Lung Pathology Flashcards
Define asthma
Paroxysmal contraction of airways resulting in decreased airflow due to reversible airway obstruction over a period of time
Restricted airway causes - increased production of mucus, enlarged smooth muscle, narrowed bronchiole
Types of asthma
Extrinsic -
- children predominate
- exposure to external agent e.g. Pollen, chemicals, (occupational), drugs Aspergillus
Intrinsic
- adults predominate
- causes include exercise, infection, stress
Causes of asthma
Genetic - atopic individual those who have hay fever and eczema
Environmental- pollution, smoke, particular allergens
Viral bacterial infection
Medication beta blockers and NSAIDS
Emotional factors and stress
What happens at the mast cells
Allergen binds to IgE Mast cells degranulate Histamine and leukotrienes released Inflammation of the lung tissue Introduces other inflammatory cells to the area cause epithelia also shredding, goblet cell discharge, plasma leak and oedema
Signs of asthma at the lung tissue
Shedding of bronchial epithelial cells - due to specific failure on intercellular adhesion mechanisms
Thickening of epithelial basement membrane
Eosinophils and by products of their degranulation
(Charcot Leyden crystals)
Increased bronchial gland mass with increased mucus- curschmanns spirals
Increased smooth muscle
Inflammation of bronchial mucosa: t lymphocytes, eosinophils, +/- neutrophils
What is status asthmaticus
Hyperinflation - not due to emphysema
Petechial haemorrhages
Mucoid plugging of large and small airways
Atelectasis (resorption collapse distal to mucoid impaction in segmental bronchi)
What are the components of COPD
Chronic obstructive pulmonary disease
Chronic bronchitis
Emphysema
Chronic bronchitis facts
Essentially a clinical diagnosis
May be prone to recurrent infections
‘Blue bloater’
Increased mass of bronchial mucus glands
Emphysema
Essentially a pathological/morphological diagnosis
Pink puffer clinically
Loss of alveolar walls and dilatation of air spaces clinically
Chronic bronchitis definition
A persistent cough with sputum production for at least 3 months over the past 2 consecutive years
Causes of chronic bronchitis
Tobacco smoking
Atmospheric pollution
The pathological changes in the large airways in chronic bronchitis
Increase in submucosal gland mass
Increase no of goblet cells
Increase in smooth muscle
Chronic inflammatory cell infiltrate of lamina propria
Define emphysema
Abnormal permanent enlargement of air spaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis
Morphological types of emphysema
Centrilobular - 75% cases generally caused by cigarette smoking
Panacinar (panlobular) - associated with alpha 1 antitrypsin deficiency
Paraseptal (distal acinar) - cause unclear may be a cause of spontaneous pneumothorax
Irregular emphysema - associated with scarring clinically not significant
Other Types of emphysema
Compensatory emphysema - response to loss of lung elsewhere e.g. Through surgery
Senile emphysema - age related
Obstructive emphysema - tumour, overinflation e.g. Congenital abnormality
Bullous emphysema - associated with bullae often with a background of centrilobular emphysema
Interstitial emphysema - air in connective tissue of lung, pleura or mediastinum
Centrilobular emphysema facts
Common
Linked with tobacco smoking and atmospheric pollution
Involves preferentially the centre of the acinus around the terminal bronchiole
Complications of COPD
Cor pulmonale
Respiratory failure
Polycythaemia
Lung cancer - double the incidence in male bronchitis
Pneumothorax - ruptured Bullae can occur if there is coexistant emphysema
What is Interstitial pulmonary fibrosis
A condition characterised by progressive interstitial scarring leading to respiratory incapacity, and effacement of the lung architecture, which in extreme cases may result in a honeycomb pattern
What is honeycomb lung
‘Cysts’ several mm to >1cm diameter, in background of dense fibrous scarring
Most prominent in subpleural parenchyma at the lung bases
Honeycomb lung causes
Antecedent lung diseases:
Idiopathic interstitial pneumonia (UIP, DIP)
DAD
Inorganic dust exposure
Interstitial granulomatous disease e.g. Infections, hypersensitivity pneumonia (EAA), sarcoidosis, berylliosis
Histiocytosis X
Types of interstitial fibrosing alveolitis
Idiopathic (cryptogenic [CFA] ) - diagnosis is by exclusion - incidence 3-5/1000000 Secondary including - connective tissue diseases - dust and smoke inhalation - asbestos - EEA, sarcoidosis - shock lung, radiation - drugs
Morphological patterns of interstitial pulmonary fibrosis
Mortality rates
AIP - acute interstitial pneumonia -60%
UIP - usual interstitial pneumonia - nearly 80%
DIP - desquamate interstitial pneumonia - nearly 40%
NSIP - non specific interstitial pneumonia -10%
GIP, LIP probably not as important
What is acute interstitial pneumonia
Individuals are well
Signs of URTI
they have progressive rapid respiratory failure
High mortality
Essentially signs of diffuse alveolar damage
Necrosis of alveolar lining cells with exudate
Hyaline membranes are frequently seen
Later organisation by fibrosis occurs
Hugh mortality
Signs, symptoms and pathology of usual interstitial pneumonia
Insidious onset of dyspnoea, in adults 40-70 years
Progressive down hill course, median survival 4-5 years
