Benign Lung Pathology Flashcards
Which of these 3 cross-sections would most likely work best at transmitting the fluid?
1 = size of lumen – 1 and 2 will allow greater volume of flow in short space of time
2 =wall strength - 1 may collapse as very thin, 2 and 3 probably strong enough
What are the 3 most important characteristics of airways?
- Size of lumen
- Wall strength
- Wall support
In this diagram, each length of the vertical blue line represents a set area of a gas exchange surface, and increased thickness, as in No 3, represents increased width and density of that gas exchange surface. The red arrow represents the gas being transferred across the surface. In this example, if we say a wide arrow represents 1 litre per second of gas transfer and a narrow arrow represents ½ litre per second, then which one enables the greatest gas transfer?
No 1 has 2 quantities of thin surface area = 2 litres per second.
No 2 has 1 quantity of thin surface area = 1 litre per second.
No 3 has 2 quantities of thick surface area = 1 litre per second.
What does the quality and thickness of alveolar walls affect?
Gas exchange
What is one of the key features of inflammation that could result in the wall of a tube narrowing the lumen?
Swelling (Tumour)
Acute inflammatory cells like neutrophils release chemicals such as proteases and active oxygen species to kill micro-organisms. What is the downside of these on the local tissues?
The downside is damage to the normal healthy cells / tissues and thereby potentially triggering further inflammation and damage
Histological view of tissue damage in airway
What are the 4 ways the tissues may respond locally after an episode of acute inflammation?
1 - complete resolution,
2 - chronic inflammation,
3 - loss of tissue
4 - scarring
What are acute inflammatory cells like neutrophils and macrophages replaced by as inflammation becomes chronic?
lymphocytes or macrophages forming granulomas
How can fibrosis affect the lungs?
fibrosis restricts expansion of the lung parenchyma
What can inflammation result in?
- swelling
- tissue damage
- tissue loss
- fibrosis
What is asthma?
Reversible intermittent narrowing of conducting airways
What is non-atopic asthma? When does it tend to develop?
Non-allergic asthma, or non-atopic asthma, is a type of asthma that isn’t related to an allergy trigger like pollen or dust, and is less common than allergic asthma. The causes are not well understood, but it often develops later in life, and can be more severe.
What are the 2 types of asthma?
Atopic (extrinsic) and non-atopic (intrinsic)
What can trigger asthma?
Allergens (pollen, house dust mite, animals), drugs (NSAIDs), cold, exercise, infections, emotion
Pathogenesis behind the trigger causing asthma?
Sensitisation to trigger followed by re-exposure to trigger causing airway narrowing
What morphological abnormalities are present in asthma? (wall, lumen)
Wall; thick (inflammation, tissue hyperplasia) and contracted (smooth muscle)
Lumen - mucus
Clinical presentation of asthma?
SOB, Wheeze, cough, hyperinflation
Airway during asthma exacerbation
What causes SOB and wheeze in asthma?
Tubes thickened and narrowed
What 3 main things cause the tubes to thicken and narrow in asthma?
- Smooth muscle contraction, (see hyperplastic/hypertrophied smooth muscle in bronchioles and bronchi)
- Inflammation, (wall of conducting airways is swollen with vasodilatation, fluid and inflammatory cells)
- Mucus (goblet cells and mucus glands are increased in number/size and increase in mucus filling lumen)
Asthma pathogenesis when exposed to allergen:
- Allergen/cold air etc triggers basophils/eosinophils
- These release histamine, prostaglandins and leukotrienes
- These cause;
- contraction of smooth muscle
- inflammation; vascular dilation and oedema
- increase mucus production
- Airway surrounded by thickened smooth muscle which contracts and narrows the lumen
-
Inflammatory cells; cause vasodilation of vessels and oedema
- This thickens the bronchial wall and narrows the lumen
- Mucus in lumen narrows it even further
How does sensitisation occur during asthma?
- APC (with MHC II) presents antigen to Th2 cells
- Th2 cells release certain cytokines (IL-4);
- Cause B cells to switch from producing IgM to IgE
- Recruite and stimulate various inflammatory cells
- Antigen is then encountered again (cells are already there)
- Antigen reacts with IgE to cause widespread release of histamine/PGs/leukotrienes for eosinophils/basophils
Which 3 main changes occur during asthma?
- inflammation
- smooth muscle contraction
- mucus production
What is chronicobstructive pulmonary disease a combination of?
Chronic bronchitis & emphysema
How is chronic bronchitis defined?
