Chapter 21_2 flashcards

Question 1

Obstructive Pulmonary Disease: Definition & Examples

Answer 1

Characterized by an increase in resistance to airflow from trachea and larger bronchi to terminal/respiratory bronchioles. Examples: Asthma, COPD (Chronic Bronchitis, Emphysema), Bronchiectasis, Sleep-disordered breathing.

Question 2

Restrictive Pulmonary Disease: Definition & Examples

Answer 2

Characterized by reduced expansion of lung tissue, with decreased total lung capacity (TLC). Lungs are stiff and noncompliant. Examples: Pulmonary fibrosis, pneumoconiosis, thoracic cage deformities, pneumothorax, pleural effusion, sarcoidosis.

Question 3

Asthma: Definition & Key Feature

Answer 3

Chronic inflammatory disorder causing reversible airway constriction due to bronchial hyperreactivity. Each attack can lead to inflammatory changes and bronchial remodeling.

Question 4

Asthma: Epidemiology & Disparities

Answer 4

Affects ~25 million in US (8%). More prevalent in children (boys > girls) and adult women. Higher rates in poverty, Black race, and Puerto Rican Hispanic ethnicity. Higher mortality in African Americans. [Text]

Question 5

Asthma: Etiologies/Triggers

Answer 5

Allergies (most common: dust mites, pet dander, pollen, molds), occupational exposures, viral infections (rhinovirus, RSV), GERD (esp. nocturnal asthma), exercise-induced, air pollution, aspirin/NSAID sensitivity (AERD).

Question 6

Asthma: Pathophysiology (Inflammatory Cascade)

Answer 6

Allergens trigger immune response (Th2 cells, IgE, mast cells, eosinophils, basophils). Mast cell degranulation releases histamine (bronchospasm, inflammation) and leukotrienes (bronchoconstriction, hyperreactivity, edema, eosinophilia). T cells release interleukins. Chronic inflammation leads to airway remodeling.

Question 7

Asthma: Airway Remodeling

Answer 7

Pathological changes from chronic inflammation: Hyperplasia of goblet cells (mucus hypersecretion), subepithelial collagen proliferation/fibrosis (stiffens airways), smooth muscle hypertrophy (decreases elasticity/bronchodilation ability). [Text]

Question 8

Asthma: Symptoms

Answer 8

Wheezing, cough, dyspnea, chest tightness. Prolonged exhalations common. Severe attacks: use of accessory muscles, distant breath sounds, diaphoresis, difficulty speaking.

Question 9

Asthma: Diagnosis (PFTs & Other Tests)

Answer 9

PFTs: FEV1 decreases during attack, FEV1/FVC ratio diminishes. Diagnosis often confirmed by >12% and >200mL increase in FEV1 after SABA. Methacholine challenge test (positive if FEV1 drops =20%). FeNO measurement (adjunct for airway inflammation). Sputum/blood eosinophils, IgE levels.

Question 10

Asthma Classifications (NIH/NHLBI 2020 - Box 21-2)

Answer 10

Mild Intermittent, Mild Persistent, Moderate Persistent, Severe Persistent. Based on symptom frequency/severity, nighttime awakenings, SABA use, activity interference, FEV1, FEV1/FVC.

Question 11

Asthma Classification (ATS/ERS - Box 21-3)

Answer 11

Based on “difficulty to treat” (level of treatment needed for control). Mild: controlled with as-needed ICS-formoterol or low-dose ICS + SABA. Moderate: controlled with low/medium-dose ICS-LABA. Severe: uncontrolled despite high-dose ICS-LABA or requires it.

Question 12

Asthma Endotype-Phenotype Classification (Box 21-4)

Answer 12

T2 High Asthma (Allergic/Eosinophilic): Early onset allergic, Late-onset eosinophilic, Aspirin-exacerbated respiratory disease (AERD). Biomarkers: High eosinophils, IgE, FeNO.
T2 Low Asthma (Non-T2/Non-Allergic): Obesity-associated, Smoking-associated (Asthma-COPD overlap), Very late onset. Biomarkers: High neutrophils.

