Obstructive Lung Disease Flashcards

1
Q

What are obstructive lung diseases? List examples.

A

Airway diseases leading to outflow obstruction.

E.g. emphysema, chronic bronchitis, asthma, bronchiectasis

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2
Q

What makes up COPD?

A

Emphysema
Chronic bronchitis
- permanent and coexist = grouped together to make COPD

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3
Q

Is asthma reversible?

A

Initially yes, but chronic irreversible obstruction can eventually occur

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4
Q

What is bronchiectasis?

A

Permanent dilation of the bronchi due to destruction of their walls

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5
Q

What happens in emphysema?

A

Destruction of the air spaces distal to the terminal bronchioles
Irreversible enlargement

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6
Q

What is the most common form of emphysema?

A

Centriacinar emphysema - respiratory bronchioles are affected but distal alveoli remain normal

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7
Q

What is the appearance of centriacinar emphysema?

A

Holes in lung parenchyma = emphysematous airspaces (dilated respiratory bronchioles)

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8
Q

What is anthracosis?

A

Due to centriacinar emphysema.

Holes appear black due to the carbon pigment deposition seen in the lungs of smokers (tar in cigarette smoke)

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9
Q

What makes the centriacinar pattern?

A

Normal alveoli exist between the areas of emphysema

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10
Q

What is the pathogenesis behind emphysema?

A

Cigarette smoking and inhaled pollutants produce oxidants, causing an ongoing accumulation of inflammatory cells in the lungs.
Oxidants and proteolytic enzymes - proteases (mainly elastases) released from inflammatory cells destroy elastic tissue in airspaces’ walls.

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11
Q

What does smoking impair?

A

Activity of the alpha-1 antitrypsin (anti-protease)

Genetic predisposition to emphysema occurs in patients with alpha-1 antitrypsin deficiency

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12
Q

What type of emphysema do patients with an alpha-1 antitrypsin deficiency have?

A

Panacinar type of emphysema

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13
Q

What is bullous emphysema?

A

Several dilated airspaces become confluent (amalgamated) creating large bullae (bubbles)

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14
Q

What does emphysema show in a chest X-ray?

A

Hyperinflated chest

  • flattened diaphragm
  • inflation of apex above clavicle
  • horizontal orientation of ribs
  • decreased bronchovascular lung markings
  • overtaking of the heart shadow by opacity of hyperinflated lungs
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15
Q

What is the clinical picture of emphysema?

A

Obstruction to expiration due to loss of elastic recoil of airspaces (due to destruction of elastic fibres in the walls by elastases)
Airways collapse during expiration & patients purse their lips to prevent this from happening = pink puffers
Patient’s chests become hyperinflated due to air trapping “barrel chest”, develop dyspnoea
Advanced cases = right side heart failure “cor pulmonale”
Most have some degree of chronic bronchitis

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16
Q

What is chronic bronchitis?

A

Persistent cough with sputum production for at least 3 months in at 2 consecutive years

17
Q

What is the initiating factor for chronic bronchitis?

A

Noxious inhaled substances e.g. cigarette smoke (90% of patients are smokers)

18
Q

What happens to the bronchi in chronic bronchitis?

A

Mucus hypersecretion, inflammation, recurrent infections, fibrosis

19
Q

What can happen to patients with chronic bronchitis?

A

May become hypoxaemic and cyanosed (blue) & edema from right side heart failure = Blue bloaters

20
Q

What is the pathogenesis behind chronic bronchitis?

A

Chronic inflammation in bronchi and bronchioles
Metaplasia of surface lining epithelium (change into goblet cells or squamous epithelium)
Mucus hypersecretion = contributes to airway obstruction
Obstruction predisposes infection.
Smoking also interferes with movement of cilia & resp epithelium = preventing clearance of mucus and infective organisms

21
Q

Final thing to note for COPD:

A

Element of small airway disease exists - bronchioles show marked narrowing of their walls by inflammation and fibrosis
= chronic bronchiolitis
= contributes to obstruction in COPD

22
Q

What is asthma?

A

Reversible bronchoconstriction caused by a variety of stimuli

23
Q

Name the several types of asthma.

A

Atopic asthma (allergy induced)
Non-topic asthma (triggered by resp viral infections, air pollutants, cold, exercise)
Drug-induced asthma (NSAIDs)
Occupational asthma (inhalation of toxic industrial gases and fumes)

24
Q

Type I hypersensitivity

A

Introduction of allergen
Stimulates TH2 responses and IgE production
IgE binds to mast cells = secrete mediators responsible for inflammation

25
What type of hypersensitivity is atopic asthma?
Type I hypersensitivity
26
Describe the pathogenesis of Type I hypersensitivity in atopic asthma.
TH2 cells - release cytokines --> production of IgE, eosinophils, mucus production
27
What does cross linking of IgE onto mast cells lead to?
Leads to mast cell degranulation and release of performed mediators causing immediate phase reaction.
28
What occurs in the immediate phase reaction of atopic asthma?
Bronchoconstriction Increased vascular permeability --> bronchial wall oedema Mucus production and plugging of airways Leukocyte recruitment
29
What is the late phase of atopic asthma pathogenesis?
Marked by leukocyte recruitment - eosinophils, neutrophils and more lymphocytes Major basic protein produced by eosinophils damages the lining epithelium of the airways
30
Describe what happens in the airway remodeling in asthma.
Structural changes in bronchial walls Irreversible element of chronic obstruction - Basement membrane thickening - Hypertrophy/hyperplasia of bronchial smooth muscle - Hypertrophy of submucosal glands and hyperplasia of goblet cells lining the epithelium - Damage to the lining epithelium
31
What is seen in the Chest X-ray of someone with acute severe asthma.
Hyperinflated chest showing: - flattened diaphragm - inflation of apex above clavicle - horizontal orientation of ribs - normal heart shadow - preservation of lung markings (different from the lung in emphysema)
32
What is bronchiectasis?
Permanent dilation of the bronchi and bronchioles due to the destruction of their walls.
33
What causes bronchiectasis?
Repeated cycles of infection with subsequent destruction of the bronchial smooth muscles and elastic tissues and healing by fibrosis.
34
What is cystic fibrosis?
A genetic disorder of ion transport (Cl) that affects fluid secretion in the exocrine glands of the resp, gastrointestinal and reproductive tracts.
35
What is the mode of inheritance for CF?
Autosomal recessive
36
What is the primary defect in CF?
Abnormal function of an epithelial chloride channel encoded by CFTR gene on chromosome 7 - main manifestations stem from the defective chloride channel and its interactions with a neighbouring sodium channel
37
What happens to the mucus produced in the airways in those with CF?
Sodium is drawn out of mucus = thick, dehydrated, viscid and difficult to clear Thick mucus results in recurrent infections
38
Which individuals are likely to suffer from bronchiectasis?
Those with CF.