Pulmonary Diseases Flashcards
Chronic Bronchitis: Epi
Smokers
Chronic Bronchitis: Symptoms
Wheeze, productive cough, dyspnea (especially exertional), muscular wasting
Chronic Bronchitis: Signs/Dx Criteria
Airway edema + fibrosis, cyanosis, hyperinflation, ↓breath sounds, black lung fields on CT, reduced FEV1/FVC ratio (<70% exp.), impaired gas exchange (V/Q mismatch), ↑ dead space, hypoventilation
Chronic Bronchitis: Type
Obstructive (COPD)
Chronic Bronchitis: Pathophysiology
Hypertrophy of mucus glands + goblet cells in bronchioles, basement memb thickening
Chronic Bronchitis: Etiologies
Smoking exacerbates
Chronic Bronchitis: Treatment
Stage I: risk factor reduction, flu/pneumo vaccine, SABA. Stage II: LABA, rehab. Stage III: inhaled corticosteroids. Stage IV: long-term O2 therapy, surgery. SMOKING CESSATION!
Emphysema (Centriacinar): Epi
Smokers
Emphysema (Centriacinar): Symptoms
Wheeze, productive cough, dyspnea (especially exertional), muscular wasting
Emphysema (Centriacinar): Signs/Dx Criteria
Airway edema + fibrosis, cyanosis, hyperinflation, ↓breath sounds, black lung fields on CT, reduced FEV1/FVC ratio (<70% exp.), impaired gas exchange (V/Q mismatch), ↑ dead space, hypoventilation
Emphysema (Centriacinar): Type
Obstructive (COPD)
Emphysema (Centriacinar): Pathophysiology
Destruction of acinar walls by ↑elastase activity → loss of radial traction, increased lung compliance
Emphysema (Centriacinar): Etiologies
Smoking, mostly affects upper lobe, spares alveoli
Emphysema (Centriacinar): Treatment
Stage I: risk factor reduction, flu/pneumo vaccine, SABA. Stage II: LABA, rehab. Stage III: inhaled corticosteroids. Stage IV: long-term O2 therapy, surgery. SMOKING CESSATION!
α1-Antitrypsin (AAT) Deficiency (aka Panacinar Emphysema): Epi
2% of COPD pts
α1-Antitrypsin (AAT) Deficiency (aka Panacinar Emphysema): Symptoms
Wheeze, productive cough, dyspnea (especially exertional), muscular wasting
α1-Antitrypsin (AAT) Deficiency (aka Panacinar Emphysema): Signs/Dx Criteria
Airway edema + fibrosis, cyanosis, hyperinflation, ↓breath sounds, black lung fields on CT, reduced FEV1/FVC ratio (<70% exp.), impaired gas exchange (V/Q mismatch), ↑ dead space, hypoventilation
α1-Antitrypsin (AAT) Deficiency (aka Panacinar Emphysema): Type
Obstructive (COPD)
α1-Antitrypsin (AAT) Deficiency (aka Panacinar Emphysema): Pathophysiology
Congenital cause of COPD; autosomal co-dominant, mutation in SERPINA1 gene leads to excess protease activity, increased lung compliance
α1-Antitrypsin (AAT) Deficiency (aka Panacinar Emphysema): Etiologies
Mostly affects lower lobes
α1-Antitrypsin (AAT) Deficiency (aka Panacinar Emphysema): Treatment
Same + IV pooled AAT
Bronchiectasis: Symptoms
Hemoptysis, productive cough
Bronchiectasis: Signs/Dx Criteria
Soap bubble appearance on CXR, PMNs and mucus in airways on histology
Bronchiectasis: Type
Obstructive (COPD)
Bronchiectasis: Pathophysiology
Chronic necrotizing infection of bronchi → permanently dilated airways, hemoptysis
Bronchiectasis: Etiologies
Bronchial obstruction, Kartagener’s, smoking, CF
Bronchiectasis: Treatment
