Benign Respiratory Pathology Flashcards
Asthma
Chronic inflammatory disorder of the airways. Paroxysmal bronchospasm. Wheeze. Cough. Variable bronchoconstriction that is at least partially reversible. Mucosal inflammation & oedema. Hypertrophic mucous glands & mucus plugs in bronchi. Hyper inflated lungs.
Clinicopathological classification: Atopic , non-atopic, aspirin-induced, allergic bronchopulmonary aspergillosis
Type I hypersensitivity reaction: Allergen - dust, pollen, animal products. Cold, exercise, reparatory infections. Many different cell types and inflammatory mediators involved
Degranulation of IgE bearing mast cells: histamine initiated bronchoconstriction & mucus production obstructing air flow. Eosinophil chemo taxis. Persistent or irreversible changes: bronchiolar wall smooth muscle hypertrophy,
Mucus gland hyperplasia, respiratory bronchiolitis leading to centrilobular emphysema.
Obstructive pulmonary disease
Localised or diffuse obstruction of air flow. Caused by: Tumour or foreign body, Distal alveolar collapse (total) or over expansion (valvular obstruction). Distal retention pneumonitis (endogenous lipid pneumonia) and bronchopneumonia or Distal bronchiectasis (bronchial dilatation): If one bit of lung expandssquishes adjacent bit.
Bronchiectasis
Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue.
Results from chronic necrotizing infection. Rare for now due to antibiotics working. Site: Bronchus/bronchioles.
Cause: Infections. Signs/ symptoms: Cough, fever, copious amounts of foul smelling sputum.
Infections: predisposing conditions e.g. Cystic fibrosis, Primary ciliary dyskinesia, Kartagener syndrome, Bronchial obstruction (tumour or foreign body), Lupus, rheumatoid arthritis, inflammatory bowel disease, GVHD.
May be localised – resectable. Complications - pneumonia, septicaemia, metastatic infection, amyloid
Chronic obstructive pulmonary disease
combination of chronic bronchitis & emphysema
Chronic interstitial lung disease
Very heterogeneous group. Usually diffuse and chronic. Diseases of pulmonary connective tissue and walls of alveoli. Restrictive lung disease.
Causes often unknown. Increased tissue in alveolar-capillary wall. Inflammation + fibrosis.
Signs and symptoms: Decreased lung compliance. Increased gas diffusion distance. Dyspnoea increasing for months to years. Clubbing, fine crackles, dry cough. Interstitial fibrosis and chronic. Inflammation with varying radiological and histological patterns. Common end-stage fibrosed “honeycomb lung”.
Examples: idiopathic pulmonary fibrosis, many pneumoconiosis , sarcoidosis, collagen vascular diseases-associated lung diseases.
Increased tissue in alveolar-capillary wall.
Idiopathic Pulmonary Fibrosis
5000 new cases a year. Affects middle aged/elderly. 5 year survival. Sub pleural, lower lobes affected first and most severely. Adjacent to normal alveolar walls.
Sarcoidosis:
Non-caseating perilymphatic pulmonary granulomas, then fibrosis. Hilar nodes usually involved. Other organs may be affected eg skin, heart, brain. Hypercalcaemia and elevated serum ACE.
Pneumoconiosis.
“Dust diseases”. Non-neoplastic lung diseases due to inhalation of mineral and organic dusts in workplace. Cause a fibrotic/allergic reaction. Have to be <3um small.
Silicosis
Silica: sand and stone dust. It kills phagocytosing macrophages, when they die they form fibrosis. Also can reactivate TB. Increased risk of lung carcinoma. Can get mixed dust pneumoconiosis (miners getting this dust too.)
Hypersensitivity Pneumonitis:
Extrinsic allergic alveolitis. Type III hypersensitivity reaction organic dusts. Farmer’s lung: actinomycetes in hay, Pigeon Fancier’s lung: pigeon antigens. Repeated episodes lead
Acute interstitial lung disease:
Diffuse alveolar damage- exudate and death of type 1 pneumocytes form hyaline membranes lining the alveoli followed by type II pneumocyte hyperplasia. Histologically acute interstitial pneumonia.
Adult respiratory distress syndrome: (shock lung) shock, trauma, infections, smoke, toxic gases, oxygen, radiation.
Cystic fibrosis
Mostly affects Caucasians. Fluid secretion in exocrine glands and epithelial lining of resp, GI & reproductive organs.
Bronchioles distended with mucus, hyperplasia mucus secreting glands. Multiple repeated infections. Severe chronic bronchitis and bronchiectasis. Exocrine gland ducts plugged by mucus. Atrophy and fibrosis of gland. Impaired fat absorption. Small bowel: mucus plugging meconium ileus. Liver: plugging of bile canaliculi cirrhosis. 95% males infertile. Median survival 41 years in UK.
Atopic asthma
Children & young adults. Common: 33.9% UK children 12-14 years with “wheeze” in 2002. 1 in 10 UK children diagnosed with asthma. 590,000 teenagers. 9 – 15% adult onset asthma is occupational. The commonest occupational lung disease.
Chronic bronchitis
cough & sputum for 3 months in each of 2 consecutive years. Site: Bronchus.
Cause: Chronic irritation: Smoking & air pollution Middle aged & old. 1 in 20 of >65yr consult GP per year.
Pathology: Mucus gland hyperplasia and hypersecretion, secondary infection by low virulence bacteria, chronic inflammation. Chronic inflammation of small airways of the lung causes wall weakness & destruction thus centrilobular emphysema.
40-45, mile late in disease, common infections, large heart –> blue bloater
Emphysema – Classification
Centrilobular (centiacinar) caused by Coal dust and smoking.
Panlobular (panacinar) - >80% a1 antitrypsin deficient (rare, autosomal dominant) , severest in lower lobe bases
Paraseptal (distal acinar) - Upper lobe sub pleural bullae adjacent to fibrosis. Pneumothorax if rupture
Site: Acinar of the alveoli. Symptoms: Dyspnoea: progressive and worsening.
50-75, severe early in disease, rare infections and small heart, hyper inflated lungs pink puffer. Compensation depends on 20+ years underground, whether smoked or not etc.
