MS UNIT 5 PT.5

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Last updated 11:24 PM on 10/19/26
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59 Terms

1
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neutrophils, CD8+ T-lymphocytes, and macrophages

which inflammatory cells dominate the chronic inflammatory response in COPD

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excess mucus production and airway plugging

in COPD, Bronchial submucosal glands enlarge, leading to ____

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elastin in alveolar septa

Destruction of ____ decreases the natural elasticity of the lungs and removes radial traction on small bronchioles

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radial support

During exhalation of COPD, the loss of _____ causes airways to collapse prematurely, trapping air within the distal air spaces (hyperinflation)

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Alveolar wall destruction

____ reduces the capillary bed surface area needed for gas exchange, causing severe Ventilation-Perfusion (V/Q) mismatching

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Ventilation-Perfusion (V/Q) mismatching

Alveolar wall destruction reduces the capillary bed surface area needed for gas exchange, causing severe ____

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Chronic hypoxia

____ causes reactive pulmonary vasoconstriction, leading to pulmonary arterial hypertension and eventually Cor Pulmonale (right ventricular enlargement and failure)

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Cor Pulmonale

Chronic hypoxia causes reactive pulmonary vasoconstriction, leading to pulmonary arterial hypertension and eventually ___ (right ventricular enlargement and failure)

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post-bronchodilator spirometry

In COPD, diagnosis requires ____ demonstrating persistent airflow obstruction

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FEV1/FVC <0.70 (70%)

Establishes the presence of non-reversible airflow limitation

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Decreased FEV1

Quantifies the severity of airflow obstruction

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Decreased FEV1

categorized under GOLD grades 1 through 4

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Increased Total Lung Capacity (TLC) & Residual Volume (RV)

Indicates severe air trapping and pulmonary hyperinflation

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Spirometry/PFTS

Golden standard of COPD

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Post-bronchodilator FEV₁/FVC < 0.70

What spirometry finding confirms persistent airflow obstruction in COPD?

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Spirometry/PFTS

Confirms diagnosis and establishes disease baseline.

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Arterial Blood Gas (ABG)

Assesses severity of hypoxemia, hypercapnia, and acid-base status

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Chest X-Ray (CXR)

Rules out differential diagnoses (e.g., pneumonia, heart failure, lung cancer).

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Centrilobular or panlobular bullae, parenchymal destruction

High-Resolution CT (HRCT) findings for COPD

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High-Resolution CT (HRCT)

Determines exact anatomical distribution and candidate suitability for surgical volume reduction.

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Levels < 11 umol/L

Serum A1-Antitrypsin findings for COPD

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Serum A1-Antitrypsin

Recommended for young patients (<45 years) or non-smokers presenting with emphysema

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Progressive Dyspnea

Persistent, exertional dyspnea that progresses over years to occur at rest.

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clear, mucoid, or purulent sputum

in COPD, Cough may be intermittent or daily, often productive of _____.

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long-term hyperinflation

in COPD, Increased anteroposterior (AP) to transverse chest diameter (1:1 ratio) caused by ____

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Pursed-Lip Breathing

Exhaling against partially closed lips to maintain positive end-expiratory pressure, preventing small airway collapse during exhalation.

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Use of Accessory Muscles & Tripod Position

Leaning forward with hands resting on knees or thighs to optimize diaphragmatic excursion

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Hyperresonant chest percussion, distant heart sounds, diminished breath sounds, coarse rhonchi, or expiratory wheezes

Physical Exam Findings of COPD

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Smoking Cessation

The most impactful intervention to halt the decline in lung function.

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Short-Acting Bronchodilators (SABA / SAMA): Albuterol, Ipratropium

used for acute symptom control in COPD

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Long-Acting Bronchodilators (LABA / LAMA): Formoterol, Salmeterol, Tiotropium

used for daily maintenance in COPD

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Inhaled Corticosteroids (ICS)

Added to LABA/LAMA for patients experiencing frequent acute exacerbation

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Phosphodiesterase-4 (PDE-4) Inhibitors (Roflumilast)

used to decrease exacerbations in severe chronic bronchitis.

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PaO2 < 55mmHg or SpO2 < 88%

Oxygen therapy is indicated for resting hypoxemia (PaO2____ or SpO2 ___).

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Low-flow supplemental oxygen (1-2 L/min)

it reduces mortality, pulmonary vascular resistance, and secondary erythrocytosis

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Annual influenza vaccination and pneumococcal vaccines (PPSV23 / PCV20)

used to to prevent infection-triggered exacerbations in COPD

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Lung Volume Reduction Surgery (LVRS)

 Resection of 20% to 30% of hyperinflated, diseased lung tissue to improve chest wall mechanics and diaphragmatic function.

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Bullectomy

Surgical excision of large, non-functional air pockets compressing healthy lung parenchyma

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Bronchoscopic Lung Volume Reduction (Endobronchial Valves)

One-way valves inserted via bronchoscope into target airways to collapse hyperinflated lobes without open surgery

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Lung Transplantation

Indicated for severe, end-stage COPD in selected candidates refractory to all medical interventions

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carbonated beverages or gas-forming

for COPD, advise avoiding ____ foods that distend the stomach and compress the diaphragm

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Primary Pathology: Permanent destruction of alveolar septa and elastic recoil.

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Primary Clinical Appearance: Mild/absent cyanosis; pink/flushed skin due to compensatory hyperventilation

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Body Habits: Often thin, emaciated, or cachectic with marked weight loss

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Dyspnea: Severe and progressive dyspnea, even at rest

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Cough & Sputum: Minimal cough; scanty or non-productive sputum.

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Arterial Blood Gases (ABGs): Near-normal PaO2 until late stages; normal or low PaCO2 (compensated hyperventilation)

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Chest Configuration: Classic Barrel Chest (increased 1:1 AP-to-transverse diameter) due to air trapping.

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Breathing Technique: Marked pursed-lip breathing and use of accessory muscles (tripod position)

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“PINK PUFFER” (PRIMARY EMPHYSEMA)

Complications: Cor Pulmonale appears only in end-stage disease; bullae/spontaneous pneumothorax risk.

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Primary Pathology: Chronic mucosal inflammation, hypersecretion of mucus, and bronchial obstruction

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Primary Clinical Appearance: Prominent cyanosis (bluish tint to skin and mucous membranes) due to severe hypoxia

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Body Habits: Frequently stocky, overweight, or obese with peripheral edema.

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Dyspnea: Moderate dyspnea; less prominent than in pure emphysema.

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Cough & Sputum: Severe, chronic productive cough with abundant mucoid/purulent  sputum.

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Arterial Blood Gases (ABGs): Marked hypoxemia (low PaO2) and chronic hypercapnia (elevated PaCO2).

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Chest Configuration: Normal or slightly increased chest AP diameter.

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Breathing Technique: Shallow respiration; less dependence on pursed-lip breathing

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“BLUE BLOATER” (PRIMARY CHRONIC BRONCHITIS)

Complications: Early onset of Cor Pulmonale (right-sided heart failure), secondary polycythemia, and peripheral edema