Asthma - Alt Pulm Fcn I Class Notes PDF

NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Asthma Intermittent attacks of bronchoconstriction caused by airway hyperresponsiveness leading to chronic inflammation and remodeling o...

NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Asthma Intermittent attacks of bronchoconstriction caused by airway hyperresponsiveness leading to chronic inflammation and remodeling of the airways. Epidemiology § Affects 25 million people (4.2 million children) in U.S. § Nearly 1 million emergency department visits and 4.9 million outpatient visits annually. § 3,517 deaths in the United States in 2021. § $81.9 billion a year (medical expenses, days of work/school missed, and deaths) in the U.S. Etiology Genetic predisposition to airway hyperresponsiveness - atopic individuals Environmental Triggers Environmental allergens - IgE-mediated (Type I) hypersensitivity Air pollution – ozone and particulate pollution Cigarette smoke Exercise and cold air Upper and lower respiratory infections 1  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Pathophysiology Acute phase response Type I hypersensitivity reaction (also see text Fig. 9-1) 1. Dendritic cell presents allergen to helper T (Th) cell 2. Th cell produces cytokines IL-4 & IL-5 that stimulate proliferation of IgE- producing B lymphocytes 3. IgE binds with IgE-specific receptors on the mast cell’s plasma membrane 4. Mast cell degranulation 5. IL-3 & IL-5 from the Th and mast cells activate eosinophils Effects of histamine on conducting airways Bronchoconstriction (bronchial smooth muscle contraction) Bronchial edema Secretion of thick mucus 2  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Late phase response Synthesis of leukotrienes & prostaglandins by mast cell (4-12 hrs later) Neutrophil & eosinophil infiltration Release of enzymes and chemicals that cause cell injury Epithelial cell sloughing Cell injury stimulates more inflammation Eosinophil mediators cause tissue injury, fibroblast proliferation, and airway scarring Toxic neuropeptides (substance P, neurokinin A, calcitonin gene-related peptide) released Consequence Airway obstruction Decreased expiratory flow rates Air trapping with hyperinflation of alveoli — increased residual volumes 3  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Structural & physiologic changes from chronic inflammation of airways Airway remodeling Bronchial smooth muscle hypertrophy Bronchial fibrosis Increased number of mucus cells & enlargement of submucousal glands Types of Asthma Attacks Slow onset acute asthma – develop over hours or days Hyperacute asthma– develop over minutes to hours Status asthmaticus - prolonged severe bronchoconstriction that can be life threatening FYI - Classification of Asthma Mild Intermittent asthma Respiratory symptoms occur no more than twice a week and are not present between asthma episodes. Nighttime symptoms occur no more than twice a month for adults, no nighttime symptoms for infants and children. No interference with activities. Lung function tests are normal when the individual is not having an acute episode. There are 0-1 exacerbations per year requiring oral steroids. 4  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Mild persistent asthma Respiratory symptoms more than twice a week but not every day. Episodes interfere with activities of daily living. Nighttime symptoms occur more than 3-4 times a month for adults and children age 5-11, 1- 2 times a month for children age 0-4. There is mild interference in activities. Lung function tests are normal when the individual is not having an acute episode. There are 2 or more exacerbations per year requiring oral steroids. Moderate persistent asthma Respiratory symptoms occur daily but not throughout the day. Inhaled short-acting bronchodilators are used daily. Episodes interfere with activities of daily living. Nighttime symptoms occur more than once a week for adults and children age 5-11, 3-4 times per month for children age 0-4. There is some limitation in normal activities Lung function tests are abnormal - more than 60%, but less than 80% of expected value. There are 2 or more exacerbations per year requiring oral steroids. Severe persistent asthma Respiratory symptoms occur throughout the day. Episodes severely limit normal physical activity. Nighttime symptoms occur frequently (as often as nightly for adults and children age 5-11, at least weekly for children age 0-4). There are severe limitations in normal