Cough and sputum for 3 months in each of 2 consecutive years
Site of bronchitis?
Bronchus
Describe the;
a) wall of the bronchus
b) mucus gland
c) mucus production
in bronchitis? What will this do to airflow?
a) thickened by inflammation
b) mucus gland hyperplasia
c) by increased mucus production
This will obstruct airflow
What will this persistent mucus in bronchitis predispose to?
Infection if mucus isn’t cleared quickly
What might happen to the wall of the airway with persistent inflammation and/or recurrent bouts of infection in bronchitis?
Airways may get scarred, become weakened and bronchiectatic
What is emphysema?
Reduction in the number alveolar walls around the bronchiole. Normal thickness walls but less of them –> less SA so reduced gas exchange
What are co-existent obstructive lung diseases associated mainly with?
Cigarette smoking
How does tobacco smoke lead to COPD?
Chemicals and heat trigger inflammation in bronchi and lung parenchyma. In the bronchi this leads to persistent inflammation, scarring, mucus hyperplasia. In the parenchyma inflammation leads to alveolar wall loss (emphysema).
What morphological abnormalities are present in bronchitis?
Chronic inflammation, mucus gland hyperplasia
What morphological abnormalities are present in emphysema?
Emphysema - alveolar wall loss, especially around the bronchioles (centriacinar)
Define centriacinar emphysema
Centrilobular emphysema primarily affects the upper lobes of the lungs
What is bronchiectasis?
Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue
If the alveolar wall is damaged and weakened by chronic inflammatory damage, what might happen to the wall on expiration?
Collapse
What is bronchiectasis due to?
secondary to chronic necrotising infection (often with pre-disposing conditions)
- Cystic fibrosis
- Primary ciliary dyskinesia, Kartagener syndrome
- Bronchial obstruction: tumour, foreign body
- Lupus, rheumatoid arthritis, inflammatory bowel disease, GVHD (graft-versus-host-disease)
Bronchi vs bronchiole?
Bronchi are the main passageway into the lungs. The bronchi become smaller the closer they get to the lung tissue and are then considered bronchioles.
What triggers/causes bronchiectasis?
Mainly obstruction (eg by tumour, thick mucus in CF) and / or infection
How does obstruction lead to bronchiectasis?
Obstruction causes infection (or infection can arise de novo)
Pathogenesis behind bronchiectasis?
- Obstruction/infection leads to inflammation
- inflammation damages wall tissues
- walls dilate but also contain inflammatory debris and mucus
What morphological abnormalities are present in bronchiectasis?
Dilated inflamed airway walls
How do the morphological abnormalities of bronchiectasis commonly present clinically?
Productive cough, may be blood, obstructive ventilatory defects, repeated infections
What is chronic ILD?
Chronic interstitial lung disease; mixed group.
Most common are:
- Idiopathic Pulmonary Fibrosis (IPF)
- Pneumoconiosis
- Sarcoid
- Hypersensitivity Pneumonitis (HP)
What does chronic ILD involve?
Often = scarring +/- inflammation in multiple areas of both lungs that reduces lung compliance (ie stiff lungs) = restrictive
What happens in idiopathic pulmonary fibrosis?
- Fibrosis of interstitium causes reduced gas exchange
- If fibrosis slowly replaces normal lung;
- Shortness of breath etc
- Increased severity of symptoms
What is idiopathic pulmonary fibrosis?
Progressive patchy scarring especially lower zones of both lungs that is fatal (mean survival 3 yrs).
Where does IPF tend to occur?
Lower zones of both lungs
Age of IPF?
Typically over 60
Speculated pathogenesis of IPF?
Speculated is repeated epithelial injury leads to inflammation and fibrosis
What morphological abnormalities are present in IPF?
Patchy interstitial fibrosis, especially lung bases at periphery
What is the cough like in IPF?
Insidious dry cough
What is Pneumoconiosis? What is it caused by?
Lung damage secondary to particle inhalation. Commonest coal dust/ silica from mining, asbestos or other fibrogenic dust inhalation from occupational exposure (eg stone or metal workers)
What triggers Pneumoconiosis
Chronic particle inhalation
What is the effect of damaged alveolar walls on the heart? What can this lead to?
Increased resistance for right ventricle –> can lead to 2ary RHF
How does chronic particle inflammation lead to Pneumoconiosis?
Particles ingested by macrophages –> trigger fibrosis (inflammation) N.B. smoking makes it worse
What morphological abnormalities are present in Pneumoconiosis?
