Flashcards in Histopathology Respiratory Pathology 1 and 2 Deck (89):
Microscopic structure of alveolar walls consist (from blood to air) of the following:
The capillary endothelium
The basement membrane
The alveolar epithelium
The alveolar epithelium
Type 1 pneumocytes – 95%
Type II pneuomocytes – secrete surfactant and rapidly replicate after injury.
The Pluera consists of
A double layer of fibrous connective tissue lined with mesothelial cells.
Diseases due to immaturity →
• Hyaline membrane disease
• Bronchopulmonary dysplasia
Hyaline Membrane Disease: Description
Complication of prematurity, less than 36 weeks gestation. Also associated with maternal diabetes, caesarean section, and amniotic fluid aspiration.
Hyaline Membrane Disease:Due to
Deficiency of pulmonary surfactant (type II not developed).
Hyaline Membrane Disease: Symptoms
Develops within hours after birth followed by cyanosis
Hyaline Membrane Disease:Histologically
There is diffuse alveolar damage with formation of hyaline membrane.
Alveoli lined by fibrosis with inflammatory cells – produce hyaline membrane.
Hyaline Membrane Disease:Treatment
Hyaline Membrane Disease: Prognosis
If infant survives resolution follows within next few days
Respiratory Infections → Types
Primary – with no underlying predisposing condition.
Secondary – when local or systemic defences are weakened
Respiratory Infections → Secondary causes
Loss or suppression of cough reflex
Acquired or congenital hypogammaglobulinaemia - reduced antibodies
Pulmonary oedema with flooding of alveoli
Bronchitis Acute epi and causes
More severe in children (larygo-tracheo-bronchitis)
Usually causes by RSV.
Other causative agents include Haemophillia influenza and strept pneumonia
Is a clinical term defined as cough and sputum for 3 months in 2 consecutive years.
This is usually due to infection affecting lower air ways and can be classified according to various criteria
1. Clinical circumstances
2. Aetiological agent
3. Anatomical pattern
Pneumonia: Clinical circumstances
Pneumonia: Aetiological Agent
Pneumonia: Complications of pneumonia
- Abscess formation (type 3 pmneumococci and klebsiella) – collection of pus
- Empyema – neutrophillic exudate (can be seen in lung and gallbladder)
- Organisation of the exudate with fibrosis
- Bacteraemia dissemination to other organs e.g. heart valves causing metastatic abscess (transient presence of bacteria in blood).
Pulmonary Tuberculosis: Definition
It is a major cause of death globally. It’s incidence is again increasing. With increase in incidence of HIV disease.
Pulmonary Tuberculosis: Caused by
- Mycobacterium T hominis (human human transfer via air droplets)
- Mycobacterium T Bovis (unpastuerised milk)
Pulmonary Tuberculosis: Types
Primary (1st occurrence)
Secondary (increased infection @ site of entry → lung)
Miliary (serious medically emergency – multiple seeds throughout body)
Pulmonary Tuberculosis: Important features which differentiate TB from other infections
- Pathogenesis and histology
- Clinical features
Pulmonary Tuberculosis: Staining
- Zihl neilson staining
Pulmonary Tuberculosis: Culture
- 5/6 weeks to grow for TB v. different to other organisms
Pulmonary Tuberculosis: Pathogenesis and histology
- Granuloma forms (inflammation)
- Neutrophillic exudate
- Histocytes and giant cell
Pulmonary Tuberculosis: Clinical features
- Strep → high grade
- TB → low grade fever + night sweats
Pulmonary Tuberculosis: Investigations
- FBC –Increased WCC, increased neutrophils
- Culture – sensitivity (afp culture)
- Skin test – eve’s test (purified protein on skin – check sensitivity)
- TB immunisation
Diseases of Vascular Organs: Types
Pulmonary congestion and oedema
Pulmonary embolism and infarction
Pulmonary congestion and oedema
Oedema: accumulation of abnormal amounts of fluid in the intercellular tissues or body cavities.
Congestion: Increased volume of blood in an affected tissue or part.
Dilated in bloodstreams
RBC containing increased
Leakage of fluid into interstitium
Two types of congestion and oedema
Oedema due to micro-vascular injury (ARDs)
Normal fluid exchange is regulated by following forces:
Colloid osmotic pressure
Crystalloid osmotic pressure
Causes of hemodynamic oedema
Increased hydrostatic pressure
Decreased osmotic pressure
Increased hydrostatic pressure (back pressure from neins)
Left sided heart failure
Pulmonary vein obstruction
Decreased osmotic pressure (cant bring fluid back in)
- Nephrotic syndrome
- Liver diseases
- Protein-losing enteropathy
Oedema due to micro-vascular injury→ causes
- Infectious agents: viruses and Mycoplasma
- Inhaled toxins: O2, SO2, Smoke
- Liquid aspiration: gastric contents
- Drugs: Busulphan
- Shock, trauma and sepsis
Pulmonary Embolism and Infarction → Description
Occlusion of pulmonary artery is almost embolic in origin
Pulmonary Embolism and Infarction → Consequences of pulmonary artery occlusion depends upon
- Size of the embolic mass
- General state of the circulation
Pulmonary Embolism and Infarction → Smaller emboli and consequence
- In patients with heart diseases who have already impaired circulation produce infarction.