Question 13

Asthma Treatment: Stepwise Approach (GINA 2022 - Fig 21-6)

Answer 13

Goal: Control asthma, prevent exacerbations. Involves patient education, environmental control, comorbidity management, medication. Step up if needed, step down if controlled >3 months.

Question 14

Asthma Treatment: Maintenance (Controller) Medications

Answer 14

Daily use. Preferred: Low-dose Inhaled Corticosteroid (ICS) + Long-Acting Beta-2 Agonist (LABA) like formoterol (e.g., formoterol/budesonide). Alternatives: LAMA (tiotropium), LTRA (montelukast), Theophylline. Immunomodulators (omalizumab) for allergic/severe.

Question 15

Asthma Treatment: Rescue (Reliever) Medications

Answer 15

For acute attacks. Preferred (GINA Track 1): Low-dose ICS-formoterol as needed. Alternative (GINA Track 2): Short-Acting Beta-2 Agonist (SABA, e.g., albuterol) as needed. SABA-only treatment no longer recommended. Cromolyn sodium (mast cell stabilizer).

Question 16

Status Asthmaticus: Definition & Pathophysiology

Answer 16

Persistent bronchoconstriction despite treatment attempts. Severe V-Q mismatching -> dramatic fall in arterial oxygenation. Can lead to cyanosis, CO2 retention, respiratory failure; potentially fatal.

Question 17

Chronic Obstructive Pulmonary Disease (COPD): Definition

Answer 17

Combination of chronic bronchitis, emphysema, and hyperreactive airway disease. Characterized by poorly reversible airflow limitation.

Question 18

COPD: Epidemiology & Major Cause

Answer 18

4th leading cause of death in US. ~16 million diagnosed (likely underreported). Smoking is major cause (also occupational/environmental exposures, AAT deficiency). More women die of COPD than men. [Text]

Question 19

Alpha-1 Antitrypsin (AAT) Deficiency

Answer 19

Genetic predisposition to COPD (rare, <1% of cases). AAT inhibits elastase; deficiency allows elastase to destroy lung tissue, leading to premature emphysema.

Question 20

Chronic Bronchitis in COPD: Characteristics

Answer 20

Hypersecretion of mucus in large/small airways, hypoxia, cyanosis. Cough present for 3 months/year for 2 consecutive years. “Blue Bloater” (cyanosis, edema from RV failure).

Question 21

Emphysema in COPD: Characteristics

Answer 21

Overdistention of alveoli with trapped air, loss of elastic recoil, obstruction to expiratory airflow, high residual CO2. “Pink Puffer” (well-oxygenated until late, pursed-lip breathing). Barrel-shaped chest.

Question 22

COPD: Pathophysiology Summary

Answer 22

Narrowing/fibrosis of bronchioles, excessive mucus (chronic bronchitis). Loss of alveolar elastic recoil, air trapping (emphysema). Smooth muscle hypertrophy. Chronic inflammation -> proteolytic-antiproteolytic imbalance -> alveolar damage.

Question 23

Cor Pulmonale in Severe COPD

Answer 23

Chronic hypoxia -> pulmonary arterial vasoconstriction (pulmonary hypertension) -> increased resistance against Right Ventricle (RV) -> RV hypertrophy and failure (cor pulmonale). Signs: JVD, ascites, hepatosplenomegaly, ankle edema.

Question 24

COPD: Breathing Stimulus Change

Answer 24

In severe COPD with chronic hypercapnia, respiratory center becomes insensitive to high CO2. Hypoxia (low O2) becomes primary stimulus for breathing (hypoxic drive).

Question 25

COPD: Diagnosis (PFTs & Other)

Answer 25

PFTs: FEV1 significantly decreased, FEV1/FVC ratio < 70% (hallmark). COPD Assessment Test (CAT), MRC Dyspnea Scale. Chest x-ray (hyperinflation, flattened diaphragm in emphysema). ABGs (chronic hypercapnia/hypoxia). AAT level for deficiency.

Question 26

COPD Classification (GOLD 2022 - Table 21-1 & Box 21-5)

Answer 26

Severity (GOLD 1-4): Based on post-bronchodilator FEV1. Groups (A, B, C, D): Based on symptom severity (MRC, CAT scores) and exacerbation history, guides treatment.

