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Respiratory Pathology - Coggle Diagram

- - - - SECONDARY
        PULMONARY
        HYPERTENSION
        
        Etiology:
        
        Hypoxemia: COPD and interstitial lung disease
        
        Recurrent pulmonary embolism
        
        Increased volume in the pulmonary
        circuit: congenital heart disease
      - PRIMARY
        PULMONARY
        HYPERTENSION
        
        Etiology is unknown; some familial forms are related to inactivating mutations of BMPR2, leading to proliferation of vascular smooth muscle
        
        Young adult females
- - - - Clinical features:
        
        Hypoxemia + Cyanosis + respiratory
        distress due to thickened diffusion barrier
        and collapse of air sacs (increased surface tension)
        
        White-out x-ray
      - Treatment:
        1) Treat underlying cause
        2) Ventlation with positive end-expiratory pressure (PEEP)
        
        Prone positioning (lying face down) is sometimes used to improve arterial oxygenation in patients with severe acute respiratory distress syndrome. It likely does so by reducing atelectasis of posterior alveoli to reduce intrapulmonary shunting and improve ventilation-perfusion matching throughout the lungs.
      - Etiology
        
        Sepsis, infection, shock, trauma, aspiration,
        pancreatitis, DIC, hypersensitivity reactions, and drugs.
        
        Activation of neutrophils induces
        protease- and free radical-mediated
        damage of type I and II pneumocytes
        
        Recovery may be complicated by interstitial fibrosis; damage and loss of type II pneumocytes leads to scarring and fibrosis
  - - - Surfactant decreases surface tension in the lung,
        preventing collapse of alveolar air sacs after expiration
      - Surfactant is made by type II pneumocytes;
        phosphatidylcholine (lecithin) is the major component
        
        Lack of surfactant leads to collapse of air
        sacs and formation of hyaline membranes
        
        Associated with:
        
        Prematurity
        
        Surfactant production begins at 28 weeks;
        adequate levels are not reached until 34 weeks
        
        Amniotic fluid lecithin to sphingomyelin ratio
        is used to screen for lung maturity; Phosphatidylcholine (lecithin) levels increase as surfactant is produced;sphingomyelin remains constant; ratio > 2 indicates adequate surfactant production
        
        Caesarian section delivery
        
        Lack of stress-induced steroids; steroids
        increase synthesis of surfactant.
        
        Maternal diabetes
        
        Insulin decreases surfactant production.
        
        Clinical features
        
        Hypoxemia with cyanosis
        
        Diffuse granularity of the lung
        ('ground-glass' appearance) on x-ray
        
        Increasing respiratory effort after birth, tachypnea with use of accessory muscles, and grunting
        
        Complications:
        
        Hypoxemia increases the risk for persistence of patent ductus arteriosus and necrotizing enterocolitis
        
        Supplemental oxygen increases the risk for free radical injury:
        
        Retinal injury leads to blindness
        
        Lung damage leads to bronchopulmonary dysplasia
- - - - Spontaneous pneumothorax is due to rupture of an emphysematous bleb; seen in young adults
        - Results in collapse of a portion of the lung
        Associated with tobacco smoking, Marfan Syndrome, mechanical ventilation.
        
        Breath sounds ↓
        
        Percussion Hyperresonant
        
        Fremitus ↓
        
        Trachea shifts to the side of collapse OR NON DEVIATION
      - Tension pneumothorax arises with penetrating chest wall injury: rib fracture, gunshot, iatrogenic
        
        Air enters the pleural space, but cannot exit.
        
        Medical emergency; treated with insertion of a chest tube side of injury; may cause increased intrathoracic pressure, mediastinal displacment, kinking of IVC, ↓ venous return and ↓ cardiac output, obstructive shock
        
        Breath sounds ↓
        
        Percussion Hyperresonant
        
        Fremitus ↓
        
        Trachea is pushed opposite to the side of injury
  - - - Presents with recurrent pleural effusions or hemorrhagic pleural effusion (exudative so protein 0.5 and ↑ LDH), dyspnea, and chest pain; tumor encases the lung
        
        Pleural thickening
        
        Histology>> Psammoma bodies; EM polygonal tumor cells with microvilli, desmosomes, tonofilaments
        
        Calretinin and cytokeratin 5/6 ⊕ in almost all
        mesotheliomas, ⊝ in most carcinomas
        - Tobacco smoking IS NOT A RISK FACTOR.
- - - - Systemic disease classically seen in African American females, Characterized by noncaseating granulomas in multiple organs
    - - Fibrosis of lung interstitium
        
        Clinical features
        
        Progressive dyspnea and cough
        
        Bilateral fibrosis on lung CT; initially seen in subpleural patches, but eventually results in extensive fibrosis with end-stage 'honeycomb' lung
        
        Anti-fibrogenic drugs slow disease progression
        
        Definitive treatment is lung transplantation.
        
        Related to cyclical lung injury;
        TGF-β from injured pneumocytes
        induces fibrosis.
      - Secondary causes of interstitial
        fibrosis such as drugs (bleomycin
        and amiodarone) and radiation
        therapy must be excluded
    - - Granulomatous reaction to inhaled
        organic antigens (pigeon breeder's lung)
        
        Chronic exposure leads
        to interstitial fibrosis
        
        Clinical:
        
        Fever, cough, and dyspnea hours after exposure
        
        Resolves with removal of the exposure
    - - Interstitial fibrosis due to occupational exposure:
        requires chronic exposure to small particles
        that are fibrogenic
        
        Alveolar macrophages engulf foreign
        particles and induce fibrosis
        
        Asbestosis
        
        construction workers, plumbers,
        and shipyard workers
        
        Fibrosis of lung and pleura (plaques) with increased risk for lung carcinoma and mesothelioma; lung carcinoma is more common than mesothelioma in exposed individuals
        
        Lesions may contain long, golden-brown fibers with associated iron (asbestos bodies), which confirm exposure to asbestos
        
        Berylliosis
        
        Beryllium miners and workers
        in the aerospace industry
        
        Noncaseating granulomas in the lung,
        hilar lymph nodes, and systemic organs
        
        Increased risk for lung cancer
        
        Silicosis
        
        sandblasters and
        silica miners
        
        Fibrotic nodules in upper
        lobes of the lung
        
        Increased risk for TB; silica impairs
        phagolysosome formation by macrophages
        
        Coal workers
        
        Carbon dust; seen
        in coal miners
        
        Diffuse fibrosis (black lung)
        Associated with rheumatoid
        arthritis (Caplan Sx)
        
        Anthracosis (collections of
        carbon-laden macrophages)