Lungs (Diseases of the Respi S.).pdf

PATHOLOGY Summer/PPT Based | Lungs (Diseases of the Respiratory System | BSOT 1-1 | NLR-RAC Topic Outline: ATELECTASIS Congenital Anomalies Atelectasis - Collapsed lu...

PATHOLOGY Summer/PPT Based | Lungs (Diseases of the Respiratory System | BSOT 1-1 | NLR-RAC Topic Outline: ATELECTASIS Congenital Anomalies Atelectasis - Collapsed lung Pulmonary Edema - Generally REVERSIBLE; except contraction Acute Lung Injury and ARDS Complications: Obstructive and Restrictive Lung Diseases o Inadequate oxygenation Fibrosing Diseases Pulmonary Vascular Diseases o ↑ Risk of infection Pulmonary Infections Tumors Type Cause Tracheal Pleura Deviation Resorption Airway Ipsilateral obstruction INTRODUCTION Compression Fluid, Air or Contralateral mass in the CONGENITAL ANOMALIES pleural cavity Contraction Pulmonary or None in initial Pulmonary Hypoplasia pleural stages fibrosis Ipsilateral if long standing - Defective development of both lungs (one may be more affected than the other) resulting in decreased weight, volume, and acini for body weight and gestational age. PULMONARY EDEMA - Caused by abnormalities that compress the lung or impede normal lung expansion in utero, such as - Leakage of excessive interstitial fluid which congenital diaphragmatic hernia and accumulates in alveolar spaces oligohydramnios. - Can result from hemodynamic disturbances - Fatal in the early neonatal period. (hemodynamic or cardiogenic pulmonary edema) or from direct increases in capillary permeability, as a Foregut Cysts result of microvascular injury - Arise from abnormal detachments of primitive foregut - Most often located in the hilum or middle mediastinum. - Classified as bronchogenic (most common), esophageal, or enteric - The wall contains bronchial glands, cartilage, and smooth muscle - (+) compression of nearby structures or are found incidentally Pulmonary Sequestration - Discrete area of lung tissue that - Lacks any connection to the airway system Hemodynamic Pulmonary Edema - Abnormal blood supply arising from the aorta or its branches - Due to increased hydrostatic pressure, as occurs Types: most commonly in left- sided congestive heart failure.  Extralobar sequestrations - Fluid accumulates initially in the basal regions of the - External to the lung and most commonly come to lower lobes because hydrostatic pressure is greatest attention in infants as mass lesions. in these sites (dependent edema). - May be associated with other congenital anomalies. - (+) Alveolar microhemorrhages and hemosiderin-  Intralobar sequestrations laden macrophages (“heart failure” cells) - Occur within the lung. - Long-standing pulmonary congestion: hemosiderin- - Present in older children, often due to recurrent laden macrophages are abundant, and fibrosis and localized infection or bronchiectasis. thickening of the alveolar walls cause the soggy lungs to become firm and brown (brown induration). Type your initials here | 1 PATHOLOGY Summer/PPT Based | Lungs (Diseases of the Respiratory System | BSOT 1-1 | NLR-RAC Edema Caused by Microvascular (Alveolar) Injury - Noncardiogenic pulmonary edema due to injury to the alveolar septa. - Primary injury to the vascular endothelium or damage to alveolar epithelial cells - inflammatory exudate -> leaks - Into the interstitial space, in severe cases, into the alveoli. - In most forms of pneumonia, edema remains localized and is overshadowed by the manifestations of infection. - An important contributor of acute respiratory distress Epidemiology syndrome - More common and associated with worst prognosis in chronic alcoholics and in smokers - Genetics ACUTE LUNG INJURY AND ARDS Clinical Manifestation: o Profound dyspnea and tachypnea Acute Lung Injury o Cyanosis and Hypoxemia o Respiratory failure - Abrupt onset of significant hypoxemia and bilateral o Diffuse bilateral infiltrates on radiographic pulmonary infiltrates in the absence of cardiac failure. examination. - Acute respiratory distress syndrome (ARDS) - severe ALI - Diffuse Alveolar Damage (DAD) – histologic OBSTRUCTIVE AND RESTRICTIVE LUNG DISEASES manifestation of ALI/ARDS Most common causes: Feature Obstructive Restrictive o Sepsis Fundamental ↑ Airway ↓ Expansion of o Diffuse pulmonary infections Pathology resistance due the lung o Gastric aspiration to obstruction parenchyma o Mechanical trauma (head injuries) with ↓ TLC Pathogenesis: Examples Bronchial Pulmonary  Endothelial Activation asthma fibrosing - Activated endothelium expresses leukocyte adhesion Emphysema diseases Chronic Chest wall molecules and chemokines → leukocyte adhesion bronchitis disorders and extravasation → inflammation and tissue injury Bronchiectasis → pneumocyte necrosis - Type II pneumocyte necrosis → ↓ surfactant → Lung Volumes ↑ ↓ diffusion defect → hypoxemia - Activated endothelium increases microvascular FEV1 ↓↓ ↓ permeability → pulmonary edema + necrotic debris FVC ↓ ↓↓ → hyaline membranes → diffusion defect → FEV1/FVC ↓ (