Flashcards in 15+16 Respiratory pathology Deck (58):
Differentiate between Type 1 and Type 2 respiratory failure.
Both PaO2 6.3
T1: hypoxic drive (CO2 less than 6.3).
T2: hypercapnic drive (CO2 more than 6.3)
What causes bronchial breathing?
BB: sound conduction through solid lung
PR: relative mvmt of inflamed pleura
What are the risk factors for lung carcinoma? (4).
Lung fibrosis (inc asbestosis + silicosis).
What are the different types of asbestos? (3).
Amphiboles: blue (most dangerous), brown.
Serpentines: white (least dangerous).
What does high level exposure to asbestos cause?
Pulmonary interstitial fibrosis.
Which type of lung cancer are prescribed occupational diseases? (4).
Asbestos related pleural fibrosis.
Lung CA in absence of asbestosis if Hx of 5years high exposure work.
What types of primary lung carcinomas are there?
Non-small cell carcinoma (85%): squamous, adenocarcinoma, large cell neuroendocrine, undifferentiated large cell.
Small cell carcinoma (15%): all neuroendocrine.
Immunocytochemistry is used to differentiate between secondary lung tumours. Which common mets show which molecules? (4types)
Colorectal: cytokeratin 7+20 +ve
Upper GI: cytokeratin 7+20 +ve
Breast: oestrogen +ve
Melanoma: S100, HMB45, MelanA +ve, cytokeratin -ve
What is the pathology of squamous carcinoma of the lung? (5).
Cells, smoking, location, paraneoplastic.
Epidermoid (desmosome linked) ± keratinisation
Central > peripheral
Hypercalcaemia due to parathyroid hormone related peptide.
What is the pathology of adenocarcinoma of the lung? (4).
Cells, location, smoking, expression.
Glandular cells, serous vacuoles in acinar/tubular/papillary structures.
Thyroid transcription factor (TTF) expressed.
What is the pathology of bronchioalveolar carcinoma? (3).
Cells, invasion, mimic.
Spread of well differentiated mucinous/non-mucinous neoplastic cells on alveolar walls.
Which proteins do neuroendocrine cells of the lung produce? (3).
What is the other name for these cells?
Neural cell adhesion molecule (CD56).
What are the different types of neuroendocrine tumours? (4).
Large cell neuroendocrine carcinoma.
Small cell carcinoma.
What is the pathology of a typical carcinoid tumour of the lung?
Behaviour, histology, associations, severity.
Often occlude bronchi.
Oganioid, bland cells, no necrosis.
Associated with MEN1.
Not smoking associated.
95% 5 year survival.
What is the pathology of atypical carcinoid tumours of the lung?
11% of lung carcinoids.
Less organoid, more atypic and nucleoli. Necrosis present.
More aggressive - 70% metastasise and 60% 5 year survival.
What is the pathology of large cell neuroendocrine carcinomas of the lung?
Cells, histology, smoking.
Organoid, eosinophilic granular cytoplasm.
Severe atypia, nucleoli and necrosis.
Associated with smoking.
What is the pathology of small cell carcinomas?
Behaviour, secretion, smoking, presentation.
Rapidly progressive and malignant.
Neurosectory granules with ACTH.
99% in smokers.
Will present with mets.
How common are lung carcinomas with multiple differentiation?
Define mixed vs combined SCC.
50% of cancers.
Mixed: >10% of component.
Combined: ant % SCC + NSCLC.
What is the pathology of large cell carcinomas? (3).
No specific morphology.
50% express thyroid transcription factor.
May be neuroendocrine.
What are the paraneoplastic effects of lung carcinomas? (6).
Acanthosis nigricans (darkened skin).
Hypercalcaemia (squamous cell)
SCC: Lambert Eaton myasthenia syndrome, ACTH, ADH.
How are lung malignancies staged?
T1: 7cm. Lung structure invasion, nodules in same lobe.
T4: Tumour in carina, invades out of lung, nodules in other lobe.
Which drugs are epidermal growth factor receptor tyrosine kinase inhibitors. (2).
How do they work?
ATP analogues that inhibit EGFR-TK (if mutation present). Inhibits mitosis. Not curative but stabilising.
In 10% of NSCLC. More common in Asian women.
What are ALK rearrangements in lung cancer?
Who are they most common in?
Which drug targets this?
Anaplastic lymphoma kinase.
inv(2)(p21;p23). ALK + EML fusion.
Activates ALK tyrosine kinase.
Non smoking Asian women.
What is a chylothorax?
Chylo: lymph in pleural cavity
Pyro: pus in pleaural cavity
What are the causes of a pleural effusion? (2).
Serous/fibrinous exudate due to inflammation in adjacent lung.
Congestive cardiac failure - transudate.
What types of pleural tumours are there?
Benign: fibroma. Rare.
