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Anatomical pathology > OBSTRUCTIVE/RESTRICTIVE DISEASE > Flashcards

OBSTRUCTIVE/RESTRICTIVE DISEASE Flashcards

1
Q

Obstructive and Restrictive Lung Diseases

A
  • Chronic non-infectious diffuse pulmonary diseases
  • Diagnosis is based primarily on pulmonary function tests
  • Patients commonly have overlapping features

Obstructive lung diseases
• Characterized by increase in resistance to airflow
• FEV1/FVC ratio of less than 0.7 – Reduced FEV1
• Due to partial or complete obstruction of the airway
• From the trachea to the terminal and respiratory bronchioles

Restrictive diseases
• Characterised by reduced expansion of lung parenchyma and decreased total lung capacity (TLC)
• FEV1/FVC ratio remains normal – Both FEV1 and FVC reduced

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2
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

A
  • Risk factors
  • Discuss common chronic obstructive lung disease, asthma and bronchiectasis
  • Underlying pulmonary pathology of two major Clinicopathologic manifestations
  • Chronic bronchitis and Emphysema.
  • Discuss four major types of emphysema
  • Define and discuss chronic bronchitis
  • Asthma
  • Definition
  • Pathology – pathogenesis, morphological findings
  • Bronchiectasis
  • Pathogenesis and morphological features
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3
Q

obstructive lung disease

A

• Definition (World Health Organisation)
• A common, preventable and treatable disease that is characterized by persistent
respiratory symptoms and airflow limitation that is due to airway and/or alveolar
abnormalities caused by exposure to noxious particles or gases.
• Common obstructive lung diseases
• Emphysema, chronic bronchitis, asthma, and bronchiectasis
• Chronic obstructive pulmonary disease (COPD)
• Chronic bronchitis and Emphysema
• RF - Cigarette smoking

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4
Q

Emphysema

A
  • Irreversible enlargement of the airspaces distal to the terminal bronchiole
  • accompanied by destruction of their walls.
  • Classification – Major subtypes
  • Centriacinar
  • Panacinar
  • Paraseptal
  • Irregular
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5
Q

CENTRIACINAR EMPHYSEMA

A

Emphysema
• Centriacinar
• Most common form - >95% of cases
• Pronounced in the upper lobes - apical segments
• Involves proximal parts of the acini (Respiratory bronchioles) and spares distal
parts (Alveoli)
• Both normal and emphysematous air spaces exist in same acinus
• Severe disease involve distal parts (alveoli) and resemble Panacinar emphysema

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6
Q

• Paraseptal EMPHYSEMA

A

• Involves distal part of acinus (Alveoli), proximal portion is normal (Terminal bronchiole)

  • Severe in the upper half of the lungs
  • More striking adjacent to pleura, septa, and margins of lobules
  • Complication
  • Occurs adjacent to areas of fibrosis, scarring, atelectasis
  • Cause of pneumothorax in young adults

• Characterised by enlarged air spaces ranging from 0.5-2.0cm

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7
Q

• Panacinar EMPHYSEMA

A
  • RF - α1-antitrypsin deficiency
  • Acini are uniformly enlarged from respiratory bronchiole to terminal blind alveoli
  • Affects lower zones and anterior margins of lung
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8
Q

Irregular emphysema

A
  • Airspace enlargement with fibrosis (irregular emphysema)
  • Irregularly involvement of acinar parts
  • Associated with scarring
  • Usually clinically insignificant
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9
Q

pathogenesis of emphysema

A

-Toxic injury and inflammation
• Damage to respiratory epithelium  Inflammation → variable degrees of parenchymal destruction

-Protease-antiprotease imbalance
• Relative deficiency of protective antiproteases → Breakdown of connective tissue components by Proteases

-Oxidative stress
• Oxidants → Tissue damage, endothelial dysfunction and inflammation
-
Infection
• exacerbation of existing disease
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10
Q

Gross morphology of emphysema

A
  • Voluminous lungs that overlap heart in the chest cavity
  • Usually, the upper 2/3 are more involved
  • Apical bullae may be present.
  • Cut surface
  • Large alveolar spaces are seen
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11
Q