Question 27

COPD: Treatment

Answer 27

Stepwise approach: SABAs, LABAs, LAMAs, ICS (often in combination inhalers). Smoking cessation, pulmonary rehab, vaccinations (flu, pneumococcal). Oxygen therapy (continuous if PaO2 =55 mmHg or SaO2 =88%). Caution with O2 in chronic hypercapnia (can depress hypoxic drive). Avoid respiratory depressants.

Question 28

Bronchiectasis: Definition & Causes

Answer 28

Uncommon disease. Chronic inflammation and dilatation of bronchi due to untreated infections (Pseudomonas, H. influenzae, S. aureus, viruses, Aspergillus), immune dysregulation, or ciliary dyskinesia. Cystic fibrosis common congenital cause.

Question 29

Bronchiectasis: Pathophysiology & Symptoms

Answer 29

Bronchiole wall destroyed, replaced by fibrous tissue; irreversibly dilated airways contain static, thick, purulent secretions. Symptoms: Persistent cough, purulent sputum, hemoptysis (50-70%), dyspnea, wheezing.

Question 30

Bronchiectasis: Diagnosis & Treatment

Answer 30

Diagnosis: CT scan (shows dilated airways), bronchography, sputum culture, PFTs (obstructive pattern). Treatment: Treat underlying infection (inhaled antibiotics for colonization/recurrent exacerbations - gentamicin, tobramycin), mucolytics, bronchodilators. Avoid long-term ICS/LABA unless concomitant COPD/asthma.

Question 31

Sleep-Disordered Breathing (SDB): Definition & Types

Answer 31

Apnea (reduction in airflow by 90% for =10s) during sleep. Types: Obstructive Sleep Apnea (OSA - intermittent upper airway collapse), Central Sleep Apnea (CSA - loss of respiratory drive from brainstem), or combination. Results in sleep disturbance, daytime sleepiness, hypoxemia.

Question 32

Obstructive Sleep Apnea (OSA): Symptoms & Risk Factors

Answer 32

Symptoms: Loud snoring, choking/gasping during sleep, unrestful sleep, daytime sleepiness. Risk factors: Obesity (most common), nasal blockage, airway anatomy. Worsened by alcohol/sedatives.

Question 33

Sleep-Disordered Breathing: Diagnosis & Treatment

Answer 33

Diagnosis: Sleep study (polysomnography) measures Apnea-Hypopnea Index (AHI). Epworth Sleepiness Scale. Treatment: Behavioral changes (alcohol/smoking cessation, weight loss). CPAP device (prevents airway closing). Oral appliance. Surgery. Hypoglossal nerve stimulation.

Question 34

Pneumothorax (Collapsed Lung): Definition & Types

Answer 34

Presence of air in the pleural cavity, causing collapse of lung tissue. Types: Primary Spontaneous (PSP), Secondary Spontaneous (SSP), Traumatic, Tension, Iatrogenic.

Question 35

Primary Spontaneous Pneumothorax (PSP)

Answer 35

Air in intrapleural space with no preceding trauma or underlying lung disease. Common in tall, young men (10-30 yrs). Etiology unclear, possibly ruptured alveoli (blebs).

Question 36

Secondary Spontaneous Pneumothorax (SSP)

Answer 36

Occurs with underlying lung disease. Air enters pleural space via ruptured blebs (overly distended/damaged alveoli). Emphysema patients at risk. Also TB, sarcoidosis, cystic fibrosis, malignancy, IPF.

Question 37

Traumatic Pneumothorax

Answer 37

Penetrating wound of thoracic cage/pleural membrane (e.g., rib fracture puncturing pleura). Opening between pleural cavity and atmosphere -> air enters pleural space, compresses lung.

Question 38

Tension Pneumothorax

Answer 38

Life-threatening. Escalating air buildup in pleural cavity (closed wound allows air in but not out) -> compresses lung, bronchioles, cardiac structures, vena cava -> inhibits venous return, compromises heart/lung function.

