Respiratory System - Pathology Lecture PDF

Respiratory system - Pathology Dr. Omar Hamdan Gastrointestinal and liver pathologist Mutah University School of Medicine-Pathology Department Undergraduate Lectures 2023  OBJECTIVES: Function and anatomy Atelectasis (Collapse) Acute respiratory distres...

Respiratory system - Pathology Dr. Omar Hamdan Gastrointestinal and liver pathologist Mutah University School of Medicine-Pathology Department Undergraduate Lectures 2023  OBJECTIVES: Function and anatomy Atelectasis (Collapse) Acute respiratory distress syndrome (ARDS) Restrictive vs. Obstructive lung diseases FUNCTION AND ANATOMY: The major function of the lung is to replenish oxygen and remove carbon dioxide from blood. https://www.amboss.com/us/knowledge/airways-and-lungs https://www.amboss.com/us/knowledge/airways-and-lungs https://www.amboss.com/us/knowledge/airways-and-lungs http://www.medicinehack.com/2011/05/microscopic-structure-of-alveolar-wall.html THE COMPONENTS OF THE ALVEOLAR WALLS (OR ALVEOLAR SEPTA) FROM THE BLOOD SIDE TO AIR SIDE : capillary endothelium basement membrane pulmonary interstitium Alveolar epithelium: made of two cell types: the flattened type I pneumocytes: 95% the rounded cells of type II pneumocytes: produce pulmonary surfactant and involved in repair of alveolar epithelium in the wake of damage to type I pneumocytes. Alveolar macrophages, mononuclear cells of phagocytic lineage, usually lie free within the alveolar space.  ATELECTASIS https://teachmesurgery.com/perioperative/cardiorespiratory/atelectasis/  ATELECTASIS Loss of lung volume caused by inadequate expansion of air spaces.  THREE TYPES: Resorption atelectasis Compression atelectasis Contraction atelectasis (cicatrization atelectasis)  1.RESORPTION ATELECTASIS Due to total obstruction of a bronchus preventing air from reaching distal airways.  RESORPTION ATELECTASIS, CAUSED BY: The most common cause is Obstruction of a bronchus by: ✓ Intrabronchial mucous or mucopurelant plugs in post operative patients. ✓ Foreign body aspiration, especially in children ✓ Obstructive lung disease: bronchial asthma, bronchiectasis, chronic bronchitis ✓ Intrabronchial tumors.  2. COMPRESSION ATELECTASIS caused by accumulation of fluid, blood, or air within pleural cavity, which mechanically collapse adjacent lung. a. Pleural effusion like in Congestive Heart Failure b. Pneumothorax: air in the pleural cavity 3. CONTRACTION ATELECTASIS (CICATRIZATION ATELECTASIS) Occurs due to local or generalized fibrosis of the lung or pleura that prevents full expansion of the lung.  Atelectasis (except when caused by contraction) is potentially reversible and should be treated promptly to prevent hypoxemia and superimposed infection of the collapsed lung.  ACUTE RESPIRATORY DISTRESS SYNDROME The epidemiology and definition are evolving. Formerly considered to be the severe end of a spectrum of acute lung injury Defined as respiratory failure occurring within 1 week of a known clinical insult with bilateral opacities on chest imaging, NOT fully explained by effusions, atelectasis, cardiac failure, or fluid overload.  graded based on the severity of the changes in arterial blood oxygenation. Causes are diverse extensive bilateral injury to alveoli known histologically as diffuse alveolar damage (DAD)  SEVERE ARDS: characterized by rapid onset of life-threatening: a. respiratory insufficiency. b. Cyanosis c. Severe arterial hypoxemia that becomes refractory to oxygen therapy and may progress to multisystem organ failure.  ARDS TRIGGERS: ► pneumonia (35%–45%) ► sepsis (30%–35) ► Aspiration ► trauma (including brain injury, abdominal surgery, and multiple fractures) ► pancreatitis ► transfusion reactions.  