06: Lung Pathology Overview

Question 1

Diseases of the conducting airways

Answer 1

• Bronchi: bronchiectasis, chronic bronchitis
• Bronchioles: asthma, other injuries (inflammatory, fibrotic)
• Respiratory bronchiole and alveoli: emphysema

Question 2

Diseases of the alveoli and interstitium

Answer 2

• Alveoli
  
  • Luminal filling: pulmonary edema, pneumonia, hemorrhage, ARDS
  • Interstitial thickening (fibrosis/inflammation): usual interstitial pneumonia, sarcoidosis, hypersensitivity pneumonitis

Question 3

Bronchiectasis

Answer 3

• Permanent dilation of bronchi and bronchioles due to destruction of elastic tissue and muscle
• Gross path: dilated bronchi filled w/ mucus or acute inflammation (purulent/cloudy material), lower lobes more than upper lobes
• Microscopy: acute and chronic inflammation, variable degrees of fibrosis, dilated airways
• Disease associations: cystic fibrosis, foreign body impaction, chronic bronchitis with repeated infection, immotile cilia

Question 4

Chronic bronchitis

Answer 4

• Persistent cough w/ sputum production for 3 months in two consecutive years
• Often due to smoking
• Often results in repeated infections
• Gross path: brown discolored, mucus filled bronchi
• Microscopic: bronchial gland hyperplasia, goblet cell metaplasia, chronic inflammation, fibrosis of bronchiolar walls, loss of cilia/squamous metaplasia
• Functional significance: airway resistance (due to mucus/edema/narrowing) –> obstructive lung dz; lung capacity normal (alveolar zones unaffected)

Question 5

Asthma

Answer 5

• Chronic inflammatory disorder of airways characterized by airway hyperresponsiveness, airflow obstruction and clinical sx
• Acute bronchospasm usually reversible (allergic trigger, non-allergic airway hyper-responsiveness [e.g., medications, exercise])
• Gross pathology: hyperinflation, mucus plugging
• Microscopic: smooth muscle hypertrophy, inflammation, eosinophils, basement membrane thickening, edema
• Functional significance: ↑total lung capacity during attack, work of breathing increased 2/2 airway resistance (remodeling, mucus, inflammation, edema), obstructive lung dz

Question 6

Bronchiolitis

Answer 6

• Inflammation of bronchioles
• Infectious (viral), allergic/hypersensitivity
• Resolveable

Question 7

Bronchiolar fibrosis

Answer 7

• Smoke inhalation
• Connective tissue dz
• Post-lung transplant (constrictive bronchiolitis/bronchiolitis obliterans)
• Unresolveable

Question 8

Emphysema

Answer 8

• Obstructive disease
• Destruction of bronchiolar/alveolar wall
• Classified by pattern/location of damage within the respiratory acinus
  
  • Centriacinar emphysema: 2/2 smoking (causes acquired deactivation of A1AT); damage is to respiratory bronchiole; when severe dz, whole acinus involved; upper lobes, especially apical portions most affected
  • Panacinar emphysema: 2/2 alpha-1 antitrypsin deficiency (genetic); damage to entire acinar unit, from respiratory bronchiole to alveolar sac; more severe at bases, but more diffuse than CLE; smoking exacerbates
• Gross pathology: irregularly dilated airspaces, thin-walled and grossly apparent
• Microscopic: dilated alveoli, anthracotic pigment
• Functional significance: ↑TLC, ↑lung compliance (elastin destruction), mild V/Q mismatch (airway & capillary destruction), recoil decreased –> loss of radial traction, worse on forced experiation –> OVD

Question 9

Pulmonary edema

Answer 9

• Increased hydrostatic pressure due to left-sided heart dz, although can occur from non-cardiac causes
• Gross pathology: heavy lungs wet with frothy fluid
• Microscopic: edema fluid in alveoli spaces, more severe in lower lobes (alveolar walls congested), hyaline membranes

Question 10

Pneumonia

Answer 10

• Inflammation of lung, often infectious; replacement of air with fluid, inflammatory cells or cellular debris
• Gross pathology: consolidation of lungs (firmness), either small patches or lobar
• Microscopic: acute bacterial pneumonia (lobar or patchy) characterized by PMNs filling alveolar space

Question 11

Pulmonary hemorrhage

Answer 11

• Filling of alveolar spaces with blood, often fibrin; if repeated, hemosiderin deposition reflects chronic component
• Gross pathology: blood filled, dark red
• Microscopic: alveoli filled with blood, fibrin and if recurrent, hemosiderin (iron)
• Causes: Goodpasture’s syndrome (immunologic), **pulmonary vasculutis **(blood vessel inflammation), structural lesions with vascular erosion, trauma

Question 12

Adult respiratory distress syndrome/diffuse alveolar damage

Answer 12

• Acute alveolar injury with microvascular damage leading to edema and tissue injury
• Many causes, including pulmonary infx, shock, sepsis, pancreatitis, burns, toxic inhalations, radiation, near-drowning

Question 13

Pulmonary embolism

Answer 13

• Obstruction of pulmonary artery usually by thrombus (also by fat, bone marrow, cancer)
• Pulmonary infarct results from coagulative necrosis due to ischemic injury (loss of blood flow) to lung tissue
• Pathology: majority arise from DVT, can occlude pulmonary artery at bifurcation (saddle embolus) or pulmonary artery branches; results in infarct 10% of time, which are usually hemorrhagic; small emboli organize and recanalize; chronic PE can lead to pulmonary hypertension

Question 14

Pulmonary hypertension

Answer 14

• Abnormal elevation in blood pressure in pulmonary arterial circulation
• Gross pathology: pulmonary artery atherosclerosis and dilatation, RV hypertrophy and dilatation depending on time course of dz
• Microscopic: progressive abnormalities reflect severity and duration of HTN
  
  • Grade 1: hypertrophy of medial smooth muscle
  • Grade 2: intimal proliferation
  • Grade 3: intimal proliferation + fibrosis and luminal narrowing
  • Grade 4, 5: complex lesions w/ network of capillary-like channels, angiomatous and cavernous lesions
  • Grade 6: necrosis of vessel wall

Question 15

Vasculutis

Answer 15

• Inflammation of pulmonary blood vessels
• Primary: immune-mediated
• Secondary: infectious