Question 39

Iatrogenic Pneumothorax

Answer 39

Complication of medical/surgical procedures (e.g., transthoracic needle aspiration, thoracentesis, central line insertion).

Question 40

Pneumothorax: Symptoms & Diagnosis

Answer 40

Symptoms: Chest pain, dyspnea, increased respiratory rate. Physical Exam: Asymmetry of chest, retractions, hyperresonance on percussion, lack of breath sounds on affected side. Diagnosis: Chest x-ray (linear shadow of visceral pleura, lack of lung markings peripheral to it, mediastinal shift), CT scan. ABGs/pulse oximetry (hypoxemia).

Question 41

Pneumothorax: Treatment

Answer 41

Small PSP may resolve with O2/observation. Larger/symptomatic: Chest tube with suction to remove air and allow lung re-expansion. Tension pneumothorax: Emergency needle decompression then chest tube. Pleurodesis (intentional pleural irritation to adhere membranes) to prevent recurrence.

Question 42

Pleural Effusion: Definition & Fluid Types

Answer 42

Abnormal collection of fluid in pleural cavity, compressing lung tissue. Fluid may be: Transudate (filtrate of blood, low protein - e.g., CHF, cirrhosis, hypoalbuminemia), Exudate (cloudy, high protein - e.g., infection, inflammation, cancer, PE), Purulent (pus), Lymph (chylothorax), or Sanguineous (bloody).

Question 43

Pleural Effusion: Signs & Diagnosis

Answer 43

Signs: Dyspnea, tachypnea, sharp pleuritic chest pain. Physical Exam: Dullness to percussion, diminished/absent breath sounds over effusion, decreased tactile fremitus. Diagnosis: Chest x-ray, CT, ultrasound. Thoracocentesis for fluid analysis (distinguish transudate/exudate, culture, cytology).

Question 44

Pleuritis (Pleurisy): Definition & Symptom

Answer 44

Inflammation of the pleural membrane. Symptom: Pleuritic chest pain (sharp, worsens with coughing/deep breathing), pleural friction rub on auscultation.

Question 45

Environmental Lung Diseases (Pneumoconioses): General Cause

Answer 45

Exposure to specific airborne agents or particulate air pollution. Macrophages overwhelmed by dust/particles that reach terminal small airways and persist.

Question 46

Coal Worker's Pneumoconiosis (Anthracosis / "Black Lung")

Answer 46

Exposure to coal dust. Ranges from asymptomatic to progressive massive fibrosis. Lungs appear blackened, gray sputum, wheezes, dyspnea. Can occur with air pollution exposure.

Question 47

Asbestosis & Silicosis

Answer 47

Asbestosis: Exposure to asbestos (mineral crystal) -> pulmonary fibrosis (restrictive). Increases lung cancer risk (esp. smokers), mesothelioma. Silicosis: Inhalation of silica (quartz crystal) -> pulmonary fibrosis. Increases TB risk.

Question 48

Thoracic Cage Deformity (Kyphoscoliosis): Effect on Lungs

Answer 48

Kyphosis (cervical curve) + Scoliosis (thoracic twisting). Causes restrictive lung disease due to chest wall rigidity and limited expansion -> hypoventilation, CO2 retention, hypoxemia.

Question 49

Idiopathic Pulmonary Fibrosis (IPF): Pathophysiology & Diagnosis

Answer 49

Restrictive lung disease from repeated lung tissue injury by unidentified agent. Alveoli -> repeated inflammation (alveolitis) -> fibroblastic proliferation & fibrotic changes (stiff lung). Chest x-ray: "ground glass" appearance, later honeycomb. PFTs: restrictive pattern.

Question 50

Hypersensitivity Pneumonitis: Cause & Symptoms

Answer 50

Immunologically mediated lung disorder from prolonged, intense exposure to inhaled organic dusts (bacterial spores, fungi, animal proteins) acting as antigens. Causes alveolar inflammation. Symptoms: Acute attacks of dyspnea, cough, fever, high WBCs (4-6h post-exposure). Prolonged exposure -> pulmonary fibrosis.

