Histopathology Respiratory Pathology 1 and 2 Flashcards Preview

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Flashcards in Histopathology Respiratory Pathology 1 and 2 Deck (89):
1

Microscopic structure of alveolar walls consist (from blood to air) of the following:

The capillary endothelium
The basement membrane
The alveolar epithelium

2

The alveolar epithelium

Type 1 pneumocytes – 95%
Type II pneuomocytes – secrete surfactant and rapidly replicate after injury.

3

The Pluera consists of

A double layer of fibrous connective tissue lined with mesothelial cells.

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Diseases due to immaturity →

• Hyaline membrane disease
• Bronchopulmonary dysplasia

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Hyaline Membrane Disease: Description

Complication of prematurity, less than 36 weeks gestation. Also associated with maternal diabetes, caesarean section, and amniotic fluid aspiration.

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Hyaline Membrane Disease:Due to

Deficiency of pulmonary surfactant (type II not developed).

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Hyaline Membrane Disease: Symptoms

Tachypnoea
Dyspnoaea
Develops within hours after birth followed by cyanosis

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Hyaline Membrane Disease:Histologically

There is diffuse alveolar damage with formation of hyaline membrane.
Alveoli lined by fibrosis with inflammatory cells – produce hyaline membrane.

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Hyaline Membrane Disease:Treatment

Oxygen
Surfactant
Artificial ventilation

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Hyaline Membrane Disease: Prognosis

If infant survives resolution follows within next few days

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Respiratory Infections → Types

Primary – with no underlying predisposing condition.
Secondary – when local or systemic defences are weakened

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Respiratory Infections → Secondary causes

Loss or suppression of cough reflex
Ciliary defects
Mucus disorders
Acquired or congenital hypogammaglobulinaemia - reduced antibodies
Immunosuppression
Pulmonary oedema with flooding of alveoli

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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

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Bronchitis Chronic

Is a clinical term defined as cough and sputum for 3 months in 2 consecutive years.

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Pneumonia: Definition

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

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Pneumonia: Clinical circumstances

Primary
Secondary

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Pneumonia: Aetiological Agent

Bacterial
Viral
Fungal
Others

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Pneumonia:Anatomical pattern

Lobar Pneumonia
Bronchopneumona

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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).

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Pulmonary Tuberculosis: Definition

It is a major cause of death globally. It’s incidence is again increasing. With increase in incidence of HIV disease.

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Pulmonary Tuberculosis: Caused by

M tuberculosis:
- Mycobacterium T hominis (human human transfer via air droplets)
- Mycobacterium T Bovis (unpastuerised milk)

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Pulmonary Tuberculosis: Types

Primary (1st occurrence)
Secondary (increased infection @ site of entry → lung)
Miliary (serious medically emergency – multiple seeds throughout body)

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Pulmonary Tuberculosis: Important features which differentiate TB from other infections

- Organisms
- Pathogenesis and histology
- Clinical features
- Investigations
- Treatment

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Pulmonary Tuberculosis: Staining

- Zihl neilson staining

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Pulmonary Tuberculosis: Culture

- 5/6 weeks to grow for TB v. different to other organisms

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Pulmonary Tuberculosis: Pathogenesis and histology

- Granuloma forms (inflammation)
- Neutrophillic exudate
- Histocytes and giant cell

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Pulmonary Tuberculosis: Clinical features

- Strep → high grade
- TB → low grade fever + night sweats
- Haemoptysis

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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

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Diseases of Vascular Organs: Types

Pulmonary congestion and oedema
Pulmonary embolism and infarction
Pulmonary Hypertension

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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.

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Congestion histology

Dilated in bloodstreams
RBC containing increased

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Oedema histology

Leakage of fluid into interstitium

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Two types of congestion and oedema

Hemodynamic oedema
Oedema due to micro-vascular injury (ARDs)

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Normal fluid exchange is regulated by following forces:

Hydrostatic pressure
Colloid osmotic pressure
Crystalloid osmotic pressure
Tissue tension

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Causes of hemodynamic oedema

Increased hydrostatic pressure
Decreased osmotic pressure
Lymphatic obstruction

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Increased hydrostatic pressure (back pressure from neins)

Left sided heart failure
Mitral stenosis
Volume overload
Pulmonary vein obstruction

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Decreased osmotic pressure (cant bring fluid back in)

Hypoalbuminaemia:
- Nephrotic syndrome
- Liver diseases
- Protein-losing enteropathy

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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
- Radiation

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Pulmonary Embolism and Infarction → Description

Occlusion of pulmonary artery is almost embolic in origin

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Pulmonary Embolism and Infarction → Consequences of pulmonary artery occlusion depends upon

- Size of the embolic mass
- General state of the circulation

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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.