ARDS should not be confused with respiratory distress syndrome of the newborn; the latter is caused by a deficiency of surfactant caused by prematurity. Robbins and Cotran pathologic basis of disease, 9th edition  PATHOGENESIS: the integrity of the alveolar-capillary membrane is compromised by endothelial and epithelial injury. As early as 30 minutes after an acute insult, there is increased synthesis and release of IL- 8, IL-1 and TNF by pulmonary macrophages. leading to endothelial activation and sequestration activation & chemotaxis of neutrophils in pulmonary capillaries.  PATHOGENESIS/CONT. Activated neutrophils release reactive oxygen species & proteases that damage the alveolar epithelium and endothelium causing vascular leakiness and loss of surfactant that render the alveolar unit unable to expand. the destructive forces are counteracted by endogenous anti- proteases and anti-oxidants  In the end, it is the balance between the destructive and protective factors that determines the degree of tissue injury and clinical severity of the ARDS.  HISTOLOGY: In the acute phase of ARDS : ► The most characteristic finding is the presence of hyaline membranes ► consists of fibrin-rich edema fluid admixed with remnants of necrotic epithelial cells (similar to respiratory distress syndrome of the newborn) FIGURE 13.3A,ROBBINS BASIC PATHOLOGY, 10TH EDITION HISTOLOGY: In the organizing stage: ► proliferation of type II pneumocytes ► intraalveolar fibrosis due to organization of the fibrin-rich exudates. ► Marked thickening of the alveolar septa due to proliferation of interstitial cells and collagen deposition. FIGURE 13.3B,ROBBINS BASIC PATHOLOGY, 10TH EDITION CLINICAL FEATURES Patients are hospitalized for one of the predisposing conditions Profound dyspnea and tachypnea followed by increasing cyanosis and hypoxemia, respiratory failure, and the appearance of diffuse bilateral infiltrates on radiographic examination. Hypoxemia may be refractory to oxygen therapy  OUTCOME: The overall hospital mortality rate is 38.5%. Most patients who survive the acute insult recover normal respiratory function within 6 to 12 months, but the rest develop diffuse interstitial fibrosis leading to chronic respiratory insufficiency PREDICTORS OF POOR PROGNOSIS 1. advanced age 2. bacteremia (sepsis) 3. development of multiorgan failure  COVID-19 & ARDS HTTPS://WWW.HAMILTON-MEDICAL.COM/RU/COVID-19.HTML  COVID-19 pandemic! Variable presentations COVID-19-associated ARDS! Is it different? Some studies, 1/3 had severe ARDS Pathogenesis of COVID-19-induced ARDS: implications for an aging population COVID-19-associated acute respiratory distress syndrome: is a different approach to management warranted?  OBSTRUCTIVE VS. RESTRICTIVE DIFFUSE PULMONARY DISEASES can be classified into two Categories: 1. OBSTRUCTIVE AIRWAY DISEASES: characterized by resistance to airflow caused by partial or complete obstruction at any level. 2. RESTRICTIVE DISEASES: characterized by reduced expansion of lung parenchyma and decreased total lung capacity. Restrictive defects occur in two general conditions: 1. chest wall disorders in the presence of normal lungs: severe obesity, diseases of the pleura, and neuromuscular disorders that affect the respiratory muscles 2. acute or chronic interstitial lung diseases: ► The classic acute restrictive disease is ARDS. ► Chronic restrictive diseases include the pneumoconioses, interstitial fibrosis of unknown etiology, and sarcoidosis. A 58-year-old man with ischemic heart disease undergoes coronary artery bypass graft surgery under general anesthesia. Two days postoperatively, he experiences increasing respiratory difficulty with decreasing arterial oxygen saturation. On physical examination, his heart rate is regular at 78/min, respirations are 25/min, and blood pressure is 135/85 mmHg. The hemoglobin concentration has remained unchanged, at 13.7 g/dL, since surgery. After he coughs up a large amount of mucoid sputum, his condition improves. Which of the following types of atelectasis does he most likely have? A) Compression B) Contraction C) Resorption THANK YOU!