PA504 Pulmonary PPT- Part 1 PDF

PULMONARY CHAPTER 12 University of Mount Union Physician Assistant Studies PA 504 ATELECTASIS  ATELECTASIS  Loss of lung volume caused by inadequate expansion of air spaces  Results in shunting of inadequately oxygenated blood from the pulmonary arteries into veins → ventilation-perfusion...

PULMONARY CHAPTER 12 University of Mount Union Physician Assistant Studies PA 504 ATELECTASIS  ATELECTASIS  Loss of lung volume caused by inadequate expansion of air spaces  Results in shunting of inadequately oxygenated blood from the pulmonary arteries into veins → ventilation-perfusion imbalance & hypoxia  3 Forms  Resorption atelectasis- occurs when an obstruction prevents air from reaching distal airways  The air already present is absorbed → alveolar collapse  Most common cause- obstruction of a bronchus by a mucous plug postoperatively  Compression atelectasis- associated with accumulation of fluid, blood, or air within the pleural cavity  Examples: pleural effusion (like in CHF), pneumothorax (leakage of air into pleural cavity)  Results in mechanical collapse of adjacent lung  Contraction atelectasis- local or generalized fibrotic changes in the lung/pleura hamper expansion and increase elastic recoil during expiration ACUTE LUNG INJURY ACUTE LUNG INJURY  Encompasses a spectrum of bilateral pulmonary damage, which can be initiated by numerous conditions  Clinical Features  Acute onset of dyspnea  Decreased arterial oxygen pressure (hypoxemia)  Development of bilateral pulmonary infiltrates on chest x-ray  “noncardiogenic pulmonary edema”  ALL in the absence of clinical evidence of primary left-sided heart failure  Can progress to acute respiratory distress syndrome (ARDS) ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)  Clinical syndrome caused by diffuse alveolar capillary and epithelial damage  Histologic manifestation of ARDS = diffuse alveolar damage (DAD)  Characterized by rapid onset of life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia  Refractory to oxygen therapy  May progress to multisystem organ failure  Causes  Direct Lung Injury- pneumonia, aspiration of gastric contents, pulmonary contusion, fat embolism, near-drowning, inhalation injury  Indirect Lung Injury- sepsis, severe trauma with shock, cardiopulmonary bypass, acute pancreatitis, drug overdose, transfusion of blood products, uremia ACUTE RESPIRATORY DISTRESS SYNDROME Chest X-Ray CT Chest ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)  Pathogenesis  Integrity of the alveolar-capillary membrane is compromised, either by endothelial or epithelial injury (or both)→ increased vascular permeability & alveolar flooding, loss of diffusion capacity, widespread surfactant abnormalities (from damage to type II pneumocytes)  After insult, there is increased synthesis of interleukin 8 (IL-8), a potent neutrophil recruiter → endothelial activation  Neutrophils release products that cause damage to the alveolar epithelium and endothelium ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)  Clinical Features  Histologic Characteristics  Develops within 72 hours of insult  Alveolar edema  Predictors of poor prognosis- advanced age,  Epithelial necrosis underlying bacteremia, development of multisystem organ failure  Accumulation of Neutrophils  Should the patient survive the acute stage →  Presence of hyaline membranes lining alveolar diffuse interstitial fibrosis can occur ducts OBSTRUCTIVE VERSUS RESTRICTIVE PULMONARY DISEASE OBSTRUCTIVE VERSUS RESTRICTIVE PULMONARY DISEASE Obstructive Airway Disease Restrictive Airway Disease  Characterized by limitation of airflow, resulting from  Characterized by reduced expansion of lung an increase in resistance caused by obstruction at parenchyma accompanied by decreased total lung any level capacity  Includes emphysema, chronic bronchitis,  Includes acute & chronic interstitial lung disease bronchiectasis, and asthma (ARDS, pneumoconiosis, interstitial fibrosis, infiltrative conditions) & chest wall disorders in the  Normal or slightly decreased forced vital capacity presence of normal lungs (severe obesity, (FVC) neuromuscular disorders)  Significantly decreased expiratory flow rate  FVC is reduced (measured as forced expiratory volume at 1 second (FEV1))  Expiratory flow rate is normal or reduced proportionately  Ratio of FEV1 to FVC is characteristically decreased  FEV1 to FVC is near normal OBSTRUCTIVE LUNG DISEASE EMPHYSEMA, CHRONIC BRONCHITIS, ASTHMA, BRONCHIECTASIS OBSTRUCTIVE LUNG DISEASE  Chronic Obstructive Pulmonary Disease (COPD)  Irreversible airflow obstruction  *asthma is reversible airflow obstruction  Affects >10% of the US adult population  4th leading cause of death in the US  Encompasses chronic bronchitis and emphysema  Emphysema is diagnosed morphologically, while chronic bronchitis is defined based on clinical features  EMPHYSEMA  Characterized by abnormal permanent enlargement and destruction of the air spaces distal to the terminal bronchioles  Types  Centriacinar (Centrilobular)- affects the central or  Distal Acinar (Paraseptal)- primarily involves proximal parts of the acini, sparing