Dust accumulation and fibrosis, often centred on smaller conducting airways
Which type of particle is the most common cause of Pneumoconiosis?
coal dust/ silica from mining
Who is Pneumoconiosis more common in?
Male due to occupational exposure, as dose dependent, often older
How does Pneumoconiosis present?
Slowly increasing SOB, often picked up on CXR
What is sarcoid/sarcoidosis?
A condition where inflamed cells clump together to make small lumps called granulomas.
Multisystem granulomatous disease that most commonly involves lymph nodes and lungs
What do granulomas cause in sarcoid?
Scarring; affects lung compliance and gas exchange
Epidemiology of sarcoid?
All ages (20-60 most common), both genders, all round world, more in non-smokers, more in those of African or Northern European descent
Trigger of sarcoid?
Granulomatous inflammation leads to fibrosis (idiopathic)
Is sarcoid more common in smokers or non-smokers?
Non-smokers
What morphological abnormalities are present in sarcoid?
Non-caseating granulomas in multiple sites, often accompanied by scarring
How does sarcoid typically present?
Nodal enlargement (esp mediastinal) , respiratory symptoms (cough, SOB), constitutional symptoms (fever, fatigue, weight loss, sweats)
What is Hypersensitivity Pneumonitis (HP)?
Inflammatory and fibrotic bronchiolar response to inhaled antigens leads to hypersensitivity response to antigen in wall of bronchioles. This inflammation triggering fibrosis if antigen not removed.
Effect on interstitium in HP?
Interstitium widened by inflammatory infiltrate
What are examples of inhaled antigens in HP?
mold (eg in hay - farmer’s lung), animal faeces (eg bird fanciers lung), paint fumes, etc
What morphological abnormalities are present in HP?
Chronic inflammation around bronchioles spilling out into interstitium, sometimes accompanied by interstitial fibrosis
Clinical presentation of HP?
Respiratory symptoms (cough, SOB), constitutional symptoms (fever, fatigue, weight loss, sweats)
What is cystic fibrosis?
Disease from abnormally thickened mucus caused by chloride channel recessive gene abnormality
How many people carry defective genes in UK for CF?
1 in 25 (common)
Pathogenesis behind CF?
Reduced sodium and chloride in lumen of: respiratory tract, GI tract (inc ducts in pancreas and liver) and seminiferous tubules. This causes dehydrated mucus which is thicker and blocks the lumina, also predisposing to infections, inflammation and scarring.
What morphological abnormalities are present in CF?
- Lungs (often the most life threatening complication) – infections, bronchitis and bronchiectasis
- Pancreas – exocrine atrophy and fibrosis, small intestine in infants – blockage (meconium ileus)
- Liver – bile canalicular blockage can lead to cirrhosis
- Seminiferous tubules – 95% males infertile
What do the clinical features of CF depend on?
Depends on predominant organ involvement - Respiratory and exocrine pancreas often most prominent
What can pancreatic insufficiency in CF lead to?
Malabsorption
In this slice of lung, what do you see?
Emphysema (lost lots of alveolar walls), fibrosis, scarring
3 - smooth muscle contraction, airway swelling and luminal mucus production triggered by histamine release
What is number 1, 2, 3 and 4?
1 - bronchiectasis
2 - cigarette smoke leading to emphysema
3 - asthma
4 - CF
2 - CF
What is 1, 2, 3 and 4?
1 - cigarette smoking leading to bronchitis
2 - CF
3 - sarcoidosis
4 - asthma or HP
Loss of alveolar walls leading to enlarged airspaces; emphysema
This is one part of COPD, so bronchitis is most likely to accompany.
3 - inflammation, mucus hypersecretion in the bronchi and bronchioles
What is 1, 2, 3 and 4?
1 - bronchiectasis
2 - sarcoid
3 - bronchitis
4 - asthma
Are you more prone to cor pulmonale if your COPD is predominated by emphysema or chronic bronchitis?
Chronic bronchitis
morphological change of heart in chronic bronchitis vs emphysema?
Chronic bronchitis; prominent vessels and large heart
Emphysema; small heart (and hyperinflated lungs)
Describe cough in emphysema vs chronic bronchitis
Emphysema; late, scanty sputum
Chronic bronchitis; early in disease, copious sputum
What is the main difference in symptoms between chronic bronchitis and emphysema?
The main difference between these conditions is that chronic bronchitis produces a frequent cough with mucus. The main symptom of emphysema is shortness of breath.