Microscopy of Emphysema

A
  • Abnormally large alveoli separated by thin septa with focal Centriacinar fibrosis.
  • Dilated pores of Kohn
  • Club shaped septa
  • Small airway inflammation
  • Inflammatory infiltrates in bronchial walls
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12
Q

clinical feautures of emphysema

A

• Barrel-chest
• Dyspnoea
• Impaired expiratory airflow is the key to diagnosis
-Prolonged expiration
-Often referred to as “Pink puffers”
=Patients sits forward in hunched-over position and breathes through pursed lips - Puffer
=Blood-gas values relatively normal at rest as the patient over-ventilate to remain oxygenated - Pink

• Poor prognosis with development of Cor-pulmonale
-Congestive heart failure and secondary pulmonary hypertension

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13
Q

Treatment of emphysema

A
  1. Smoking cessation
  2. Oxygen therapy
  3. Long-acting bronchodilators
  4. Inhaled corticosteroids
  5. Physical therapy
  6. Bullectomy
  7. Lung volume reduction surgery
  8. Lung transplantation
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14
Q

Other conditions associated with lung over inflation

A

• Compensatory hyperinflation
-dilation of alveoli in response to loss of lung substance elsewhere
• Obstructive over inflation
- air trapping leading to hyperinflation – foreign body
• Bullous emphysema
-large sub pleural bullae ≥ 1 cm
• Interstitial emphysema
-entrance of air into the connective tissue stroma of the lung,
mediastinum, or subcutaneous tissues

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15
Q

Chronic Bronchitis

A

• Persistent, productive cough ≥ 3 months ≥ 2 consecutive years in the absence of any other
identifiable cause
• Common in habitual smokers / smog-laden cities

Major risk factor
• Cigarette smoke
• Damages epithelium
• Chronic inflammation
• Interferes with muco-ciliary action of the respiratory epithelium
• Prevents clearance of mucus → increasing the risk of infection

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16
Q

Pathogenesis of chronic bronchitis

A
  1. Mucus hypersecretion
  2. Acquired (CFTR) dysfunction
  3. Inflammation
  4. Infection
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17
Q

Gross morphology of bronchitis

A
  • Hyperemia, swelling and oedema of mucous membranes
  • Associated mucinous or mucopurulent secretions
  • May see casts of mucus and exudate in airways
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18
Q

Chronic Bronchitis

• Microscopy

A
  • Characteristic microscopic features
  • Chronic inflammation of the airways
  • Thickened bronchiolar wall
  • smooth muscle hypertrophy
  • Deposition of extracellular matrix in the muscle layer
  • Peri-bronchial fibrosis

• Goblet cell hyperplasia
• Enlargement of the mucus-secreting glands of the trachea and bronchi.
• Increase in the size of the mucous glands
• Assessed by Reid index - normally = 0.4
» the ratio of the thickness of the mucous gland layer to the thickness of the wall
between the epithelium and the cartilage .
• Narrowing of bronchioles → bronchiolitis obliterans.
• Squamous metaplasia - dysplasia

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19
Q

cardinal symptoms of Chronic Bronchitis

A
  • Persistent cough
  • Productive of sputum
  • Dyspnoea on exertion
  • Hypercapnia, hypoxemia, mild cyanosis

“Blue bloaters”
• Accelerate decline in lung function
• Cor pulmonale and heart failure

20
Q

differences between bronchitis and emphysema

A

Bronchitis

Age:40-45
Dyspnea: Mild; late
Cough: Early, copious sputum
infections: Common
respiratory insufficiency; Early periodic
Cor pulmonale: Common
airway resistance: Increased
Elastic recoil: Normal
chest radiograph: Prominent vessels, large heart size
Appearance: Blue bloater
Emphysema
Age:50-75
Dyspnea: Severe; early
Cough: Late; scanty sputum
Infections; Occasional
respiratory insufficiency: End-stage
Cor pulmonale: Uncommon, End-stage
Airway resistance: Normal or slightly
increased
Elastic recoil: Low
Chest radiograph: Hyperinflation; normal heart size
Appearance: Pink puffer
21
Q

asthma

A

• Heterogenous disorder of the conducting airways usually caused by an immunological process marked by episodic bronchoconstriction, inflammation of the bronchial walls; and increased mucus secretion

• Classification
 -Atopic
• IgE-mediated (type I) hypersensitivity reaction
• Onset - childhood
• Triggered by environmental allergens

-Non-atopic
•No evidence of allergen sensitization

-Drug induced
• Aspirin-sensitive asthma

-Occupational

22
Q

pathogenesis of asthma(Th2 Responses, IgE, and Inflammation)

