Lung - Pathology

Acute Lung Injury

Pulmonary edema

ARDS (Diffuse alveolar damage)

Acute interstitial pneumonia

Pulmonary Edema
1. Hemodynamic disturbances( capillary hydrostatic pressure), MCCLVF, Heart failure cells 2. oncotic pressure (Hypoalbuminemia) Renal failure, Malnutrition, Cirrhosis 3. Microvascular injury - capillary permeability, Seen in ARDS following a) Infection -viral pneumonia b) Gases, Aspiration, Drugs--heroin, Paraquat (herbicide) c) Shock, Trauma, Sepsis, DIC

ARDS:
Also known as ***Diffuse Alveolar Damage (DAD) pulmonary edema (protein rich) hyaline membrane disease hypoxemia (refractory to oxygen Rx ) Mortality in 50% of cases Clinical Manifestations: respiratory insufficiency, Cyanosis, arterial hypoxemia multi-organ failure Acute interstitial pneumonia Cause is unknown (Unlike ARDS) but Radiographic and Pathologic features, mortality similar to ARDS

Pulmonary Edema

Exaggerated lobular structures

Pulmonary Edema
Thick Alveolar septa

pink fluid (Pulmonary Edema)

Hemosiderin laden macrophages

ARDS (Diffuse alveolar damage)

Lung - Pathology

Obstructive Pulmonary Diseases

Emphysema
Chronic bronchitis Asthma Bronchiectasis

 Obstructive Pulmonary Diseases

Classical COPDs Emphysema Chronic Bronchitis Obstructive element is also seen in Bronchial Asthma Bronchiectasis

 Emphysema
Irreversible overinflation of air spaces distal to the terminal bronchioles, with destruction of their walls Types: according to distribution within the acinus

Panacinar:
Uniform involvement of the acinus Associated with 1-antitrypsin deficiency

Centriacinar:
Enlargement of central parts of the acinus (respiratory bronchioles and alveolar duct), sparing the peripheral alveoli (distal alveoli) More common and more severe in apical segments of upper lobes In heavy smokers and often associated with Chronic bronchitis

Paraseptal:
Enlargement of the distal parts of the acinus (subpleural), sparing the proximal parts (in adjacent to areas of fibrosis, scarring, or Atelectasis)

Irregular:
No uniform acinar pattern (seen with scarring)

Centriacinar vs. Panacinar

 Pathogenesis Emphysema Protease- Antiprotease Hypothesis (imbalance between proteases and protease-inhibitors) is most important Tobacco Smoking recruits PMNs, macrophages & Releases the proteases (elastase) inactivate alpha-1-antitrypsin Common disease

Age: fifth to eighth decades Clinically:

Dyspnea with prolonged expiration Cough & expectoration (when associated bronchitis) barrel shaped Chest (X-ray finding)- AP diameter

Death is due to
Respiratory failure CHF (Cor pulmonale) Rupture of bullae tension Pneumothorax

Emphysema - Gross
Bullae if rupture tension Pneumothorax ( air in pleural space) Death due to compression great vessels of heart to the point of occlusion

 Chronic Bronchitis Definition : Persistent cough with sputum production for at least 3
months in at least 2 consecutive years Cause : Initiated by smoking (by causing Chronic irritation of the bronchial mucosa) infections are secondary

Pathology: Hypertrophy of mucus glands Hyper secretion of mucus Reid Index = ratio of thickness of mucous gland layer (CD) to the
thickness between the epithelium and the cartilage (AB) (normally 0.4). The closer to 1 means theres an increase in thickness and correlated to progression of disease

Normal CD/AB = 0.4

Chronic Bronchitis
Clinical course
Bronchi & bronchioles are obstructed by mucus plugs bronchiolitis obliterans. In long-standing cases, squamous metaplasia & dysplasia (precancerous) predisposes for squamous cell carcinoma
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Emphysema Slight Cough Blood gas values NORMAL No cyanosis lean forward to breathe easier Diffusing capacity is low Over-distension severe Pink puffers

Chronic Bronchitis Severe cough Hypercapnia & Severe hypoxemia Cyanotic History of recurrent infections Purulent sputum

Blue bloaters

 Bronchial Asthma
Definition :Increased responsiveness of the bronchial tree to various stimuli that results in paroxysms of Bronchospasm reversible bronchospasm later bronchial inflammation, and obstructive lung disease Types : Extrinsic & Intrinsic Pathology of Extrinsic Asthma

Acute response
Starts within minutes and lasts about 6 hours after exposure to allergen IgE cross-linking mast cell release of mediators Results in Bronchospasm (have hard time breathing, edema (due to vascular permeability), increased mucus (causes coughing)

Late phase reaction

persist for 12+ hours & Mediators are mainly from leukocytes (Neutrophils, Eosinophils and Basophils)

Bronchial Asthma
Extrinsic Intrinsic

type-I (IgE-mediated) hyper-sensitivity or allergic reaction Triggered by environmental antigens (dust, pollens, food, ..) family history of Atopy

Not allergic

triggered by respiratory tract infections &drugs (aspirin). No family history

Bronchial Asthma - Pathophysiology

 Bronchial Asthma - Morphology

Occlusion of airways by mucous plugs.

Bronchial walls
Hypertrophy of mucous glands & smooth muscles Eosinophils. Whorled mucous plugs (Curschmanns spirals) Debris of eosinophils (Charcot-Leyden crystals)

Clinically:
Status asthmaticus (severe form of asthma attack) lasts several days respiratory failure and death disease may disappear spontaneously (atopic) Can lead to chronic bronchitis, emphysema & Cor-pulmonale.

Bronchial Asthma

 Bronchiectasis
Infection + permanent dilatation of bronchi Causes:

infections and causes of bronchial obstruction (FB, mucus plugs, tumors, sequestrations, cystic fibrosis) immotile cilia (Kartageners )syndrome (Bronchiectasis, dextrocardia -situs inversus, chronic sinusitis, and infertility)
Clinically:

Chronic cough, productive of purulent sputum Dyspnea and orthopnea in severe cases later obstructive respiratory insufficiency & Corpulmonale

Bronchiectasis Gross

Distended peripheral bronchi (Due to weakening of wall)

Bronchiectasis Gross