Bronchial asthma

Question 1

List clinical triad of bronchial asthma

Answer 1

Persistent wheezing
Chronic episodic dyspnoea
Chronic non-productive cough

Question 2

Explain when symptoms of bronchial asthma is worse and why?

Answer 2

Symptoms may be worse, or only present at nigh, due to the physiologic drop of cortisol secretion

Question 3

Classical symotom of asthma?

Answer 3

Nocturnal cough

Question 4

explain what happens in the eyes and nose of the asthmatic patient

Answer 4

Dark rings under the eyes (allergic shiners)
Dark transverse crease on the nose (allergic salute)

Question 5

A prolonged asthmatic attack whihc can be fatal

Answer 5

Status asthmaticus

Question 6

Epidemiology of allergic asthma

Answer 6

Occurs more frequently in children with strong familial tendencies

Question 7

Associatedconditions of allergic asthma

Answer 7

Patients may have hay fever or eczema

Question 8

Mechanism of allergic asthma

Answer 8

Typer 1 hypersensitivity reaction

Question 9

Causes of allergic asthma

Answer 9

Pollen, dust, drugs

Question 10

epidemiology of non-allergic asthma

Answer 10

Occurs more frequent in adults. family history or allergies

Question 11

Mechanism of non-allergic asthma

Answer 11

Not type 1 hypersensitivity reaction, IgE levels are normal

Question 12

causes of non-allergic asthma associated with what?

Answer 12

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

Question 13

Explain the gross appearance of asthma

Answer 13

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

Question 14

Explain the microscopic features of bronchial asthma

Answer 14

Bronchial asthma, microscopy
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).
Not present in pic : Charcot Leyden crystals, features of airway increased numbers of goblet cells

Question 15

list mediators invovled in pathogenesis of atopic asthma

Answer 15

Mediators: 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 16

what happen in early phase reaction of pathogenesis of atopic asthma

Answer 16

Early-phase reaction: Bronchoconstriction, increased mucus production, vasodilation, increased vascular permeability

Question 17

what happen in late phase reaction of pathogenesis pf atopic asthma

Answer 17

Late-phase reaction: Recruitment of leukocytes (eosinophils, neutrophils, more T cells e.g. Th17 cells that produce IL-17 to recruit neutrophils)

Question 18

Explain the Th2-mediated IgE response in pathogenesis of atopic asthma

Answer 18

Th2-mediated IgE response: 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