- In patients with adequate cardiovascular circulation the bronchial artery sustain the lung parenchyma and there is no infarction.
Tidal Volume (TV)
Amount of air inhaled/exhaled during each normal/quiet respiration.
Vital capacity (VC)
Amount of air exhaled after maximum inspiration.
Residual Volume (RV)
Amount of air left in lung after expiration.
Total lung cancer capacity
Vital capacity and residual volume.
Forced expiratory volume 1 in 1 Second (FEV1)
The maximum volume of air exhaled from the lungs within the 1st second after a previous maximum inspiration. Reduced with obstructed airways, pulmonary fibrosis or oedema, or muscle weakness.
Forced Expiratory Ratio (FEV1/VC)
Low in obstructive defects. Normal or high in restrictive defects.
Transfer Factor for Carbon Monoxide (TCO)
Air containing a known concentration of carbon monoxide is inhaled; the breath is held for 15 seconds and then exhaled. The amount of CO absorbed is a measure of pulmonary gas exchange. TCO is reduced in pulmonary fibrosis, oedema, embolism and anaemia.
Restrictive Airway Disease: characterised by
Reduced lung capacity – two groups
• Acute or chronic interstitial or infiltrative lung diseases e.g. ARDs, Pneumoconiosis (fibrosis of lung post exposure to particles e.g. asbestos
• Chest wall disorders e.g. poliomyelitis (resp muscle trunk), kyphoscoliosis, severe obesity and pleural diseases.
Pulmonary function tests
Reduced vital capacity (VC)
Normal or increased FEV1/VC ratio
Chronic Bronchitis → Defined clinically as
Cough with sputum for at least 3 months in 2 consecutive years.
Chronic Bronchitis → Two factors are important in the genesis of chronic bronchitis
Chronic irritation by inhaled substances: cigarette smoking
Microbiologic infection: H. influenza and strept. Pneumonia.
Chronic Bronchitis → Smoking predisposes to infection in different ways:
Interferes with ciliary action of the respiratory epithelium
Causes direct damage to airway epithelium
Inhibits the ability of bronchial and alveolar leukocytes to clear bacteria (macrophages can’t phagocytose)
Chronic Bronchitis → Pathogenesis
• Respiratory bronchitis affecting airways of less than 2mm
• Leads to destruction of the wall and surrounding parenchymal elastin with the development of centri-lobular emphysems
• Hyper-secretion of mucus secondary to hypertrophy of submucosal glands in bronchi and increased number of goblet cells of small airways
Chronic Bronchitis → Severe cases symptoms
Emphysema → Description
This is an anatomical term defined as permanenet enlargement of airspaces distal to the terminal bronchioles together with destruction of their walls (hyperinflation if no destruction).
Emphysema → 6 different types of emphysema
Emphysema → Centrilobular Emphysema
• Mostly seen in heavy cigarette smokers
• It involves respiratory bronchioles (central part of lobules) particularly of upper lobes.
• Dust laden macrophages are seen in the wall with inflammation around bronchi and bronchioles.
Emphysema →Panlobular Emphysema
• Mostly seen in patients with α1 antitrypsin deficiency: acute phase serum protein which inhibitis the action sof collagenase, elastase and other proteases (secreted by dying macrophages and macrophages).
• It involves all air spaces distal to the terminal bronchioles particularly in lower lobes.
Emphysema → α1 antitrypsin deficiency:
• Death: alveolar macrophages → contain lysosomal bags with enzymes when macrophages die, the enzymes are released in alveoli. Normally α1 antitrypsin neutralises those enzymes to prevent damage from enzymes to alveoli.
Emphysema → Paraseptal Emphysema
• It involves air spaces at the periphery of the lobules typically adjacent to the pleura. Upper lobes are most frequently involved.
Emphysema → Irregular Emphysema
• It irregularly involves the respiratory acinus.
• Commonly seen around old healed scars at lung apices therefore pathogenesis thought o be air trapping caused by fibrosis.
Emphysema → Bullous emphysema
• Not a separate category but refers to the presence of balloon-like foci of emphysema over 10mm in diameter
→ Spontaneous pneumothorax (young adult male with isolated bullous burst causing a collapse.