Seen with CFA but may also be associated with collagen vascular diseases, especially rheumatoid arthritis and scleroderma
Pathology - heterogenous, non-uniform inflammatory and fibrosing process, fibroblastic foci, honeycomb damage
Signs, symptoms, pathology of desquamative interstitial pneumonia
Uncommon
Occurs in Middle Aged smokers
Dyspnoea and cough
Usually responds to steroid treatment
Relatively good prognosis
Now believed to be related to respiratory bronchiolitis
Pathology- increased numbers of macrophages in alveolar spaces, uniform interstitial fibrosis
Signs and symptoms of non-specific interstitial pneumonia
Dyspnoea
Cough
Middle aged adults
Underlying connective tissue disease in some patients
Steroid responsive in most patients
Microscopy –> uniform interstitial inflammatory and fibrosing process
Antigens implicated in extrinsic allergic alveolitis
Wide range
Including drugs
In a significant number NO antigen can be found
What is extrinsic allergic alveolitis otherwise known as
Hypersensitivity pneumonitis
Clinical presentation of hypersensitivity pneumonitis
Acute: follows exposure to large amounts of antigen. Sudden onset of dyspnoea, fever, chills. Symptoms subside following cessation of exposure, reappear on rexposure
Chronic: results from prolonged exposure to small amounts of antigen. Insidious onset of dyspnoea, dry cough, fatigue, reticulonodukar infiltrates on CXR, can progress to irreversible lung damage if exposure persists.
Hypersensitivity pneumonitis radiological features
Lower love ground glass and fine nodular densities characteristic
Hypersensitivity pneumonitis histological features
Variable lymphoplasmocellular infiltrate centred on small airways and alveolar ducts
Small non-necrotising loose granulomas
Foamy macrophages
BOOP like pattern in 50% of cases
BOOP - bronchiolitis-obliterates-organising-pneumonia
Occupational disease in the lung
Occupational asthma Pneumonitis with ARDS appearance - acute respiratory distress syndrome Hypersensitivity pneumonitis Emphysema Pulmonary or pleural fibrosis Malignancy - lung, pleura
Types of fibrogenic dusts
Silicosis
Asbestos
Hard metal disease - tungsten, cobalt
What is the most prevalent chronic occupational disease worldwide
Silicosis
Occurrence of crystalline silica
Silicone dioxide basic component of sand, quartz, granite
Second most common mineral in the earths crust
Airborne silica produced by
Sandblasting
Rock drilling
Foundry work
Quarrying
What does silicosis do to the lungs
Collagenous nodules form within the lungs and in the mediastinal lymph nodes
It is irreversible
Low mortality but of severe tends to cause respiratory incapacity
Many cases asymptomatic
Often long latency between exposure and development of silicosis
Pathology -well defined nodular opacities in the upper and posterior lung zones
Lung nodules may coalesce to form confluence complicated nodules
Microscopy of silicosis
Whorled laminated well circumscribed nodules of collagen (onion skin)
Anthracotic pigment may also be present
May be found anywhere in the lung
Hilar lymph node involvement invariably involved and may be the sole representation of the disease
Alveolar lipoproteinosis may be seen in acute silicotic workers
Immune dysfunction in silicosis
Promotes development of mycobacterial infection - TB and atypical forms
Up to 5% cases complicated by TB
Increased risk of connective tissue disorders particularly scleroderma
Patients with silicosis have increased levels of autoantibodies in the blood
Likely due to depressed cell immunity and macrophage function
Coal workers pneumoconiosis
May be asymptomatic Variable quartz and carbon Pathological findings Coal dust macule Upper lobe predominance Histologically - accumulation of coal dust around respiratory bronchioles - nodular lesions with silicotic morphology maybe found - emphysema invariably present
Progressive massive fibrosis
Progressive from dust macules
By definition - nodules >10mm
Probably related to quartz/silica content of inspired particles
Not related to cigarette smoking
May progress in the absence of any coal mining exposure
Pulmonary massive fibrosis pathology
Upper zone predominant - related to poor lymphatic drainage Locally destructive rubbery Cavitation may occur but exclude TB Microscopy - Black lipid debris Deposition of cholesterol clefts Necrosis Giant cells
Asbestos types
Amphibioles
Serpentine
Amphiboles
Crocidolite and amosite (blue and brown asbestos)
Stiff, straight and brittle
Fibres less prevalent
More pathogenic as impacted in airways and lungs
Serpentines
Chrysotile white asbestos
Cleared reasonably effectively from airway
Less pathogenic than amphiboles
Asbestos chest disease
Can affect pleura and lungs and can benign and malignant
Asbestos benign disease
Pleural plaques
Benign pleural thickening
Pleural effusion
Interstitial fibrosis (asbestosis)
Pleural plaques
Fairly common
Non neoplastic and invariably asymptomatic
Irreversible and composed of hyalinised collagen possibly also showing calcification
Implies asbestos exposure
BUT
Does not indicate asbestosis
Asbestos malignant disease
Mesothelioma - 90% associated with asbestos exposure often decades previously
Bronchiogenic carcinoma
- invariably associated with accompanying asbestosis
- all forms of lung cancer may occur but particularly adenocarcinomas
Other cancers
-laryngeal carcinoma
Colon cancer ?