A

• Presentation of antigen to naïve CD4+ helper T cells

-IL-4
• Stimulates class switching to IgE and promotes the development of additional Th2 cells
  • IL-5
    • Development and activation of eosinophils

-IL-13
• Enhances IgE production
• Stimulate mucus secretion by epithelial cells

23
Q

Pathogenesis of Asthma (Sensitization and activation of Mast Cells)

A
  • Activated by high-affinity IgE Fc receptors
  • Release of mediators by mast cell (degranulation)
  • Vasoactive amines. – histamine
    » Smooth muscle contraction
    » Increases vascular permeability
    » Mucus secretion.
  • Enzymes – Proteases (Chymase/Tryptase)
    » tissue damage
  • Proteoglycans – heparin and chondroitin sulphate
    » package and store the amines
24
Q

Pathogenesis of asthma (Sensitization and activation of Mast Cells)

A

• Lipid mediators
- Leukotrienes
» Leukotrienes C4 and D4 are vasoactive and spasmogenic,
» Leukotriene B4 is highly chemotactic for neutrophils, eosinophils, and monocytes.

  • Prostaglandin D2.
    » Causes intense bronchospasm and mucus hypersecretion secretion.

-Platelet-activating factor (PAF)
» causes platelet aggregation, histamine release, bronchospasm, increased vascular permeability, and vasodilation