Treat underlying cause
Bronchiolitis: Signs/Dx Criteria
Evidence of fibrosis, inflammation on histology
Bronchiolitis: Type
Obstructive (COPD)
Bronchiolitis: Pathophysiology
Inflammation of bronchioles, fibrosis
Bronchiolitis: Etiologies
RSV, allergic / hypersensitivity
Bronchiolitis: Treatment
Treat underlying cause
Bronchiolitis Obliterans: Signs/Dx Criteria
Evidence of fibrosis, inflammation on histology
Bronchiolitis Obliterans: Type
Obstructive (COPD)
Bronchiolitis Obliterans: Pathophysiology
Inflammation of bronchioles, fibrosis
Bronchiolitis Obliterans: Etiologies
Lung transplant, CTD
Bronchiolitis Obliterans: Treatment
Treat underlying cause
Asthma: Epi
Clean kids
Asthma: Symptoms
Wheeze, cough, chest tightness during attacks
Asthma: Signs/Dx Criteria
Decline in FEV1 of 20% from baseline, pulsus paradoxus, hypoxemia, hyperinflation, thick wall/narrow lumen, mucus plugging
Asthma: Type
Obstructive (COPD)
Asthma: Pathophysiology
Airflow obstruction (reversible), bronchial hyperresponsiveness, V/Q mismatch during attacks, alveolar hyperventilation during attacks (hypoventilation if severe, due to fatigue + dead space); Th2 phenotype
Asthma: Etiologies
Genetic (FCεR1, CD14, IL-4, IFN, etc.), environment (URIs, stress, allergen re-exposure), prenatal exposures
Asthma: Treatment
Inhaled corticosteroids, LABAs; O2 / intubation if severe; Omalizumab is useful in high-risk pts, binds all circulating IgE, blocks mast cell cross-linking without affecting complement
Idiopathic Pulmonary Fibrosis (IPF) / Usual Interstitial Pneumonia (UIP): Epi
Older male smoker with fam. Hx
Idiopathic Pulmonary Fibrosis (IPF) / Usual Interstitial Pneumonia (UIP): Symptoms
Dyspnea (exertional), dry cough
Idiopathic Pulmonary Fibrosis (IPF) / Usual Interstitial Pneumonia (UIP): Signs/Dx Criteria
Clubbing, hypoxemia, bibasilar crackles, impaired gas exchange, dermatomyositis, Raynaud’s, sclerodactyly, positive six-minute walk test, ground glass opacity/reticular opacity/honeycombing, TLC < 75% expected
Idiopathic Pulmonary Fibrosis (IPF) / Usual Interstitial Pneumonia (UIP): Type
Restrictive (ILD)
Idiopathic Pulmonary Fibrosis (IPF) / Usual Interstitial Pneumonia (UIP): Pathophysiology
Fibrosis and thickening of alveolar walls and interstitium, honeycomb lung appearance, bases>apices
Idiopathic Pulmonary Fibrosis (IPF) / Usual Interstitial Pneumonia (UIP): Etiologies
Idiopathic; can also have drug-induced, radiation-related, or connective tissue disease-related ILD
Idiopathic Pulmonary Fibrosis (IPF) / Usual Interstitial Pneumonia (UIP): Treatment
O2, pulmonary rehab, avoid lung injury / antigen, anti-inflammatory therapy (corticosteroids), lung transplant
Pneumonoconiosis: Epi
Workers
Pneumonoconiosis: Symptoms
Dyspnea (exertional), dry cough
Pneumonoconiosis: Signs/Dx Criteria
Clubbing, hypoxemia, bibasilar crackles, impaired gas exchange, dermatomyositis, Raynaud’s, sclerodactyly, positive six-minute walk test, ground glass opacity/reticular opacity/honeycombing, TLC < 75% expected
Pneumonoconiosis: Type
Restrictive (ILD)
Pneumonoconiosis: Pathophysiology