Malignant: secondary adenocarcinoma (lung/breast). Primary malignant mesothelioma (rarer).
What is the pathology of a malignant mesothelioma?
>90% asbestos related, may be low level exposure. 15-60yr latent period.
Mixed spindle and epithelioid cells.
How does a malignant mesothelioma spread?
Initial nodule and effusion, later obliterating pleural cavity, invading chest wall.
Mets uncommon due to fatality .
What is a fibrous pleural plaque?
On lower thoracic wall and diaphragmatic parietal pleura.
Low level asbestos exposure.
No physiological effect. Not premalignant.
What types of illness are lung infections commonly secondary to?
Mucociliary escalator - physical obstruction, poor cough reflex, Kartagener's syndrome, cystic fibrosis.
Immunity - obvious, smoking, hypoxia (macrophage).
What is pneumonia?
Inflammatory exudate in alveoli and distal small airways with consolidation.
What causes bronchopneumonia and how is it distributed?
Low virulence bacteria, fungi.
Common, patchy and bronchocentric.
What causes lobar pneumonia, and how does it affect the lungs?
90% Strep pneumoniae.
Klebsiella pneumoniae -elderly, diabetic, alcoholic.
Lobes with overlying pleuritis. congestion, hepatisation, and resolution without scarring.
What causes atypical pneumonia's in non-immunosuppressed patients? (5)
Coxiella burnetti (Q-fever).
What causes atypical pneumonia's in immunosuppressed patients? (6)
What are the non-infective pneumonias? (4).
Lipid (retention pneumonitis).
Cryptogenic organising pneumonia.
Bronchiolitis obliterans organising pneumonia.
How does pulmonary tuberculosis usually resolve or progress? (4)
Limited spread to bone, kidney.
Name three causes of pulmonary vasculitis:
What is bronchiectasis?
Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue. Results from chronic necrotising infection.
What is chronic obstructive pulmonary disease?
A combination of chronic bronchitis and emphysema.
Define chronic bronchitis.
Cough and sputum for 3 months in each of 2 consecutive years.
Mucus gland hyperplasia with 2o infection + chronic inflamm -> wall weakness + destruction.
What is emphysema?
Abnormal permanent dilation of airspaces distal to terminal bronchiole with destruction of the wall and without obvious fibrosis.
Describe the three classifications of emphysema:
Panlobular: >80% α1 antitrypsin deficient, lower lobes.
Paraseptal: upper lobe bulllae + fibrosis.
What are the two stereotypes for COPD?
Bronchitis - blue bloater, large heart, younger.
Emphysema - pink puffer, small heart, hyper inflated lungs, older.
What is asthma?
Paroxysmal bronchospasm with wheeze, cough, and partially reversible bronchorestriction.
Describe atopic asthma and common stimuli:
Type 1 hypersensitivity reaction. Smooth muscle hypertrophy, mucus gland hyperplasia.
Dust, pollen, animals, cold, exercise.
What is interstitial lung disease?
Increased tissue in alveolar-capillary wall.
Decreases lung compliance, increases gas diffusion distance.
Idiopathic pulmonary fibrosis,
Collagen vascular diseases
What is acute interstitial lung disease?
Exudate and death of type 1 pneumocytes. Type 2 pneumocyte hyperplasia.
= Adult respiratory distress syndrome.
What is chronic interstitial lung disease?
Increasing dyspnoea, clubbing, crackles, fine cough.
Interstitial fibrosis and chronic inflammation.
What is idiopathic pulmonary fibrosis?
Cryptogenic fibrosing alveloitis.
Sub-pleural, lower lobes affected most.
Bosselated pleural surface due to interstitial fibrous tissue contraction.
What is sarcoidosis?
Non-caseating perilymphatic pulmonary granulomas, then fibrosis.
May affect other organs. Hypercalcaemia and elevated ACE.
Young adult females.
What are pneumoconiosis?
Non neoplastic lung diseases due to inhalation of mineral dusts in the workplace.
How does silicosis produce a disease state?
Silica kills macrophages, causing fibrosis and fibrous silicotic nodules.
Increased risk of lung carcinoma. TB reactivation.
What is asbestosis?
Interstitial fibrosis with visible asbestos bodies. Increased risk of lung cancer.
What is hypersensitive pneumonitis?
Who gets it?
Type III hypersensitivity reaction to organic dusts.
Farmers (actinomycetes), pigeon fanciers.
Inflammation and non caseating granulomas.
What is cystic fibrosis?
Inherited multiorgan disorder of epithelial cells affecting fluid secretions.
Caucasians, autosomal recessive.
CFTR gene on 7q31.2.
What does cystic fibrosis cause? (6).
Hyperplasia of mucus glands.
Mucus distended bronchioles.
Atrophy of pancreas with impaired fat absorption, enzyme secretion and vitamin deficiencies.