distal alveoli distal portion of acini  More common & severe in the upper lobes (apical segments)  Occurs adjacent to areas of fibrosis, scarring, or  Most commonly seen as a consequence of cigarette smoking in atelectasis, more severe in upper half of lungs people who do NOT have a congenital deficiency of α1-antitrypsin  Seen most often in cases of spontaneous  Panacinar (Paralobular)- acini are uniformly pneumothorax in young adults enlarged, from respiratory bronchiole to terminal blind alveoli  Irregular- acinus is irregularly involved  Occurs more commonly in the lower lung zones  Associated with scarring  Type that occurs with α1-antitrypsin deficiency  EMPHYSEMA  Pathogenesis  Exposure to substances such as tobacco smoke & inhaled pollutants → ongoing inflammation & accumulation of neutrophils, macrophages, and lymphocytes in the lung  Elastases, cytokines, and oxidants are released → epithelial injury & proteolysis of the ECM  Antielastases (α1-antitrypsin) stop this cycle  80% of patients with congenital α1-antitrypsin deficiency develop symptomatic panacinar emphysema EMPHYSEMA  Clinical Features  Dyspnea- first symptom, steadily progressive  Weight loss  Barrel chested  Prolonged expiration, hunched over position  Reduced FEV1 with normal or near-normal FVC  Ratio of FEV1 to FVC is reduced  Blood gases relatively normal  “Pink Puffers”- adequate oxygenation, prominent dyspnea  Secondary pulmonary hypertension CHRONIC BRONCHITIS  Defined by the presence of a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years  Common among cigarette smokers and urban dwellers in smog-ridden cities  Pathogenesis  Environmental irritants (cigarette smoking) induce hypertrophy of mucous glands in the trachea and main bronchi → marked increase in mucin-secreting goblet cells in the surface epithelium of smaller bronchi and bronchioles  Irritants cause inflammation with infiltration of CD8+ lymphocytes, macrophages, & neutrophils CHRONIC BRONCHITIS  Clinical Features  Prominent cough and production of sputum  Hypercapnia, hypoxemia, cyanosis – “blue bloater”  With progression, complicated by pulmonary hypertension and cardiac failure  Recurrent infections & respiratory failure may occur COPD IMAGING Emphysema Chronic Bronchitis ASTHMA  Chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough  Hallmarks  Intermittent and reversible airway obstruction  Chronic bronchial inflammation with eosinophils  Bronchial smooth muscle cell hypertrophy and hyperreactivity  Increased mucous secretion  ASTHMA  Pathogenesis  Etiologic Factors- genetic predisposition to type I hypersensitivity (atopy), acute and chronic airway inflammation, bronchial hyper-responsiveness to a variety of stimuli  Atopy- associated with an excessive type 2 helper T (TH2) cell reaction against environmental antigens  IL-4- stimulates IgE production  IL-5- activates eosinophils  IL-13- stimulates mucus production and promotes IgE production  IgE coats submucosal mast cells  Two Phases  Early (immediate)- bronchoconstriction, increased mucous production, variable vasodilation  Late- inflammation with activation of eosinophils, neutrophils, and T cells  Repeated bouts of inflammation lead to airway remodeling (structural changes in bronchial wall)  ASTHMA  Types  Atopic- most common  Type I IgE-mediated hypersensitivity reaction  Begins in childhood, positive family history of atopy and/or asthma common  Asthma attacks often preceded by allergic rhinitis, urticaria, or eczema  Triggered by environmental antigens- dusts, pollen, animal dander, foods  Non-Atopic  Triggers- respiratory infections due to viruses, inhaled air pollutants  Humoral and cellular mediators are common to both atopic and non-atopic → treat in similar way  Drug-Induced  Aspirin most common agent  Inhibits the cyclooxygenase pathway of arachidonic acid metabolism → increased leukotrienes → bronchial spasm  Occupational  Stimulated by fumes (epoxy resins, plastics), Organic/chemical dusts, & gases (toluene) ASTHMA  Clinical Features  Attack- severe dyspnea with wheezing  Last from one to several hours  Progressive hyperinflation of the lungs with air trapped distal to the bronchi  Status asthmaticus- severe paroxysm that does not respond to therapy and persists for days to weeks  Hypercapnia, acidosis, severe hypoxia BRONCHIECTASIS  The permanent dilation of bronchi and bronchioles caused by destruction of the muscle and the supporting elastic tissue, resulting from or associated with chronic necrotizing infections  NOT a primary disease  Characteristic symptoms- severe persistent cough & expectoration of copious amount of purulent sputum  Episodic, precipitated by upper respiratory tract infections  Clubbing of the fingers  Hypoxemia, hypercapnia, pulmonary hypertension, cor pulmonale  Predisposing Conditions  Bronchial obstruction- tumors, foreign bodies, impaction of mucous  Cystic Fibrosis  Necrotizing or suppurative pneumonia- Staphylococcus aureus, Klebsiella BRONCHIECTASIS  Morphology  Affects the lower lobes bilaterally  Airways dilated as much as 4x their usual diameter  Fibrosis of the bronchial and bronchiolar walls  “Tram Tracks”