25
Status asthmaticus
* Unremitting asthmatic attack * Lungs are distended by over inflation * Small areas of atelectasis * Most striking: occlusion of bronchi and bronchioles by thick mucus plugs
26
Sputum(of asthma)
* Curschmann spirals * Extrusion of mucus plugs from mucous glands * Numerous eosinophils * Charcot-Leyden crystals * Composed of eosinophil protein galectin-10
27
Asthma | • Microscopy - Airway remodeling
1. Thickening of airway wall 2. Sub-basement membrane fibrosis 3. Increased vascularity 4. Increase in size of submucosal glands 5. Increase in number of airway goblet cells 6. Hypertrophy + hyperplasia of bronchial smooth muscle
28
Asthma | Clinical features
* Chest tightness, dyspnea, wheezing, coughing (+/- sputum) * Classic attack - several hours * Status asthmaticus – days or even weeks * Between the attacks, patients may be virtually asymptomatic
29
Bronchiecstasis
• Bronchiectasis is a disorder in which destruction of smooth muscle and elastic tissue by chronic necrotising infections leads to permanent dilation of bronchi and bronchioles • Associated with • Congenital or hereditary conditions that predispose to chronic infections (cystic fibrosis), immunodeficiency states, primary ciliary dyskinesia, and Kartagener syndrome. • Severe necrotizing pneumonia • Bronchial obstruction • Immune disorders • idiopathic
30
pathogenesis of bronchiecstasis
Obstruction and infection
31
Gross Morphology of bronchiecstasis
* Affects lower lobes bilaterally * May be diffuse or localised * Dilated airways – up to 4x in size * Bronchi can be followed to pleural surface * Bronchi appear cystic and are filled with mucopurulent secretions
32
Bronchiectasis | • Microscopy
• Acute and chronic inflammatory exudation • Desquamation of epithelial lining • Ulceration • Squamous metaplasia of the remaining epithelium • Necrosis destroys the bronchial or bronchiolar walls and forms a lung abscess • Fibrosis of the bronchial and bronchiolar walls
33
Exudation of bronchiecstasis
The bronchus has residual epithelium (Square) with necrotizing inflammation (Circle) with subsequent bronchial destruction, and inflammation extending into the adjacent lung parenchyma, characteristic of bronchiectasis
34
symptoms/signs of bronchiectasis
* Sever persistent cough * Foul smelling, sometimes bloody, sputum * Dyspnoea and orthopnea in severe cases * Hemoptysis – may be massive * Exacerbated by URTI
35
Restrictive lung diseases
• characterized by inflammation and fibrosis of the lung interstitium associated with pulmonary function studies indicative of restrictive lung disease. • Reduction in diffusion capacity, lung volume, and lung compliance • Chronic Diffuse Interstitial (Restrictive) Diseases • Chest wall disorders • Neuromuscular diseases such as poliomyelitis • Severe obesity • Pleural diseases • Kyphoscoliosis
36
• Chronic Diffuse Interstitial (Restrictive) Diseases
* Chronic interstitial and infiltrative diseases * Interstitial fibrosis of unknown etiology * Idiopathic Pulmonary Fibrosis * Nonspecific Interstitial Pneumonia * Cryptogenic Organizing Pneumonia * Pulmonary Involvement in Autoimmune Diseases * Pneumoconiosis
37
Idiopathic Pulmonary fibrosis (cryptogenic fibrosing alveolitis)
• progressive interstitial pulmonary fibrosis and respiratory failure * Pattern of lung injury – usual interstitial pneumonitis * Patchy  subpleural regions and lower lobes * Fibrosis in various stages of development * Variable inflammation
38
• Morphology of Idiopathic Pulmonary fibrosis (cryptogenic fibrosing alveolitis)
* Usual interstitial pneumonia (UIP) * Gross – Cobblestone pleural surface * Retraction of scars along the interlobular septa * Firm, rubbery white areas of fibrosis * Affects lower lobes, the sub pleural regions, and along the interlobular septa
39
microscopy of Idiopathic Pulmonery fibrosis (cryptogenic fibrosing alveolitis)
• Hallmark - patchy interstitial fibrosis of varying age and intensity » Early lesion – Hypercellular - fibroblastic foci » Late lesion – Hypocellular, dense fibrosis with destruction of alveolar architecture » Honeycomb fibrosis - formation of cystic spaces lined by hyperplastic type II pneumocytes or bronchiolar epithelium » Mild to moderate inflammation » Squamous metaplasia and smooth muscle hyperplasia » Pulmonary hypertension - intimal fibrosis and medial thickening » acute exacerbations - DAD
40
Restrictive lung diseases | Clinical features
* Progressive dyspnoea * Dry cough * Clubbing * Fatigue and weight loss * Progress to respiratory failure in 5years
41
Factors that influence the development of dust-borne pneumoconiosis
• Dust retention - dust concentration, duration of exposure, and effectiveness of clearance mechanisms • Particle size - dangerous particles are from 1 to 5 μm in diameter because they can reach the terminal small airways and air sacs • Particle solubility and cytotoxicity • Particle uptake by epithelial cells or egress across epithelial linings • Activation of the inflammasome which occurs following phagocytosis • Tobacco smoking, which worsens the effects of all inhaled mineral dusts, but particularly those caused by asbestos.
42
Pneumoconiosis
• non-neoplastic lung reaction to inhalation of mineral dusts encountered in the workplace, now also includes disease induced by chemical fumes and vapors
43
Coal Workers’ Pneumoconiosis
* Inhalation of coal particles * Anthracosis * Coal macules - 1 to 2 mm in diameter * if larger = Nodules. * Carbon-laden macrophages; * Delicate network of collagen fibers. * Located primarily adjacent to respiratory bronchioles
44
silicosis
Silicosis • Inhalation of pro-inflammatory crystalline silicon dioxide (silica) • Early stages - Small, barely palpable, discrete pale to blackened nodules in hilar lymph nodes and upper zones of the lungs. * Late stages - Hard, collagenous scars * Softening and cavitation - superimposed tuberculosis or to ischemia. * Hallmark lesion * Central area of whorled collagen fibers with a more peripheral zone of dust-laden macrophages * Examination of the nodules by polarized microscopy reveals weakly birefringent silicate particles
45
Asbestosis
Asbestosis • Inhalation of pro-inflammatory crystalline hydrated silicates that are associated with pulmonary fibrosis and various forms of cancer – activation of inflammasome Asbestosis • Diffuse pulmonary interstitial fibrosis • Presence of asbestos bodies • Golden brown, fusiform or beaded rods with a translucent center that consist of asbestos fibers coated with an iron-containing proteinaceous material • They arise when macrophages phagocytose asbestos fibers; the iron is derived from phagocyte ferritin • Similar iron-protein complexes called ferruginous bodies. * Early * Fibrosis around respiratory bronchioles * Late stages * Pleural plaques - Well-circumscribed plaques of dense collagen + calcified
46
Asbestos-related disease:
* Recurrent pleural effusion * Parenchymal interstitial fibrosis - asbestosis * Lung carcinoma * Mesothelioma * Laryngeal, ovarian neoplasms * Increased risks for systemic autoimmune diseases and cardiovascular disease

Anatomical pathology (13 decks)

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