Resp path - Chronic bronchitis & asthma

Question 1

What is chronic bronchitis

Answer 1

persistent cough with sputum production for at least 3 months in at least 2 consecutive years, in the absence of any other identifiable cause

Question 2

Explain the pathogenesis of chronic bronchitis

Answer 2

Continual irritants (smoking, infection, pollution) to the lungs cause the airways to become swollen and inflamed.
Constant irritants leads to enlargement of the mucus-secreting glands of the bronchial tree, an increase in the number of goblet cells, which results in increased mucus secretion.
The smooth muscle in the airways becomes hypertrophied and narrows the bronchioles.
Extra mucus is produced to trap any irritants and prevent them entering the lungs.
The cilia become unable to cope with excessive secretions and therefore the mucus blocks the airways. This is known asReversible Airways Obstruction.
The mucus goes deeper into the lungs and becomes harder to clear.
Excessive secretions are predispose to infection.
The walls of the bronchioles become inflamed, continual inflammation causes gradual destruction of the bronchioles, resulting in fibrosis -Irreversible Airways Obstruction.
If the inflammation spreads to the blood vessels this will lead to capillary bed wall atrophy. This increases the pressure of the pulmonary circulation. Pulmonary arteries may become distended (stretched)and blood may back track into the right side of the heart resulting in right sided hypertrophy (enlargement)and heart failure. This is known asCor Pulmonale.

Question 3

What happens if the inflammation spreads to the blood vessels?

Answer 3

this will lead to capillary bed wall atrophy

Question 4

How does cor pulmonale start?

Answer 4

If the inflammation spreads to the blood vessels this will lead to capillary bed wall atrophy. This increases the pressure of the pulmonary circulation. Pulmonary arteries may become distended (stretched)and blood may back track into the right side of the heart resulting in right sided hypertrophy (enlargement)and heart failure. This is known asCor Pulmonale

Question 5

Microscopic features of chronic bronchitis

Answer 5

In the wall of this large bronchus is cartilage (♦) and the bronchial wall is expanded from increased size of mucus-secreting glands (∗) along with chronic inflammatory cell infiltrates (□) to expand the bronchial wall and promote airway obstruction.
At the right, above the respiratory epithelium, is increased mucus (✚) in the airway.

Question 6

how does chronic bronchitis look like grossly?

Answer 6

Hyperaemia, swelling and edema of mucous membranes, with excessive mucinous or mucopurulent secretions

Question 7

Histological changes in chronic bronchitis

Answer 7

Submucosal gland hypertrophy producing increased Reid index.
Chronic inflammation
Enlargement of mucus-secreting glands of * trachea and bronchi
Increased number of goblet cells
Squamous metaplasia and dysplasia of bronchial epithelium
Narrowing of bronchioles by mucous plugging, inflammation and Fibrosis
_/+bronchiolitis obliterans
Submucosal gland hypertrophy producing increased Reid index. The Reid index is the thickness of mucous glands in relation to thickness of the wall; in chronic bronchitis, it is > 0.40

Question 8

clinical findings of chronic bronchitis

Answer 8

Smoking history of >40yrs
-Mostly present with slowly increasing dyspnoea on exertion and chronic productive cough that is worse in the morning;):
-Patients adapt to hypoventilation with decreased oxygenation and hypercarbia, appear to be cyanotic with weight gain from peripheral oedema.

Question 9

complications of COPD

Answer 9

Complications of COPD=
Progressive lung dysfunction causing pulmonary hypertension, cor pulmonale, death due to heart failure.
Death due to acute respiratory failure from superimposed infections,
Fatal pneumothorax from rupture of subpleural blebs (in emphysematous patients)

Question 10

What is interstitial emphysema?

Answer 10

Air leaking from the lung causing clear air bubbles within the subcutaneous adipose tissue of the chest wall.
Entrance of air into the connective tissue of the lung, mediastinum, or subcutaneous tissue producesinterstitial emphysema.

Question 11

What increases the risk of pulmonary interstitial emphysema?

Answer 11

Trauma
Mechanical ventilation

Question 12

Clinical presentation of bronchial asthma

Answer 12

Classic clinical triad :persistent wheezing, chronic episodic dyspnoea, and chronic non-productive cough.
Symptoms may be worse, or only present at night, due to the physiologic drop in cortisol secretion.
Nocturnal cough, which may be the only symptom, is a classic symptom of asthma.
Dark rings under the eyes (“allergic shiners”) and
Dark transverse crease on the nose (“allergic salute”).
Status asthmaticus is a prolonged asthmatic attack, which can be fatal.

Question 13

Allergic asthma epidemiology

Answer 13

Occurs more frequently in children with strong familial tendencies.

Question 14

conditions associated with allergic asthma

Answer 14

Eczema
Hay fever

Question 15

Type of hypersensitivity of allergic asthma

Answer 15

type 1

Question 16

triggers of allergic asthma

Answer 16

Pollen, dust, drugs

Question 17

Non-allergic asthma epidemiology

Answer 17

Occurs more frequently in adults. No family history of allergies

Question 18

Mechanism of non-allergic asthma

Answer 18

Not type I hypersensitivity reaction; IgE levels are normal.

Question 19

causes of non-allergic asthma

Answer 19

viral infection(e.g., rhinovirus, parainfluenza)
Exercise,
cold air,
drugs,
gastroesophageal reflux,
Occupational asthma.
Cardiac asthma.

Question 20

Explain the Th2 mediated IgE response of atopic asthma

Answer 20

Exaggerated Th2 response to normally harmless environmental antigens, secreting cytokines (IL-4, IL-5 and IL-13) that promote inflammation (including eosinophil recruitment) and mucus secretion, as well as stimulating B cells to produce IgE antibodies that bind to Fc receptors on submucosal mast cells. Upon repeated allergen exposure, mast cell degranulation and production of cytokines and other mediators occurs, inducing the early-phase (immediate hypersensitivity) and late-phase reactions

Question 21

Distinguish between early and late phase rxn in asthma

Answer 21

Early-phase reaction: Bronchoconstriction, increased mucus production, vasodilation, increased vascular permeability
Late-phase reaction: Recruitment of leukocytes (eosinophils, neutrophils, more T cells e.g. Th17 cells that produce IL-17 to recruit neutrophils)

Question 22

Mediators that respond to pharmacologic interventions

Answer 22

Those that respond to pharmacologic intervention include leukotrienes C4, D4, E4, acetylcholine, IL-5, galectin-10 (forms Charcot-Leyden crystals that induce inflammation and mucus production).

Question 23

Gross appearance of bronchial asthma

Answer 23

Overinflated lungs with small areas of atelectasis,
Thick mucus plugs occluding bronchi and bronchioles

Question 24

Microscopic appearance of bronchial asthma

Answer 24

Between the bronchial cartilage (♦) on the right and the bronchial lumen (▪) filled with mucus on the left
Submucosa widened by smooth muscle hypertrophy (∗),oedema, and an inflammatory infiltrate with many eosinophils.(atopy).