Question 51

Pulmonary Edema: Most Common Cause & Pathophysiology

Answer 51

Most common cause: Left Ventricular Failure (LVF). Weakened LV -> blood backs up into LA, pulmonary veins, capillaries -> increased hydrostatic pressure in pulmonary capillaries -> fluid leaks into alveolar interstitial spaces.

Question 52

Pulmonary Edema: Symptoms, Diagnosis, Treatment

Answer 52

Symptoms: Severe respiratory distress, pink frothy sputum, confusion, stupor (if severe hypoxia). Auscultation: Coarse, loud crackles. Diagnosis: Clinical presentation, Chest x-ray (congested vasculature, infiltrates). Treatment: Decrease hydrostatic pressure (treat LVF with diuretics, digitalis, ACE inhibitors), oxygen.

Question 53

Pulmonary Embolism (PE): Definition & Origin

Answer 53

Clot that traveled to pulmonary arterial circulation, causing obstruction. Usually originates as DVT in leg or atrial thrombus in right heart.

Question 54

Pulmonary Embolism (PE): Presentation, Diagnosis, Treatment

Answer 54

Presentation: Often vague, without warning; can be fatal. Cough, dyspnea, chest pain. Diagnosis: D-dimer test (if normal, PE unlikely), CT pulmonary angiography. Treatment: DOACs (first-line), thrombolytics (tPA for hemodynamic instability), anticoagulation for =3 months. Inferior vena cava filter for multiple PEs.

Question 55

Pulmonary Hypertension: Definition & Types

Answer 55

Abnormally high pressure in pulmonary arteries (PAP >25 mmHg at rest or >30 mmHg with exercise). Primary: Genetic, abnormal vessel structure. Secondary: Due to other factors (elevated pulmonary venous pressure, increased flow, obstruction, hypoxemia - e.g., COPD).

Question 56

Pulmonary Hypertension: Pathophysiology (Secondary to Hypoxia) & Symptoms

Answer 56

Chronic hypoxia -> pulmonary arterial vasoconstriction -> increased pulmonary vascular resistance -> increased RV workload -> RV hypertrophy -> RV failure (cor pulmonale). Symptoms: Syncope, dyspnea on exertion, fatigue.

Question 57

Pulmonary Hypertension: Diagnosis & Treatment

Answer 57

Diagnosis: X-ray, echocardiography (preferred screening), Doppler US, right heart catheterization (PAP). PFTs, CT scan. Treatment: Vasodilators (calcium channel blockers, epoprostenol, bosentan, tadalafil, macitentan, selexipag), oxygen. Improve RV function.

Question 58

Adult Respiratory Distress Syndrome (ARDS): Definition

Answer 58

Diffuse alveolar injury, pulmonary capillary damage, bilateral pulmonary infiltrates, and severe hypoxemia in critically ill patients.

Question 59

ARDS: Risk Factors & Pathophysiology

Answer 59

Common risk factor: Sepsis. Also trauma, drug overdose, massive transfusion, pancreatitis, aspiration. Inflammatory trigger -> mediators damage alveolar-capillary membrane -> fluid leaks into alveoli -> alveoli collapse, airways narrow, lung compliance decreases -> severe hypoxemia/hypercapnia. Fibrotic phase possible.

Question 60

ARDS: Defining Feature & Berlin Criteria

Answer 60

Defining feature: Arterial hypoxemia that does NOT improve with oxygen administration. Berlin Criteria: Respiratory symptoms within 1 week of insult, bilateral opacities on CXR (not fully explained by effusion/collapse), respiratory failure not fully explained by cardiac failure/fluid overload, moderate-severe oxygenation impairment (PaO2/FiO2 ratio).

Question 61

ARDS: Diagnosis (ABGs) & Treatment

Answer 61

ABGs: PaO2 =50 mmHg, PaCO2 =50 mmHg (consistent with respiratory failure). Chest X-ray: pulmonary edema. Treatment: Mechanical ventilation (often with sedation/neuromuscular blockade), nutritional support, DVT/GI ulcer prophylaxis. Prone positioning. Possible: Inhaled nitric oxide/prostacyclin, corticosteroids, ECMO.