activities. Lung function tests are abnormal - less than 60% of expected value. There are 2 or more exacerbations per year requiring oral steroids. GINA Guidelines Based on difficulty to treat Severe asthma: Uncontrolled despite optimized treatment or requiring high dose ICS- LABA to prevent it from becoming uncontrolled Moderate asthma: Well controlled on step 3 or 4 treatment Mild asthma: Well controlled with ICS-formoterol or low dose ICS plus PRN SABA 5  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Chronic Obstructive Pulmonary Disease Chronic obstructive pulmonary disease (COPD) is a term used to describe long-term airway obstruction and is generally applied to the disease processes of chronic bronchitis and emphysema. Chronic asthma is sometimes considered a form of COPD. Emphysema Reduced alveolar recoil and destruction of the alveolar septa Etiologies a1-antitrypsin deficiency (primary emphysema) Autosomal recessive gene mutation Aa Aa AA Aa aA aa Autosomal recessive pedigree Homozygotes have a 70-80% chance of developing emphysema Inhibition of a1-antitrypsin (secondary emphysema) Tobacco smoking (20% chance of developing emphysema) Air pollution 6  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Pathophysiology a1-antitrypsin deficiency and/or inhibition of a1-antitrypsin Breakdown of elastin surrounding alveoli by proteases leading to hyperinflation of alveoli and air trapping Eventually see septal destruction leading to permanent enlargement of alveolus (bullae and bleb formation) Loss of septal alveolar capillaries and reduced surface area for gas exchange Clinical Consequences Hypoxemia and hypercapnea Increased anterior-posterior diameter of chest Polycythymia Pulmonary hypertension and RV failure 7  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Chronic Bronchitis Chronic inflammation of the bronchi with hypersecretion of mucus and a productive cough for at least 3 consecutive months in a year for two consecutive years. Etiology Chronic exposure to irritants Cigarette smoke Environmental pollutants Occupational exposure to irritants Pathophysiology Recurrent, chronic irritation and inflammation Bronchial edema Bronchoconstriction and eventually hypertrophy of bronchial smooth muscle Increased mucus secretion and eventually hypertrophy of mucus-producing cells Impaired mucus clearance Eventually see alveolar septal destruction that can lead to emphysema Clinical Consequences Airway obstruction causing hypoventilation – leads to hypoxemia and hypercapnea Impaired ciliary function 8  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Air trapping in alveoli Increased risk of infection Pulmonary hypertension and RV failure Cystic Fibrosis Inherited disorder that results in respiratory and other multisystem problems Etiology Autosomal recessive gene mutation 9  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Aa Aa AA Aa aA aa Autosomal recessive pedigree Epidemiology There are about 30,000 people living with CF in the U.S. with about 1,000 new cases per year. 1/29 Caucasians in U. S. are carriers Pathophysiology Gene defect on chromosome 7 causes abnormal expression of the protein cystic fibrosis transmembrane conductance regulator (CTFR or CFTCR) Gene mutation (categorized as Class I-V mutations) can determine disease severity CFTR protein is a chloride channel present on the surface of many epithelial cells that produce sweat, mucus, and digestive enzymes Sweat glands: The CFTR defect results in reduced epithelial reabsorption of Cl- with a corresponding decrease in Na+ reabsorption, resulting in increased Na+ and Cl- in the sweat 10  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Sweat gland Epithelial linings (Respiratory, GI and other): The CFTR defect results in reduced epithelial secretion of Cl- with a corresponding decrease in Na+ and H20 secretion, resulting in a thick and viscous mucus Epithelium Clinical Consequences Pulmonary Airway obstruction Bacterial infections (bronchitis and pneumonia) Bronchial fibrosis Sinus issues – sinusitis, polyps, sinus infections, 11  NURS 7054 Advanced Pathophysiology II for DNP Students Alterations of Pulmonary Function - Class Notes Digestive Chronic pancreatitis leading to pancreatic insufficiency and malabsorption syndromes Endocrine Type 1 diabetes mellitus Reproductive Sterility in males Complications Antibiotic resistant pneumonias Hemoptysis Bullae formation leading to pneumo/hemothorax Pulmonary hypertension eventually leading to right ventricular failure (RVF) 12