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Obstructive Airway Disorders - Coggle Diagram

- - - - Bronchospasms
      - Inflammatory response
    - - Acute bronchoconstriction
      - Mucosal edema
      - Mucous plug formation
      - Airway wall remodeling
    - - Wheezing
      - Breathlessness
      - Chest thightness
      - Coughing worse at night
- - - - Hyper-secretion of bronchial mucus
      - Inflammation of the major and small airways
      - Associated with chronic smoking and exposure to environment pollutants
    - - chronic inflammation and edema
      - Hyperplasia of bronchial mucous gland and smooth muscle
      - Destruction of cilia
      - Squamous cell metaplasia
      - Bronchial wall thickening and fibrosis
    - - Coughing
      - Sputum production
      - Severe respiratory impairment
      - Hypoxemia and cyanosis "blue bloaters"
- - - - Triggered by cigarette smoking, air pollution, and certain occupation
      - Increase in the size of alveolar duct, loss of alveoli, loss of gas-exchanging surface area and a decrease in bronchiolar musculature
      - Decreased airflow or gas exchange "pink puffer"
    - - Alveola destruction secondary inflammatory response
      - Inactivate Alpha1-antitrypsin
    - - Based on patient's history and physical findings
        
        Difficulty breathing, use of accessory muscles, progressive dyspnea, hunched forward, barrel chest, pursed-lip, minimal coughs
        
        Increased functional RC, increased RV, increased TLC, increased FEV, decreased FVC
    - - Atrovent, albuterol, guaifensesin, corticosteroid, theophylline, low dose oxygen, smoking cessation, avoid triggers
- - - - Defect in chromosome 7 prevalent in Caucasian young man
      - Affect pancreas, intestinal tracts, sweat glands, sweat glands and the lungs, and causes infertility
        
        Excessive production and secretion of mucus plug occluding the glands and ducts
      - Development of chronic lung disease due accumulation of viscid mucus in the bronchi, impaired mucociliary clearance and lung infection with P. aeruginosa
        
        Increase sputum viscosity and need for high consumption of 02
    - - Young children with coughing thick, tenacious sputum, recurrent pulmonary infection, and recurrent bronchitis
      - Dyspnea, tachypnea, sternal retraction, unequal breath sounds, moist basilar crackles and rhonchi, barrel chest
      - Diagnostic tests are positive for pilocarpine iontophoresis, genetic test, 72 hour stool collection, arterial blood gas, decreased vital capacity, decreased airflow rate, increased airway resistance, patchy atelectasis, bronchiectasis, cystic lung fields, peribronchial thickening
    - - Antibiotic, chest physical therapy, mucolytic agent and pancreatic enzyme replacement, nutritional therapy
- - - - Aspiration (atypical)
      - Inhalation (typical)
      - Contamination from the systemic circulation
    - - Breaching of the defense mechanism
        
        Multiplying and triggering pulmonary inflammation
        
        A “red hepatization” stage follows and is marked by the filling of alveoli with fibrinous exudates
        
        Cells degenerate with cell death. Eventually, the bacteria are opsonized by WBCs, a yellow exudate forms, these exudates are then absorbed, and resolution begins.
        
        Recent infection shows rapid filling of the alveolar capillaries with a frothy, serous, and blood-tinged fluid.
    - - Chill, fever, severe malaise, purulent sputum, coughs, patchy Xray
      - To treat or optimize ventilation and diffusion
        
        Possible admission to administer appropriate antibiotic, rehydrate, chest physiotherapy, deep breathing, sputum expectoration
- - - - Causes by severe trauma, burn, sepsis, aspiration of gastric acid, shock , drug overdose, inhaled toxin like smoke inhalation
      - Triggers cause the immune system to activate the complement system and to initiate neutrophil sequestration in the lung
        
        Increased permeability of the pulmonary vascular and flooding of the alveoli with proteinaceous fluid
        
        Edema fluid accumulation and surfactant inactivation
        
        Hyaline membrane forming causing impaired gas exchange and profound hypoxia
        
        Onset of symptoms within 12 to 18 hours of triggers
        
        Coughs, dyspnea, sputum production, hypoxemia, increase heart rate, +crackles and rhonchi to respiratory failure
    - - -Refractory hypoxemia
        -ABG gas showing hypoxia, acidosis, and hypercapnia
        -diffuse white-out in XRAY
        
        Identify the underlying cause and address it
        
        Provide adequate oxygen with a ventilator
- - - - C/o Chest pain, dyspnea, blood-streaked sputum, and increased shallow respiratory rate
        
        Diagnosis test: Va/Q lung scan, ABG, ECG, Chest XRAY, cardiac enzyme
    - - Thrombi from LE to emboli lodge in pulmonary vasculature
      - Occlusion causes high pulmonary arterial pressure due to vasoconstriction
      - Increased alveolar dead space from vascular obstruction and hypoxemia from right-to-left shunting.
      - Impaired transfer of carbon monoxide due to loss of gas exchange surface
      - Right-sided failure followed with hypotension
      - Hypoxemia due to impaired gas exchange
    - - Venous stasis due to prolonged bed rest, venous endothelial injury, and hyper-coagulability state
    - - AROM, heparin, lovenox, pneumatic leg compression, hydration
    - - Thrombolysis, embolectomy, and caval filters