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Anatomical Pathology > obstructive and restrictive > Flashcards

obstructive and restrictive Flashcards

1
Q

Obstructive lung diseases

A

Characterized by increase in resistance to airflow

• FEV1/FVC ratio of less than 0.7 – Reduced FEV1

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2
Q

Restrictive diseases

A

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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3
Q

four major types of emphysema

A

Centriacinar
• Panacinar
• Paraseptal
• Irregular

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4
Q

Emphysema

• Definition:

A

Irreversible enlargement of the airspaces distal to the terminal bronchiole
• accompanied by destruction of their walls.

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5
Q

Centriacinar

A

Most common form
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 –

A

volves 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

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7
Q

Panacinar

A

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

Emphysema

• Pathogenesis

A

Toxic injury and inflammation
Protease-antiprotease imbalance
Oxidative stress
Infection

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9
Q

Emphysema

• Gross morphology

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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10
Q

Emphysema

• Microscopy

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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11
Q

Emphysema

• Clinical features

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

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12
Q

Emphysema

• Treatment

A

Smoking cessation

  1. Oxygen therapy
  2. Long-acting bronchodilators
  3. Inhaled corticosteroids
  4. Physical therapy
  5. Bullectomy
  6. Lung volume reduction surgery
  7. Lung transplantation
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13
Q

Chronic Bronchitis

• Definition

A

Persistent, productive cough ≥ 3 months ≥ 2 consecutive years in the absence of any other
identifiable cause

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14
Q

Chronic Bronchitis

• Pathogenesis

A
  1. Mucus hypersecretion
  2. Acquired (CFTR) dysfunction
  3. Inflammation
  4. Infection
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15
Q

Chronic Bronchitis

• Gross morphology

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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16
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
17
Q

Chronic Bronchitis

• Cardinal symptoms:

A 
Persistent cough
• Productive of sputum
• Dyspnoea on exertion
• Hypercapnia, hypoxemia, mild cyanosis
•
“Blue bloaters
18
Q

Asthma

• Definition

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

19
Q

Asthma Classification

A 
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
20
Q

Asthma

• Pathogenesis

A

Th2 Responses, IgE, and Inflammation
• 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

Sensitization and activation of Mast Cells
• 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

21
Q

Status asthmaticus

A

Unremitting asthmatic attack
• Lungs are distended by over inflation
• Small areas of atelectasis
• Most striking: occlusion of bronchi and bronchioles by thick mucus plugs

22
Q

Asthma

• Sputum

A

Curschmann spirals
Numerous eosinophils
Charcot-Leyden crystals

23
Q

Asthma

• Clinical features

A

Chest tightness, dyspnea, wheezing, coughing (+/- sputum)
• Classic attack - several hours
• Status asthmaticus – days or even weeks
• Between the attacks, patients may be virtually asymptomatic

24
Q

Bronchiectasis

• Definition

A

disorder in which destruction of smooth muscle and elastic tissue by chronic
necrotising infections leads to permanent dilation of bronchi and bronchioles

25
Q

Bronchiectasis

• Pathogenesis

A

Obstruction and infection

26
Q

Bronchiectasis Morphology – Gross

A

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

27
Q

Bronchiectasis

• Microscopy

A

• 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

28
Q

Bronchiectasis cardinal symptoms

A 
Sever persistent cough
• Foul smelling, sometimes bloody, sputum
• Dyspnoea and orthopnea in severe cases
• Hemoptysis – may be massive
• Exacerbated by URTI
29
Q

Restrictive lung diseases

• Clinical features

A 
Progressive dyspnoea
• Dry cough
• Clubbing
• Fatigue and weight loss
• Progress to respiratory failure in 5years
30
Q

• Pneumoconiosis

A

non-neoplastic lung reaction to inhalation of mineral dusts encountered in the workplace, now also includes disease induced
by chemical fumes and vapors

31
Q

Factors that influence the development of dust-borne pneumoconiosis

A

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

32
Q

Silicosis

A

Inhalation of pro-inflammatory crystalline silicon dioxide (silica)

33
Q

Asbestosis

A

Inhalation of pro-inflammatory crystalline hydrated silicates that are associated with pulmonary
fibrosis and various forms of cancer – activation of inflammasome

Anatomical Pathology (13 decks)

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