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Tidal Volume (TV)

Amount of air inhaled/exhaled during each normal/quiet respiration.

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Vital capacity (VC)

Amount of air exhaled after maximum inspiration.

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Residual Volume (RV)

Amount of air left in lung after expiration.

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Total lung cancer capacity

Vital capacity and residual volume.

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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.

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Forced Expiratory Ratio (FEV1/VC)

Low in obstructive defects. Normal or high in restrictive defects.

48

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.

49

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.

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Pulmonary function tests

Reduced vital capacity (VC)
Normal or increased FEV1/VC ratio

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Chronic Bronchitis → Defined clinically as

Cough with sputum for at least 3 months in 2 consecutive years.

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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.

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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)

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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

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Chronic Bronchitis → Severe cases symptoms

• Hypercapnia
• Hypoxaemia
• Cyanosis
‘BLUE BLOATERS’

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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).

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Emphysema → 6 different types of emphysema

Centrilobular emphysema
Panlobular emphysema
Paraseptal emphysema
Irregular emphysema
Bullous emphysema
Interstitial emphysema

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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.

59

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.

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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.

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Emphysema → Paraseptal Emphysema

• It involves air spaces at the periphery of the lobules typically adjacent to the pleura. Upper lobes are most frequently involved.

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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.

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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.

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Interstitial Emphysema

• 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)

65

Bronchiectasis: Definition


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.

66

Bronchiectasis: Clinical manifestations

Cough
Fever and the expectoration of copious amounts of foul-smelling purulent sputum.

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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.

68

Bronchiectasis: Pathophysiology

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.

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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

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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.

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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.

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Bronchial Asthma: Mediated by a

Type 1 hypersensitivity reaction.

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Bronchial Asthma: Release of histamine and othe chemical mediators leads to

• Bronchoconstriction – causing wheezing, tachypnoea and dyspnoea
• Increased vascular permeability – oedema
• Mucus hyper-secretion

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Bronchial Asthma: Serum:

• IgE levels are raised

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Bronchial Asthma: Investigations

• Skin test with offending antigen results in an immediate wheel and flare reaction

76

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.

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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

78

Bronchial Asthma: Types

• Atopic
• Non-atopic
• Aspirin induced
• Occupational
• Allergic broncho-pulmonary aspergillosis

79

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%

80

Bronchogenic Carcinoma →Risk factors

Cigarette smoking
Abestos
Radiation
Oncogenes

81

Bronchogenic Carcinoma →Cigarette smoking

Increased risk of lung cancer
• Average smoker 10x increased risk
• Heavy smoker 20x increased risk

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Bronchogenic Carcinoma →Substances harmful in smoking

Polycyclic aromatic hydrocabons such as benzo(a)oyrene
Phenol derivative
Radioactive elements: polonium – 210, carbon-14

83

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.

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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.

85

Bronchogenic Carcinoma →Oncogenes

• C mymc in small cell carcinoma
• K-ras in adenocarcinoma

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Bronchogenic Carcinoma →Scarring

• Controvertial

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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.

88

Bronchogenic Carcinoma Paraneoplastic ectopic hormones

• ACTH and ADH from small cell carcinoma
• PTH from squamous cell carcinoma
• Finger-clubbing and hypertrophic pulmonary osteoarthropathy

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Bronchogenic Carcinoma Classification of lung Carcinoma

Squamous cell carcinoma
Adenocarcinoma
Bronchio-alveolar carcinoma
Large cell undifferentiated carcinoma
Neuroendocrine tumours:
• Carcinoid
• Atypical carcinoid
• Small cell carcinoma
• Large cell neuroendocrine carcinoma

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