Robbins 9th ed - Chapter 15 - Pulmonary Oedema + Obstructive Airways (1)

Question 1

What is meant by Haemodynamic Pulmonary Oedema? What is its most common cause?

Answer 1

This is pulmonary oedema resulting from either increased hydrostatic pressure (e.g. left heart failure, most common cause), or reduced oncotic pressure. This is as opposed to pulmonary oedema due to microvascular injury / increased capillary permeability (e.g. sepsis).

Question 2

What are “heart-failure cells”?

Answer 2

Haemosiderin-laden macrophages

Question 3

How is pulmonary oedema different when it is caused by infection rather than by left heart failure?

Answer 3

If caused by infection/pneumonia, pulmonary oedema is due to microvascular injury and increased capillary permeability. This means that the fluid leaked out is exudate rather than transudate.

Question 4

What is a finding in RFTs of obstructive airways disease?

Answer 4

The FEV1 is reduced, and the FEV1/FVC ratio is less than 0.7, due to prolonged expiratory phase.

Question 5

Name five different obstructive airway diseases.

Answer 5

COPD (Chronic bronchitis, Emphysema), Asthma, Bronchiectasis, Bronchiolitis

Question 6

What are the major pathological changes of Chronic Bronchitis?

Answer 6

In the bronchus: Mucous gland hyperplasia + hypersecretion

Question 7

What are the major pathological changes in Asthma, during the acute phase of an attack?

Answer 7

Antigen binding to IgE-coated mast cells causes mediator release, which cause bronchospasm, oedema and mucous secretion.

Question 8

What are the major pathological changes in Emphysema?

Answer 8

In the acinus: Airspace enlargement, wall destruction

Question 9

What is a lobule? What is its size, and what is its relationship to the bronchopulmonary segment and to the acinus?

Answer 9

A bronchopulmonary segment contains thousands of lobules. A lobule is about 3-7mm in diameter. Each lobule is a cluster of acini. Each acinus is the collective group of airways distal to a single terminal bronchiole (an acinus is in the respiratory zone rather than the conducting zone).

Question 10

Is emphysema reversible or irreversible?

Answer 10

Irreversible.

Question 11

What is centriacinar emphysema?

Answer 11

Also called “centrilobular” emphysema, this is the most common form of emphysema (95% of clinically significant cases), whereby the wall destruction occurs in the respiratory bronchioles, and the distal alveoli are spared.

Question 12

Name three different processes that contribute to the destruction of alveolar walls, causing emphysema, in cigarette smokers.

Answer 12

1) Inflammatory mediators
2) Oxidative stress
3) Protease-antiprotease imbalance

Question 13

Why is emphysema called an OBSTRUCTIVE airways disease?

Answer 13

Emphysematous small airways do not have the normal elastic recoil in their walls. This means that they tend to collapse upon exhalation, and there is gas-trapping.

Question 14

What vascular changes can occur secondary to emphysema?

Answer 14

Pulmonary Hypertension and cor pulmonale (right heart failure).

Question 15

COPD involves which two major pathologies of airways?

Answer 15

Emphyesma and Chronic Bronchitis

Question 16

What is the clinical definition of chronic bronchitis?

Answer 16

Productive cough lasting at least three months and occurring in at least 2 consecutive years.

Question 17

Which tissue is hypertrophied in chronic bronchitis?

Answer 17

Submucosal glands become hypertrophied, and the Goblet cells increase in number. This results in hypersecretion of mucus.

Question 18

What are the pathological features that make chronic bronchitis an obstructive airways disease?

Answer 18

Mucus plugging, inflammation and fibrosis. These all cause narrowing of bronchioles.

Question 19

What is the predominant pathology in the airways of “Blue Bloaters”? And in “Pink Puffers”?

Answer 19

Blue bloaters = Chronic bronchitis (CO2 retainers)

Pink puffers = Emphysema (relatively normal blood gases at rest)

Question 20

What is the classic trigger in atopic asthma?

Answer 20

Environmental allergens that produce a wheal-and-flare reaction in the patient, such as pollen, dust mites, etc.

Question 21

What are the classic triggers in non-atopic asthma?

Answer 21

Viral infection, Cold air, Exercise.

Question 22

Which tissues become hypertrophied and hyperplastic in chronic atopic asthma?

Answer 22

Mucus glands become hypertrophied, smooth muscle proliferates.

Question 23

Name four immune cells involved in the immediate phase of the acute atopic asthma attack, and explain what they do.

Answer 23

1) TH2 cells detect the antigen on APCs, and trigger:
2) B-cells to produce IgE, which triggers:
3) Mast cells to release IL-5, which triggers:
4) Eosinophils to release their granular contents

Question 24

What happens in the late phase of an acute asthma attack?

Answer 24

A few hours after the immediate phase, the late phase involves persistent bronchospasm and oedema, neutrophil and monocyte and eosinophil infiltration, damage to the respiratory epithelium cause by inflammatory cells.

Question 25

What is bronchiolitis obliterans?

Answer 25

This is when the lumen of small airways becomes completely obliterated by fibrosis.

Question 26

What is a major morphologic feature of bronchiectasis?

Answer 26

There is significant dilation of the bronchi and bronchioles, caused by destruction of smooth muscle and elastic tissue, caused by chronic infections.

Question 27

What is the key difference between atopic asthma and non-atopic asthma, with regard to an investigation finding?

Answer 27

Non-atopic asthma shows no evidence of allergen sensitivity: skin testing is usually negative, and serum IgE levels are normal.