Risk of cancer
Non smoker RR =1
Asbestos and no smoker = rr 5
Asbestos and smoker RR = 55
How is asbestos inhalation assessed
Inspection for the pressence of asbestos bodies
- characteristics beaded rod shaped structures coated with iron salts
Only a few asbestos fibres become coated in the way to become visible and their presence indicates significant asbestos inhalation
Digestion of tissue and manually counting asbestos fibres by microscopy
What is pulmonary hypertension
When the means pulmonary arterial pressure is greater than 25mmHg at rest or 30mmHg during exercise
Primary pulmonary hypertension
Rare
Females > males
Often affects young adults
Very poor prognosis - transplant may be necessary
Secondary pulmonary hypertension
Left to right cardiac shunts Venous back pressure - mitral stenosis Hypoxaemic lung disease - chronic bronchitis - emphysema Drugs Vascular obstruction - repeated Pulmonary thromboembolism
Cause of pulmonary hypertension
Prepulmonary Increased pressure and flow - congenital heart disease Pulmonary - disruption +\- loss of lung parenchyma - emphysema - vascular obstruction -- chronic thromboembolism - hyooxaemia -- COPD -- living at high altitudes Post pulmonary -- mitral stenosis
Pulmonary hypertension morphology
Muscularisation of the arterioles Medical thickening of muscular arteries Intimal thickening Plexiform lesions Fibrinoid necrosis
Pathophydiology of acute asthma
Trigger which causes inflammation in the bronchioles -> airway hyper responsiveness And smooth muscle contraction And increased mucous secretion -> Airway obstruction and then clinical symptoms Inc mast cell Inc eosinophil Inc NKT Inc T helper 2
Lung mechanics in asthma
Incomplete expiation as the airways close prematurely leads to hyperinflation can’t breath out so inspiration is difficult
Tachypnoea
Positive end expiratory pressure (PEEP)
-gas trapping
- dynamic hyperinflation breath in and can’t completely breath out
- auto PEEP
Inc work of breathing and patient can tire
Inc residual volume due to unable to breath out, inc elastic load on respiratory muscle
Respiratory muscle must Uber come this for breathing so may tire
AutoPEEP / intrinsic positive end reps pressure
What are the abnormalities in measurements
Dec FEV1, FEV1/FVC
Dec FVC as airways close prematurely
Inc RV obstruction
Inc FRR and TLC
Asthma presentation
Cough
Tight chest
Wheeze
Dyspnoea
Asthma history
Pro drone of a cough, rhinorrhea, wheeze, fever, GI Speed of onset Associated illness Precipitating exposure Number of admission No of ITU admission and intubation Best peak flow Dec in activity
Asthma examination
Inc resp rate Accessory muscles -sternocleidomastoid Tachycardia Talking in full sentence - difficult due to dyspnoea Wheeze polyphonic
How to recognise asthma severity
Moderate PEFR 50-75% of best or predicted Acute severe PEF 33-50% best/predicted Resp rate more than 25 breaths min HR 110 above Inability to com
Pathophydiology of acute asthma
Trigger which causes inflammation in the bronchioles -> airway hyper responsiveness And smooth muscle contraction And increased mucous secretion -> Airway obstruction and then clinical symptoms Inc mast cell Inc eosinophil Inc NKT Inc T helper 2
Lung mechanics in asthma
Incomplete expiation as the airways close prematurely leads to hyperinflation can’t breath out so inspiration is difficult
Tachypnoea
Positive end expiratory pressure (PEEP)
-gas trapping
- dynamic hyperinflation breath in and can’t completely breath out
- auto PEEP
Inc work of breathing and patient can tire
Inc residual volume due to unable to breath out, inc elastic load on respiratory muscle
Respiratory muscle must Uber come this for breathing so may tire
AutoPEEP / intrinsic positive end reps pressure
What are the abnormalities in measurements
Dec FEV1, FEV1/FVC
Dec FVC as airways close prematurely
Inc RV obstruction
Inc FRR and TLC
Asthma presentation
Cough
Tight chest
Wheeze
Dyspnoea
Asthma history
Pro drone of a cough, rhinorrhea, wheeze, fever, GI Speed of onset Associated illness Precipitating exposure Number of admission No of ITU admission and intubation Best peak flow Dec in activity
Asthma examination
Inc resp rate Accessory muscles -sternocleidomastoid Tachycardia Talking in full sentence - difficult due to dyspnoea Wheeze polyphonic
How to recognise asthma severity
Moderate PEFR 50-75% of best or predicted Acute severe PEF 33-50% best/predicted Resp rate more than 25 breaths min HR 110 above Inability to com