Inorganic antigen leads to inflammation
Pneumonoconiosis: Etiologies
Silicosis, asbestosis
Pneumonoconiosis: Treatment
O2, pulmonary rehab, avoid lung injury / antigen, anti-inflammatory therapy (corticosteroids), lung transplant
Sarcoidosis: Epi
N. Europe, Af-Am
Sarcoidosis: Symptoms
Dyspnea (exertional), dry cough
Sarcoidosis: Signs/Dx Criteria
Clubbing, hypoxemia, bibasilar crackles, impaired gas exchange, dermatomyositis, Raynaud’s, sclerodactyly, positive six-minute walk test, ground glass opacity/reticular opacity/honeycombing, TLC < 75% expected
Sarcoidosis: Type
Restrictive (ILD)
Sarcoidosis: Pathophysiology
Systemic non-necrotizing granulomatous disease, usually near airways; multi-system, can also get skin plaques, lupus pernio, uveitis with synechiae, hilar adenopathy on CXR
Sarcoidosis: Etiologies
Unknown; often reversible
Sarcoidosis: Treatment
O2, pulmonary rehab, avoid lung injury / antigen, anti-inflammatory therapy (corticosteroids), lung transplant
Hypersensitivity Pneumonitis: Epi
BIRDS
Hypersensitivity Pneumonitis: Symptoms
Dyspnea (exertional), dry cough
Hypersensitivity Pneumonitis: Signs/Dx Criteria
Clubbing, hypoxemia, bibasilar crackles, impaired gas exchange, dermatomyositis, Raynaud’s, sclerodactyly, positive six-minute walk test, ground glass opacity/reticular opacity/honeycombing, TLC < 75% expected
Hypersensitivity Pneumonitis: Type
Restrictive (ILD)
Hypersensitivity Pneumonitis: Pathophysiology
CD4+ Th1 humoral immune response overreacts, leading to Type III + IV hypersensitivity, centrilobular nodules, airway thickening + fibrosis
Hypersensitivity Pneumonitis: Etiologies
Birds, fungi, bacteria, chemicals
Hypersensitivity Pneumonitis: Treatment
O2, pulmonary rehab, avoid lung injury / antigen, anti-inflammatory therapy (corticosteroids), lung transplant
ARDS (Acute RDS): Symptoms
Acute onset tachypnea, dyspnea
ARDS (Acute RDS): Signs/Dx Criteria
Hyaline membranes, hypoxemia, diffuse crackles, bilateral infiltrates, consolidation
ARDS (Acute RDS): Type
Restrictive (Resp. Failure)
ARDS (Acute RDS): Pathophysiology
Diffuse alveolar damage, ↑alveolar capillary permeability, inflammatory injury from neutrophils, necrosis lead to hyaline membranes
ARDS (Acute RDS): Etiologies
Pulmonary infxn, shock, sepsis, burns, near-drowning, etc.
ARDS (Acute RDS): Treatment
Treat underlying cause, lung protective ventilation (6cc/kg VT), max plateau of 30cm H2O, conservative fluids, ECMO
NRDS (Neonatal RDS): Epi
Premie
NRDS (Neonatal RDS): Symptoms
Dyspnea, hypoxia
NRDS (Neonatal RDS): Signs/Dx Criteria
Hyaline membranes, hypoxemia, diffuse crackles, bilateral infiltrates, consolidation
NRDS (Neonatal RDS): Type
Restrictive (Resp. Failure)
NRDS (Neonatal RDS): Pathophysiology
Congenital surfactant deficiency, alveolar collapse
NRDS (Neonatal RDS): Etiologies
Maternal diabetes, C-section, premature
NRDS (Neonatal RDS): Treatment
Maternal steroids, artificial surfactant
Guillain-Barre: Symptoms
Dyspnea, tachypnea
Guillain-Barre: Signs/Dx Criteria
Respiratory failure, restrictive ventilatory defect, hypoxia, hypercapnia, respiratory acidosis