neutrophil, and helper, memory T-cells to Cell mediators (histamine, prostaglandin sites of allergen exposure. D2, and cysteinyl leukotrienes) contract The mediators released by these cells airway smooth muscle (ASM) directly, also cause ASM contraction that is and may also stimulate reflex neural largely reversible by beta-agonist pathways 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 ‐ ‐ Factors that Lesson Probability Episodic Wheeze (high-pitched whistling sound, usually upon of Asthma ‐ Lack of improvement exhalation) following anti-asthmatic ‐ Episodic Cough (often worse at medications night) ‐ Onset of symptoms ‐ Episodic Shortness of breath or >50 yrs difficulty breathing ‐ Concomitant symptoms ‐ Episodic Chest tightness such as chest pain, lightheadedness, syncope, ‐ Characteristic triggers or palpitations ‐ History of cigarette smoking  Physical exam findings ‐ Wheezing (may not be ‐ Acute Exacerbation present between episodes or ‐ Tachypnea, tachycardia, prolonged mild exacerbations expiratory 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 decreased mental status, worsening ‐ Tripoding, unable to recline hypercapnia, SpO2