Lung Pathology Flashcards
WHAT ARE THE DIFFERENT MODES FOR OLD TO GET?
Vapour.
Gases.
Dusts.
Fume.
What is vapour or gases?
Liquid or solid substance suspended in air.
Including mists.
What is dust?
Aerosolised solid particles. Size from 1 to less than 100 nanometers.
What is a fume?
Normally vapour or gas.
When do most occupational lung disorders occur?
After a period of latent (asymptomatic) exposure.
What improves prognosis in OLDs? What do you need to weigh up though?
Earlier recognition
Identify and cease exposure
Health versus income
Loss of employment
Eg allergic OA
What is the problem with historical exposure factors for OLD? What effect does this have on prognosis?
Recognised years later
Not normally exposed
Supportive measures
Little/no impact on prognosis
Benefits advice
Eg asbestosis
What factors do you have to think about when looking at OLDs?
Susceptibility
Genetic/individual vs population
Severity
No sx vs disability/death
Reversibility
Reversible vs irreversible
Employment
Working vs employed
What are the most common OLDs?
Asthma.
Allergic alveoli’s.
Bronchitis/empyhsema.
Non-malignant pleural disease.
Mesothelioma.
How can occupational asthma be caused?
90% Asthma induced by sensitisation (allergy) to an agent inhaled at work.
10% Asthma induced by massive accidental irritant exposure at work (direct airway injury).
How much of adult onset asthma does occupational asthma take up?
9-15%.
What happens with occupational asthma prolonged exposure?
Ongoing exposure worse prognosis
Early identification important
Treat or even cure
What would some tests of occupational asthma show?
Normal spirometry.
Work-effect confirmed by seal PEF.
Positive IgE to wheat flour.
What is an example of allergic sensitisation?
Extrinsic allergic alveolitis
Note, Asthma is also one
Where was extrinsic allergic alveolitis first recognised?
Farmers
How can extrinsic allergic alveolitis be caused?
Occupational or environmental.
What is extrinsic allergic alveolitis?
An interstital lung disease
Upper lobe predominant, gas trapping, ground glass, progresses to fibrosis.
How is extrinsic allergic alveolitis classed?
Duration
Acute (may be self-limiting).
Subacute.
Chronic (scarring).
What are the different occupational hazards for extrinsic allergic alveolitis?
Microorganisms.
Animals.
Vegetation.
Chemcials.
What are the different microorganisms causing for EAA?
FARMERS!
wood pulp workers, sewage workers, maple bark strippers, cheese washers, metalworking engineers, mushroom workers, suberosis, bagassosis
What animals, vegetation and chemicals can cause EAA?
Animals
Birds, wheat weevil, fish meal, rodent handlers
Vegetation
Coffee, wood
Chemicals
Vineyard sprayers, insecticide, isocyanates, anhydrides, plastics
What does prognosis of EEA depend on?
Early recognition and avoiding exposure.
What is an example of Chronic inflammation?
COPD.
What percentage of COPD happens within occupational exposure?
10-15%.
What historic VGDF substances cause COPD?
Coal, silica, grain
What is an occupational hazard that can cause COPD?
Dust exposure.
What deficiency makes a person more likely to develop COPD?
Alpha-1 antitrypsin deficiency.
What are some asbestos-related lung diseases?
Pleural plaques
Diffuse pleural thickening.
Asbestosis.
Lung cancer.
Mesothelioma
What is asbestos?
Naturally occurring mineral fibre
Used for millenia
Insulating, fire-retardant, tensile strengh
What are pleural plaques and why are they important in asbestos-related lung diseases?
Pleural collagen, often calcified.
Marker of exposure.
Not pre-malignant.
Aetiology unclear.
What is diffuse pleural thickening and what can it cause in asbestos-related lung disease?
Follows benign effusion
Obliteration of costophrenicangle
Can cause
Restriction due to thickened pleura
SOB, respiratory failure
Is there any treatment for diffuse pleural thickening?
No effective treatment.
May progress slowly (without further treatment).
What is asbestosis and what does it show in asbestos-related lung disease?
Pulmonary fibrosis
Subpleural, basal, UIP pattern.
With/without plaques.
History of heavy exposure.
Is there any treatment for asbestosis?
No effective treatment.
May progress (without further exposure).
What is mesothelioma in asbestos-related lung disease?
Rapidly progressive and usually incurable pleural cancer
Lung encased by tumour
How does mesothelioma present in asbestos-related lung disease?
Often presents as an unexplained pleural effusion
Progressive breathlessness, chest pain, weight loss
Average survival 8-14 months.
How can you prevent OLDs?
Requirement under COSHH.
Focus on exposure prevention or minimisation.
What procedures can you do to help prevent OLDs?
Elimination (eg asbestos)
Substitution (eg latex to nitrile gloves)
Engineering controls (eg exhaust ventilation)
Worker education
RPE (masks and respirators)
What can you do if there is an individual risk to a patient?
Yearly questionnaire/spirometry/CXR
Identify ill health early
Prevent further harm by reducing/preventing exposure
Review control measures to protect other workers
What are some chronic obstructive diseases?
