Lung Flashcards
One-sentence summary of asthma pathogenesis
Widespread reversible narrowing of the airways that changes in severity over short periods of time
Asthma pathogenesis (immediate and late phase)
Sensitisation to allergen; followed by…
Immediate phase = mast cell degranulation –> mediator release –> inc. vascular permeability, eosinophil and mast cell recruitment and bronchospasm
Late phase = tissue damage, increased mucous production, muscle hypertrophy
Histological features of asthma
Hyperaemia Eosinophils w/ Charcot Leyden crystals Goblet cell hyperplasia Hypertrophic constricted muscle Mucus plugging (may be spiral-shaped- Curschmann's spiral) Inflammation
COPD definition
Chronic cough productive of sputum; most days for ≥3 months over ≥2 consecutive years
One-sentence summary of COPD pathogenesis
Chronic injury to airways elicits local inflammation and reactive changes
Histological features of COPD
Dilatation of airways
Hypertrophy of mucous glands
Goblet cell hyperplasia
One-sentence summary of bronchiectasis pathogenesis
Permanent abnormal dilatation of the terminal bronchi
Causes of bronchiectasis
Congenital (CF, ciliary dyskinesia [i.e. Kartagener’s syndrome])
Inflammatory (post-infectious, obstruction, 2nd to bronchiolar disease and interstitial fibrosis, asthma)
Pathophysiology of CF
Autosomal recessive
CFTR gene on Chr 7 –> abnormal –> defective Cl- ion transfer so less water transfer to secretions
S/S affect all organs (from abnormally thick secretions)
Histological features of pulmonary oedema
Intra-alveolar fluid on histology
“Heart failure cells” = iron-laden macrophages
Histological features of ARDS and RDS
Basic pathology the same = diffuse alveolar damage
Gross pathology: Fluffy white infiltrates in all lung fields Lungs expanded/firm Plum-coloured lungs, airless >1kg mass
Micro-pathology:
1. Capillary congestion 2. Exudative phase 3. Hyaline membranes 4. Organising phase
Pathology and organisms of bronchopneumonia
Low virulence organisms (staph, H. influenzae, strep, pneumococcus)
Pathology = patchy bronchial and peribronchial distribution, lower lobes, inflammation surrounding the airways themselves and is within the alveoli
Pathology and organisms of lobar pneumonia
Affects entire lobe; infrequent due to ABx; 90-95% pneumococci (i.e. strep)
Stages of lobar pneumonia:
(1) Congestion Hyperaemia, Intra-alveolar fluid
(2) Red hepatization Hyperaemia, Intra-alveolar neutrophils (non-atypical)
(3) Grey hepatization Intra-alveolar connective tissue
(4) Resolution Restoration of normal architecture
Pathology and organisms of atypical pneumonia
Mycoplasma, viruses (CMV, influenza), Coxiella, chlamydia, etc. i.e. CMV pneumonia in those immunosuppressed
Interstitial inflammation without the accumulation of intra-alveolar inflammatory cells
Chronic inflammatory cells within alveolar septa with oedema ± viral infections
What type of alveolar parenchyma loss is caused by smoking?
Centred on bronchioles- centrilobular
What type of alveolar parenchyma loss is caused by alpha-1 antitrypsin deficiency?
Diffuse loss- panacinar
What is a granuloma?
Collection of histiocytes, macrophages ± giant multinucleate cells
Pathogenesis of sarcoidosis
Abnormal host immunological response to variety of commonly encountered antigens, probably environmental in origin
Lung pathology of sarcoidosis
Discrete epithelioid and giant cell granulomas, preferential distribution in upper zones with a tendency to peri-lymphatic and peri-bronchial –> advanced disease becomes fibrocystic
Diagnostic features of sarcoidosis
Non-caseating granuloma, elevated serum ACE, hypercalcaemia (1a-hydroxylase)
Presentation of pulmonary vasculitis
Present as life threatening haemorrhage, chronic haemoptysis, mass lesion, interstitial lung disease
Match the site of origin to the type of lung cancer:
Airways, pleura, central/peripheral, peripheral alveolar spaces
Adenocarcinoma, mesothelioma, SCLC, SCC
Airways (SCC)
Peripheral alveolar spaces (Adenocarcinoma)
SCLC can arise either centrally or peripherally
Mesothelioma is a tumour of the pleura
Name a benign lung tumour
Chondroma
Pathogenesis of SCC
Squamous epithelium is much more resilient, but it does NOT have cilia –> leads to a build-up of mucus
Within this mucus, you will get loads of carcinogens –> more carcinogens accumulate
Normal epithelium –> hyperplasia –> squamous metaplasia –> dysplasia –> carcinoma in situ –> invasive carcinoma