• This is inflation of the interstitium of the lung by air, commonly due to traumatic rupture of an airway. It may extend into the mediastinum or sub-cutis.
• → air present in the soft tissues (surgical emergency)
This is a chronic necrotizing infection of the bronchi and bronchioles leading to, or associated with, abnormal and permanent dilation of these airways, particularly in lower lobes.
Bronchiectasis: Clinical manifestations
Fever and the expectoration of copious amounts of foul-smelling purulent sputum.
Bronchiectasis: Develops in association with following conditions
- Bronchial obstruction due to tumour or foreign body
- Congenital or hereditary condition e.g. cystic fibrosis and immobile cilia and Kartagener’s syndrome
- Necrotizing pneumonia.
There is dilation of bronchi and bronchioles with inflammatory infiltration especially polymorphs during acute exacerbation. The inflammation and associated fibrosis extends into the adjacent lung tissue.
Bronchial Asthma: Definition
Is a disease characterised by hyperactive airways leading to episodic, reversible bronchoconstriction, owing to increased responsiveness of the trachea-bronchial tree to various stimuli.
→ Transient constriction of bronchioles: Type 1 hypersensitivity (Ige) – mast cells
Bronchial Asthma: Hypersensitivity
Mast cells (FC) receptors of mast cells – release histamine (vasodilation, bronchoconstriction).
The next time the body recognises the antigens: antigen-antibody reaction takes place.
Bronchial Asthma: Epi
Begins in childhood
Triggered by – a variety of environmental agents including dust, pollens, food and animal dander.
Often a family history of atopy.
Bronchial Asthma: Mediated by a
Type 1 hypersensitivity reaction.
Bronchial Asthma: Release of histamine and othe chemical mediators leads to
• Bronchoconstriction – causing wheezing, tachypnoea and dyspnoea
• Increased vascular permeability – oedema
• Mucus hyper-secretion
Bronchial Asthma: Serum:
• IgE levels are raised
Bronchial Asthma: Investigations
• Skin test with offending antigen results in an immediate wheel and flare reaction
Bronchial Asthma: Symptoms
• Rarely symptoms persist for days (status asthamaticus) leading to respiratory failure and even death.
• Grossly the lungs are overdistended; bronchi and bronchioles are occluded by mucus plugs.
Bronchial Asthma: Pathophysiology
• Mucus plgus contains crushmann spirals (whorls of shed epithelium), large number of eosinophils and charcot – leyden crystals.
• Mucus glands hypertrophy
• Thickening of BM
Bronchial Asthma: Types
• Aspirin induced
• Allergic broncho-pulmonary aspergillosis
Bronchogenic Carcinoma →Epi
One of the commonest malignancies
Accounts for one third of all cancer deaths in males
Occurs between ages 40-70 years
Overall 5 year survival rate is 4-7%
Bronchogenic Carcinoma →Risk factors
Bronchogenic Carcinoma →Cigarette smoking
Increased risk of lung cancer
• Average smoker 10x increased risk
• Heavy smoker 20x increased risk
Bronchogenic Carcinoma →Substances harmful in smoking
Polycyclic aromatic hydrocabons such as benzo(a)oyrene
Radioactive elements: polonium – 210, carbon-14
Bronchogenic Carcinoma →Asbestos
• Lung cancer is the most frequent malignancy in persons exposed to asbestos
• Abestos workers who do not smoke have a five times increased risk and those who smokes have a 50-90 times greater risk of developing lung cancer.
• Among asbestos workers one death in five is due to lung cancer and one death in ten is due to mesothelioma
• A latent period of 20 years between exposure and development of cancer.
Bronchogenic Carcinoma → Radiation
• Increased incidence of lung cancer among survivors of the Haroshima and Nagaski atomic bombs blasts.
• Lung cancer rates among non-smoking uranium minor is four times higher than those of general population.
• Exposure to radon gas is also linked to increased lung cancer risk.
Bronchogenic Carcinoma →Oncogenes
• C mymc in small cell carcinoma
• K-ras in adenocarcinoma
Bronchogenic Carcinoma →Scarring
Bronchogenic Carcinoma →Clinical Features
• Weight loss, cough and haemophtysis are common presenting features.
• Patients may present with metastisi and common sites include lymph node, bone, brain, liver and adrenals.
• Paraneoplsatic effects are common and are due to ectopic hormones.
Bronchogenic Carcinoma Paraneoplastic ectopic hormones
• ACTH and ADH from small cell carcinoma
• PTH from squamous cell carcinoma
• Finger-clubbing and hypertrophic pulmonary osteoarthropathy