Chronic bronchitis and/or emphysema
Asthma
Bronchiectasis
WHAT IS COPD?
Collection of lung diseases that cause IRREVERSIBLE obstruction to airflow out of the lungs.
What are the causes of COPD?
Smoking
A1AT
IV drug use
Industrial exposure to chemicals
WHAT IS CHRONIC BRONCHITIS?
https://www.youtube.com/watch?v=Y29bTzKK_P8
Bronchial tubes inflammation
IRREVERSIBLE
What is chronic bronchitis defined as?
Cough, sputum production on most days for 3 months of 2 successive yrs
What are the different layers of the airways?
Mucosa
Epithelial cells
Goblet cells
Lamina propria
Basement membrane
Loose connective tissue
Submucosa
Smooth muscle
Connective tissue
Cartilage (bronchi)
What does smoking cause?
What does this cause?
In chronic bronchitis
Hypertrophy and hyperplasia of the mucinus glands (bornchi)
Hypertrophy and hyperplasia of goblet cells (bronchioles)
Increase in mucus
Cilia also become short and less motile
Harder to move mucus
Air trapping
How can pulmonary hypertension happen in chronic bronchitis?
Decreased gas exchange causign vasocontriction
Large proportion
Increases pulminary vascular resistance
Develops pulmonary hypertension
Right side of heart enlarges
Cor pulmonale
How can a person become cyanosed in chronic bronchitis?
CO2 trapped in alveoli takes up more space
O2 unable to fill alveoli
Less goes into the blood
More CO2 in alveoli means less CO2 can come out the blood
More CO2 in blood less O2
What is the reid index?
Size of the mucinus glands relative to the rest of the layers
Who does chronic bronchitis affect?
Affects middle aged heavy smokers
Some following pollution chronically
Recurrent low grade bronchial infections
What are the symptoms of chronic bronchitis?
Wheeze
Crackles
Cough
Production of mucus (sputum)
What are the signs of chronic bronchitis?
Hypoxemia
Hypercapnia
These cause cyanosis
Pulmonary hypertension
Result of low O2
Causing cor pulmonale
Tachypnoea
Use of accessory muscles
Hyperinflation
What are the differential diagnosis for chonic bronchitis?
Alpha1-Antitrypsin Deficiency
Asthma
Bronchiectasis
Chronic Obstructive Pulmonary Disease (COPD)
Chronic Sinusitis
Gastroesophageal Reflux Disease
Influenza
What are the investigations for chronic bronchitis?
Chest X-ray
Rule out other lung conditions, such as pneumonia.
ECG
Right venticle and atria enlargment (cor pulmonale)
Sputum (bacteria).
A pulmonary function test
CT scan
ABG: PaO2 decrease ± hypercapnia
What are the management options for chronic bronchitis?
Reduce risk factors.
Medications
A bronchodilator.
Theophylline is an oral medication that relaxes the muscles in your airways.
General
Short-acting antimuscarinic (ipratropium) or salbutamol
Mild/Moderate
Long-acting antimuscarinic (tiotropium) or salmeterol
Corticosteroids if severe plus long acting
Beclamethosone
Antibiotics
Pulmonary rehabilitation. It often consists of exercise, nutritional counseling, and breathing strategies.
WHAT IS EMPHYSEMA?
What are the different types?
https://www.youtube.com/watch?v=TEuSV_7gWA8
Enlargement of alveolar airspaces with destruction of elastin in walls.
Centri-acinar
(proximal part of acinus due to smoking)
(top of lungs)
Pan-acinar
(All acinar affected)
(Genetic condition alpha1-antitrypsin)
(Bottom of lungs)
Paraseptal acinar
(Distal acinus)
(Periphery of lungs)
(Pneuthorax)
What are the causes of emphysema?
Cigarette smoking. (MAINLY)
Alpha-1-antitrypsin deficiency
Coal dust exposure
Cadmium toxicity
What happens when the alveoli becomes irritated by smoke?
What does this do?
What happens when exhaling?
Triggers an inflammatory response, immune cells come in
Releasing inflammatory mediators
(Proteases, Collangenases)
Breaks down the collagen and elastin in the alveoli wall
Bernoulli principle
Exhalation of air has a lower pressure and pulls the airway inwards, ormal airways can withstand this
Emphysema airways have less elastin and collagen therefore collapse
Leads to air trapping
What happens when air comes into emphysema lungs?
Lungs are more compliant
Lungs overinflate
What happens in alpha-1 antitrypsin deficiency?
Macrophages produce proteases
Helps clear debris
Can damage tissue
Alpha-1 antitrypsin is a protease inhibitor
Protects against damage
Deficiency means proteases can damage lungs
What are the oxygen and carbon dioxide levels in emphysema?
‘pure’ emphysema appears with reduced PaCO2 and normal PaO2 at rest due to overventillation (‘pink puffers’)
What are the symptoms of emphysema?
Dyspnea - shortness of breath
Exhaling through pursed lips to keep lungs inflated
Cough - sputum
Weight loss due to metabolic demands
1/3 of lung capacity is destroyed before symptoms
What are the signs of emphysema?
Barrel chest - overinflated chest on x-ray
Flattened diaphragm
Pulmonary hypertension
Right heart failure
What are the differential diagnosis of emphysema?
Bronchiectasis
Bronchitis
Lymphangioleiomyomatosis
What are the investigations for emphysema?
Blood tests
Hb level increase secondary polycythaemia.
Chest x-ray
This helps to show hyperexpansion of the lungs.
ECG or Echocardiogram
Right heart failure (a complication of emphysema and COPD).
Pulmonary/Lung Function tests
Spirometry is the best test to detect airflow limitation and obstruction.
Blood gases
Normal, later stages of disease, low oxygen and high carbon dioxide levels.
High resolution CT
Best test for detecting emphysema and bullae (big dilated air spaces).
What is the treatment for emphysema?
Stop smoking
General
Idotropium or salbutamol
Mild/intermediate
Tiotropium (antimuscarinic)) and salmeterol
Severe
corticosteroids (beclemethosone)
What are the complications of COPD?
Pneumothorax
Cor pulmoale
Acute exaccerbations
Infection
WHAT IS BRONCHIECTASIS?
https://www.youtube.com/watch?v=rTcVPHszU5E
Irreversible dilation of the bronchioles
What are the causes of bronchiectasis?
**_Congenital_** Cystic fibrosis (CF);
Post-infection
TB
HIV
**_Other_** Bronchial obstruction (tumour, foreign body)
What is the pathology of bronchiectasis?
Infection and imparied drainage
Activates neutrophilic proteases and cytokines causing inflammation
Increaed mucus and increased stagnent bacteria
Cycle starts again
What are the signs and symptoms of bronchiectasis?
Chronic cough - foul smelling sputum
Flecked with blood sometimes.
Finger clubbing
Coarse inspiratory crepitations.
Wheeze
What are the differential diagnosis for bronchectasis?
Alpha1-Antitrypsin Deficiency
Aspiration Pneumonitis and Pneumonia
Asthma
Bronchitis
Chronic Obstructive Pulmonary Disease (COPD)
Cystic Fibrosis
Emphysema
Gastroesophageal Reflux Disease
What are the tests for bronchiectasis?
Sputum culture
HRCT chest
To assess extent and distribution of disease.
Spirometry
Obstructive.
Chest X-Ray
Cystic shadows, thickened bronchial walls
What is the management for bronchiectasis?
Stop smoking
Airway clearance exercises
Bronchodilators
Corticosteroids
Antibiotics
What are the complications with bronchiectasis?
Pneumonia
Emphysema
Septicaemia
Amyloid formation.
WHAT IS ALPHA-1 ANTITRYPSIN DEFICIENCY?
A deficiency in alpha-1 antitrypsin
What does alpha-1 antitryspin do?
What is the gene that codes for it?
What chromosome is it on?
Inactivates elastase (a protease)
SERPINA1
Long arm of chromosome 14
What happens when there is infection or inflammation in the lungs?
What does A1AT do?
What happens if there is no A1AT?
Neutrophils
Neutrophils make neutrophil elastase
Break down bacteria but also elastin in the walls
Liver makes alpha-1 antitrypsin which travels to lungs and inhibits this
Neutrophil elastase breaks down alveoli wall
Alveoli lose elasticity and structural intengrity
When would you favour alpha 1-antitryspin deficiency as a dignosis?
Never smoked
Young
What are the symptoms of alpha-1 antitrypsin deficiency?
Shortness of breath
Wheezing
Mucus production
Chronic cough
Cirrhosis
Inability to make coagulation factors
Build up of toxins
What investigations are done for alpha-1 antitrypsin deficiency?
Bloods
A1AT low
Biopsy
Liver - Periodic-acid shiff stain
What is the treatment of alpha-1 antitrypsin deficiency?
Augmentation therapy
IV infusion of normal protein
Slow of halts progression
Inhlaers
Oxygen
Liver transplant
WHAT ARE INTERSTITIAL LUNG DISEASES?
Disease of the alveoli primarily
Scarring
Fibrosis
What are the symptoms of interstitial lung diseases?
Dry cough
Digital clubing
Diffuse inspiratory crackles
Dysponea
What can acute interstitial lung diseases cause?
Acute respiratory distress syndrome
What are the causes of acute respiratory distress syndrome?
Shock
Trauma
Infections
Gas inhalation
Narcotic abuse
What are the symptoms of acute respiratory distress syndrome?
Tachypnoea
Dyspnoea
Pulmonary oedema
What are some Chronic interstitial diseases? (Differential diagnosis of eachother)
Idiopathic
Pneumoconiosis
Extrinsic Allergic Alveolitis/ Hypersensitivity pneumonitis
Sarcoidosis, connective tissue disease etc.
What is pneumoconiosis?
Lung disease caused by inhaled dust Organic or inorganic dust (mineral)
What happens in coal workers’ pneumoconiosis?
Coal is ingested by alveolar macrophages (dust cells)
They aggregate around bronchioles
The consequences vary from trivial to lethal.